Fitness Interface
Access to the world is mediated by evolved fitness interfaces, not guaranteed veridicality.
The reference library
Modern human suffering is, in many cases, accurate biological signaling in a mismatched environment - not disorder inside the individual. This library holds the work behind that claim, in the order the argument runs: what the organism needs, how those systems work, where the environment breaks the fit, how the inputs can be repaired, and the evidence under all of it.
Library snapshot as of 2026-08-11.
Need
The premises the framework builds on. Their canonical home is the locked stack, where the layers are laid out in order; this is a flat browse. Every code deep-links into its layer there.
Access to the world is mediated by evolved fitness interfaces, not guaranteed veridicality.
Motivational-emotional outputs are treated as prima facie informative about the organism's regulated conditions, by default. The signal is read as information about input conditions and current state, not as noise to be suppressed. This is a diagnostic default, not a presumption of veridicality (OF1 stands) and not a contraindication to symptom relief where indicated. The default is displaced by positive evidence of decoupling or direct physiological perturbation: developmental miscalibration carried forward, chronic dysregulation, acute organic disease or state shift (sleep deprivation, inflammation, endocrine perturbation, delirium), structural damage, and substance or medication effects.
Inclusive fitness - survival and reproduction - is the loss function of selection, not of the organism's runtime computation.
The organism contains evolved, domain-sensitive, interacting functional adaptations.
Modern environments often push these adaptations outside their expected or regulatable operating ranges.
Many aversive outputs are intelligible defensive signals under mismatch, not evidence of defective design.
Human regulation is constitutively socially scaffolded; social context is likely the highest-leverage cross-cutting input dimension.
Systems are recurrently coupled; perturbations propagate and can self-maintain across domains.
Proxy cues can activate systems without meeting the conditions that normally regulate or terminate them.
Defensive systems err toward over-activation under asymmetric error costs.
The architecture contains partially competing motivational programs and tradeoff structures.
The architecture calibrates to developmental and ongoing environmental input within evolved ranges.
Motivational programs have phylogenetically determined priority relations. Older, survival-critical systems can suppress or commandeer newer systems.
Mechanism resolution conditions are not fully interchangeable. Improvement in one mechanism can buffer or modulate consequences in another, especially where mechanisms are recurrently coupled (DA3), but cross-system buffering does not generally replace the specific resolution conditions of an impaired mechanism. Well-being is often bottlenecked by severe unresolved deficits in individual mechanisms and is not well described as a simple average across mechanism states.
Architecture parameters (drive gains, thresholds, calibration setpoints) vary between individuals within heritable ranges.
Chronic unresolved activation accumulates as allostatic load.
Markets can industrialize proxy exploitation of unmet regulatory needs.
Cortical override of subcortical activation is metabolically expensive, and chronic defensive activation downregulates the cortical override machinery itself. Interventions that change the organism's actual input conditions are therefore frequently more durable and less effort-dependent than interventions targeting cognitive override alone. The environment is a primary intervention layer for systemic and population-scale change, and is currently underweighted by major institutions. This does not preclude individual-level cognitive, pharmacological, or psychotherapeutic interventions where indicated; the claim is about default leverage and systemic design, not exclusivity or head-to-head comparative efficacy in individual cases.
Operate
Places where separate research traditions arrive at the same structure. That is harder to dismiss than any single study.
Natural selection operates on inclusive fitness - survival plus reproduction weighted by relatedness - establishing a single loss function that all evolved motivational architecture serves, as demonstrated independently by Darwinian selection theory, Hamilton's kin-selection formalism, and experimental altruistic-punishment findings that humans enforce cooperation at personal cost where inclusive-fitness logic predicts.
The human organism contains evolved, domain-sensitive, interacting functional adaptations rather than a general-purpose learner - supported independently by Tooby & Cosmides' design-principle derivation, Panksepp's conserved subcortical affective-motivational systems, and Bowlby's attachment-as-primary-motivational-system framework.
Modern post-agricultural, post-industrial environments push evolved adaptations outside their expected operating ranges in systematic and predictable ways - established independently by Eaton & Konner's discordance hypothesis, Li/van Vugt/Colarelli's mismatch-identification framework, Boyd & Richerson's gene-culture coevolution constraint (matched must include cultural scaffolding), and Henrich's WEIRD empirical diagnostic showing Western populations anchor the extreme end of the cross-cultural distribution.
The core affective-motivational systems (SEEKING, FEAR, RAGE, CARE, PANIC/GRIEF, PLAY, LUST) are anatomically and functionally conserved across mammals and extend into birds for specific systems - established independently by Panksepp's deep-brain-stimulation and cross-species neuroscience, Bowlby's attachment cross-mammalian homology, and Hrdy's cross-primate parental/alloparental evidence.
Human regulation is constitutively socially scaffolded: the organism's default expectation is proximity to trusted co-regulators, and this scaffolding is architectural rather than optional - established independently by Coan's Social Baseline Theory fMRI program, Bowlby's attachment theory, Hrdy's cooperative-breeding thesis, Dunbar's social-brain hypothesis, and Holt-Lunstad's mortality meta-analysis showing 50% survival advantage from strong social relationships.
Motivational pursuit ('wanting', mediated by mesolimbic dopamine) is dissociable from hedonic satisfaction ('liking'), creating an open-loop vulnerability where proxy cues can activate the SEEKING system without providing the conditions that normally terminate or resolve it - established independently by Berridge & Robinson's incentive-salience neuroscience, Tinbergen's supernormal-stimuli ethology, and Panksepp's SEEKING-circuit affective neuroscience.
Chronic or developmental adverse experiences cascade across physiological systems in a dose-response manner, with effects that propagate and self-maintain across domains (metabolic, immune, neural, behavioral) - established independently by Felitti's ACE Study clinical epidemiology, McEwen's allostatic-load neuroendocrinology, and Panksepp's cross-system inhibition evidence for affective-system propagation.
Defensive systems evolved under asymmetric error costs err reliably toward over-activation (false-positive) because the cost of missing a true threat historically exceeded the cost of reacting to a non-threat - established independently by Nesse's smoke-detector principle in evolutionary psychiatry, Haselton & Buss's Error Management Theory in evolutionary social psychology, and the Öhman/Mineka fear-module visual-attention program in cognitive neuroscience.
Chronic unresolved activation of stress-response systems produces cumulative physiological damage across multiple organ systems (allostatic load), reversible in part by environmental correction - established independently by McEwen's neuroendocrinology of allostasis and allostatic load, Felitti's ACE dose-response clinical epidemiology, and Sapolsky's primate stress physiology linking hierarchy type to cortisol and downstream pathology.
Threat detection and defensive response are mediated by phylogenetically ancient subcortical circuits (amygdala, periaqueductal gray, hypothalamus) that operate pre-attentively and can override cortical processing - established independently by Panksepp's FEAR-system neuroanatomy, the Öhman/Mineka backward-masking fear-module research program, and Nesse's clinical evolutionary psychiatry linking panic and anxiety to these defensive systems.
Humans have specialized architecture for reciprocal exchange, cheater detection, norm enforcement, and coalitional identity - supported independently by Fehr & Gächter's experimental altruistic-punishment findings, Boehm's reverse-dominance coalition dynamics in hunter-gatherer anthropology, and Tomasello's shared-intentionality comparative-cognition research.
Specific physiological and behavioral systems calibrate during specific developmental windows to environmental inputs within evolved parameters; inputs outside those parameters produce persistent miscalibration - established independently by Bowlby's attachment developmental calibration, McEwen's HPA-axis calibration neuroendocrinology, and Felitti's ACE Study dose-response evidence for durable effects of early-life exposure.
Many aversive psychological and physiological outputs (anxiety, low mood, pain, grief, fatigue, anger) are intelligible defensive signals produced by architecture that is functioning correctly in response to inputs outside its expected operating range - established independently by Nesse's 'good reasons for bad feelings' evolutionary psychiatry, Panksepp's affective neuroscience of conserved aversive systems, and Fehr & Gächter's finding that anger/moralistic outrage is the proximate mechanism for prosocial norm enforcement rather than a dysregulation.
Reproductive motivation (desire, attraction, pair-bonding) is a distinct architectural system independent of general-purpose pursuit, with sex-differentiated substrates and a characteristic proxy gradient from real partner to pure proxy - established independently by Panksepp's LUST-circuit affective neuroscience, Buss's sexual strategies theory and sex-differentiated mate preferences research, and Haselton/Buss's error-management prediction of sex-differentiated perceptual biases around mating cues.
Individual differences in human behavioral and psychological traits are substantially heritable in every adequately measured domain, established independently by twin designs (Polderman et al. 2015 meta-analysis of fifty years of twin studies: 17,804 traits from 2,748 publications, average reported heritability 49%), adoption and family designs (the Plomin program: significant genetic influence on all psychological traits with corroborating adoption evidence), and molecular SNP-heritability estimated from unrelated individuals (the Yang et al. 2010 GCTA line), with Turkheimer's three laws of behavior genetics as the canonical framing. Heritability is a population statistic under a given environment distribution, not individual determinism.
Operate
Empirical results that show the mechanism doing what the framework says it does. Each grounds specific mechanisms and foundations.
Cortisol reduced ~30-40% vs baseline
What it demonstrates. Hierarchy type (not the mere existence of hierarchy) determines pathology, and a troop's social culture is transmissible and reversible within a single generation without genetic turnover.
Sapolsky's long-studied olive baboon troop in Kenya had its most aggressive adult males eliminated by a tuberculosis outbreak circa 1983 (the aggressive males were the ones willing to forgo morning socializing to raid a tourist-lodge garbage dump and consumed tubercular meat). The surviving troop - skewed to a 2:1 female-to-male ratio and disproportionately unaggressive, affiliative males - developed a dramatically more peaceful social style: more grooming, more sitting in contact, minimal displacement aggression, lower baseline cortisol. As new males transferred in over subsequent years (males leaving their natal troops at puberty), they were absorbed into the troop and adopted its low-aggression high-affiliation style, despite having grown up in typical aggressive troops. The culture was being transmitted horizontally without genetic change. This is a natural experiment, not a randomized intervention, but its explanatory power for the possibility of environmental correction of hierarchy-driven pathology is substantial.
A Pacific Culture among Wild Baboons: Its Emergence and Transmission
All 40 captive chimps abnormal; none reported in wild
What it demonstrates. Aversive behavioral outputs in captive primates are a function of environmental mismatch rather than defective design: every one of the 40 captive chimpanzees studied showed at least one abnormal behavior, while no comparable abnormal repertoire has been reported in wild chimpanzees. Strongest non-human demonstration of defensive signals under mismatch (DA1).
Birkett & Newton-Fisher (2011) systematically surveyed abnormal behaviors (stereotypies, coprophagy, self-mutilation, rocking, etc.) in captive chimpanzees across accredited zoos and sanctuaries. They found these behaviors present in every one of the 40 individuals studied. No comparable abnormal repertoire has been reported in wild chimpanzee observation. The implication: the chimpanzee phenotype includes a suite of 'abnormal' behaviors only when the environment falls outside the species' expected range. The hardware works; environment is wrong.
How Abnormal Is the Behaviour of Captive, Zoo-Living Chimpanzees?
Foster care doubles IQ recovery vs institutional care
What it demonstrates. Early developmental calibration (DA7) depends on the presence of specific social input; institutional care without an alloparental network produces durable brain, attachment, and cognitive deficits that are partially reversible by foster placement but persistently worse than never-institutionalized outcomes.
The Bucharest Early Intervention Project (Zeanah, Nelson, Fox and colleagues) randomized institutionalized Romanian children to continued institutional care vs high-quality foster care and compared both groups to never-institutionalized community children. Across neurodevelopmental, attachment, cognitive, and psychiatric outcomes, the foster-care cohort showed substantial recovery (~2× IQ improvement, reduced disorganized attachment, reduced psychopathology) compared to the institutional-care cohort, with earlier placement predicting better outcomes. But neither ever caught up fully to the never-institutionalized community controls, confirming developmental calibration windows and the severity of the mismatch between institutional care and the evolved expectable environment.
Cognitive Recovery in Socially Deprived Young Children: The Bucharest Early Intervention Project
~50% lower heart disease mortality during cohesion era
What it demonstrates. Intense social cohesion can override standard cardiovascular risk factors to produce dramatically lower heart disease mortality - and the effect erodes within a generation once cohesion breaks down, confirming the causal role of the social input rather than any genetic or dietary confounder.
Roseto, Pennsylvania was a small Italian-American immigrant community with unusually strong intergenerational family structures, tight social cohesion, and community rituals through the 1950s-60s. Stewart Wolf and colleagues documented roughly half the heart disease mortality of surrounding communities despite comparable standard risk factors (diet, smoking, occupational exposures). As the younger generation assimilated into mainstream American individualism across the 1970s-80s, the social cohesion eroded and the mortality advantage disappeared on schedule. The Roseto effect is a natural experiment for DA2/DC1: strong social scaffolding can suppress the cardiovascular consequences of allostatic load, and its removal reveals the baseline.
The Roseto effect: a 50-year comparison of mortality rates
~75% response vs ~45% on SSRI monotherapy
What it demonstrates. Treating depression by restoring resolution conditions across multiple mechanisms simultaneously (exercise, omega-3, sleep, sunlight, anti-rumination, social connection) produces remission rates comparable to or exceeding SSRI monotherapy - consistent with depression-as-mismatch-signal rather than depression-as-broken-brain.
Stephen Ilardi's Therapeutic Lifestyle Change protocol is a six-lever intervention targeting M10 (movement), M7 (sleep and sunlight), M3 (social connection), M8/M13 (omega-3 / anti-inflammation), and cognitive anti-rumination. In his clinical trials and subsequent implementations, remission rates in moderate-to-severe depression have reached ~75%, comparable to or exceeding typical SSRI monotherapy rates (~45% remission). The protocol is consistent with Cor's prediction that many depression presentations are M1/M3/M5/M6 defensive-signal cascades resolvable by restoring the resolution conditions for the affected mechanisms.
The Depression Cure: The 6-Step Program to Beat Depression without Drugs
32% vs 8% remission at 12 weeks (NNT≈4)
What it demonstrates. A Mediterranean-style dietary intervention produces clinically meaningful remission from moderate-to-severe depression at ~4× the rate of social-support control over 12 weeks, supporting the causal role of M13 (energy regulation / diet quality) and M8 (inflammation) in depression onset/maintenance rather than treating diet as a correlate.
Jacka et al. 2017 (BMC Medicine) conducted the SMILES randomized controlled trial, comparing a Mediterranean-style dietary intervention to a befriending/social-support control in adults with moderate-to-severe major depressive disorder. At 12 weeks, 32% of the dietary intervention group met remission criteria vs 8% of the control group. NNT ≈ 4. The effect is unusually large for a dietary intervention in a psychiatric population and has subsequently been partially replicated (HELFIMED and follow-up trials). SMILES grounds a causal rather than merely correlational reading of diet-depression links and supports the M13/M8/DA3 cascade.
A randomised controlled trial of dietary improvement for adults with major depression (the 'SMILES' trial)
Cohen's d ~0.8; non-inferior to SSRI in RCTs
What it demonstrates. Aerobic exercise at moderate intensity produces depression symptom reduction comparable to SSRI pharmacotherapy in head-to-head randomized trials and meta-analyses, supporting M10 (movement/regulatory) as a central mechanism in depression pathophysiology rather than a general-health adjunct.
Multiple meta-analyses (Schuch et al. 2016 J Psychiatr Res and subsequent updates) pooling dozens of randomized trials find moderate-intensity aerobic exercise produces Cohen's d ~0.8 reduction in depression severity, comparable to SSRI effect sizes in the same literatures. Several head-to-head trials (Blumenthal et al. and follow-ups) show no significant difference between exercise monotherapy and sertraline at 16 weeks, with exercise showing better long-term relapse prevention. Exercise is not a correlate or adjunct; it is a primary intervention in its own right, consistent with M10's role in the depression cascade.
Exercise as a treatment for depression: A meta-analysis adjusting for publication bias
~60% bipolar depression response within first week
What it demonstrates. Total sleep deprivation combined with morning bright light and sleep-phase advance produces 60%+ response rates in bipolar depression within days - orders of magnitude faster than pharmacotherapy - by targeting M7 (circadian regulation) directly. Demonstrates M7 as a cascade entry point.
Wirz-Justice, Benedetti, and colleagues have developed chronotherapeutic protocols for treatment-resistant bipolar depression combining one night of total sleep deprivation (to rapidly shift circadian phase), morning bright light therapy (to re-entrain M7), and sleep-phase advance (to lock in the new timing). Response rates of 60%+ within the first week are consistent across multiple European trials, compared with ~30% for pharmacotherapy alone over the same interval. The protocol works because it targets the timing architecture that many depression cascades propagate through.
Chronotherapeutics for Affective Disorders: A Clinician's Manual for Light and Wake Therapy
~40% neonatal mortality reduction; benefits at 20 years
What it demonstrates. Skin-to-skin contact between premature infants and caregivers reduces mortality, improves physiological regulation, and produces long-term developmental benefits - demonstrating R1 (C-tactile touch as regulatory input to M3) as architecture rather than comfort measure, with effects that persist two decades.
Charpak et al. developed and studied Kangaroo Mother Care in Bogotá, Colombia for low-birth-weight infants: continuous skin-to-skin contact with the mother (or other caregiver) 24 hours a day, replacing or supplementing incubator care. In low-resource settings the intervention reduces neonatal mortality by ~40% compared to standard incubator care; in high-resource settings it produces improved physiological regulation (thermoregulation, heart rate variability, weight gain) and long-term cognitive and behavioral benefits demonstrated at 20-year follow-up (Charpak et al. 2017 Pediatrics). Feldman's longitudinal work confirms the effects on stress reactivity and executive function into adolescence. Kangaroo care is the strongest evidence that R1 (C-tactile input) is a genuine regulatory channel with architecture-level consequences, not a comfort measure.
Maternal-preterm skin-to-skin contact enhances child physiologic organization and cognitive control across the first 10 years of life.
Mismatch
The same operation at the scale of a life: name the mechanism, check whether the modern environment delivers its resolution conditions, correct the inputs. These end on recognition - the full case carries mechanism, mismatch, and intervention.
Same operation, 3 times. Each row: the presenting situation, the mechanism it is a signal from, the mismatch producing it, the conventional reply, and what Cor reads the signal as.
| Case | Mechanism | Mismatch | Conventional advice | Cor prescription |
|---|---|---|---|---|
| Case 01 · The AI companion trap | M3 | A proxy bond fires the attachment system without reciprocal human co-regulation. | Use the tool responsibly; set screen limits. | An AI must not occupy a Dunbar slot. Restore reliable human co-regulators; route AI toward human connection, not to replace it. |
| Case 02 · Instagram depression | M5 | Rank circuitry built for about 150 people is forced to compare against millions of algorithmically selected lives. | Work on self-esteem; reframe comparison cognitively. | Restore a bounded reference group where position is stable, fair, and visible. Remove the global proxy; the signal is accurate to the environment. |
| Case 03 · The synthetic childhood | M4 | Developmental windows calibrate to a world designed to hold attention, not to the inputs the systems evolved to need. | Set screen-time limits; pick better apps. | Restore outdoor unstructured play, stable adult relationships, morning daylight, and movement. The windows close on whatever is present. |
A chatbot becomes the most responsive relationship in a lonely life, and the loneliness alarm goes quiet for the wrong reason.
Read the caseStatus circuitry built for bounded groups is forced to compare upward against millions of algorithmically selected lives.
Read the caseDevelopmental windows close on a world designed to hold attention, not on a world calibrated to what those systems evolved to need.
Read the caseRepair
What the framework is for: places where reading distress as a signal changes what you build or do. AI alignment leads.
Cor is the missing specification under AI alignment. Current alignment approaches treat human preferences as ground truth and train AI systems to satisfy them. But preferences are mechanism outputs - and under mismatch, mechanisms output preferences that point toward more mismatch (more variable-reward apps, more status comparison, more proxy satisfaction). Aligning AI to unverified preferences entrenches the mismatch rather than correcting it. Cor provides three things AI alignment needs: (1) a fourth evaluation axis - matched/mismatched - alongside helpful/harmless/honest; (2) constitutional knowledge of what a human organism needs before asking what it prefers; (3) a test applicable to every AI output: 'Is this creating conditions for real resolution of a mechanism, or is it activating the mechanism without resolving it?' The highest-risk patterns are AI companions (M3 proxy), status/engagement optimization (M5 proxy), and AI sexual/romantic content (M14 proxy) because the mechanisms hijacked are the deepest and most phylogenetically protected.
Current psychiatry classifies many aversive presentations as disorders and treats them with suppression (pharmacotherapy, CBT targeting the experience). Cor reframes many presentations as accurate signals of environmental mismatch: the architecture is working correctly, the environment is outside the expected range, and the signal is telling the clinician where to look. Clinical practice redesigned around Cor includes: (1) environmental audit against the mechanism inventory (M1-M14 + R1) before or alongside symptom treatment, (2) resolution-condition restoration as the first-line intervention where feasible, (3) pharmacotherapy and symptom-suppression reserved for genuinely dysregulated states (not for defensive-activation states that will resolve once the environmental input is corrected). The four categories the handoff distinguishes - defensive activation, dysregulation, damage, developmental miscalibration - each point to a different treatment approach.
Architecture, urban planning, office design, product design, school design, and healthcare facility design currently proceed without a clear account of what the human organism requires to function. Cor provides the framework. Each evolved mechanism has resolution conditions (documented in Cor's mechanism architecture) that the designed environment either satisfies or degrades. The application: design environments that satisfy resolution conditions for each mechanism - M7 light/dark cycles, M10 movement integration, M3 social density, M4 unstructured play space for children, M9 alloparental-care commons, R1 touch-positive cultures. Designers should be able to audit any proposed environment against the Cor inventory and flag which mechanisms will be compromised by default.
Individuals currently diagnose themselves through the cultural filter of psychiatric categories, productivity culture, wellness trends, or self-help frameworks. Cor provides a direct assessment: which mechanism's resolution conditions are unmet in your life right now? A tool built on the framework lets the user answer questions about their environment and get back a picture of which mechanisms are matched vs mismatched, with resolution-condition statements they can act on. This is not therapy, not diagnosis, not productivity advice; it is an audit of the inputs the user's evolved architecture currently is or is not receiving.
Current education treats children as cognitive agents to fill with information, organized around the economic value of the adult they will become. Cor reframes education as organism care: children are developing organisms with mechanism requirements that current school design routinely violates. M4 (play) requires unstructured, age-matched, unsupervised physical play - which contemporary schooling systematically removes. M7 (circadian) requires age-appropriate school start times and daylight exposure - routinely violated for adolescents. M10 (movement) requires embedded daily movement, not scheduled PE. M3 (attachment) requires stable caring relationships with specific adults - eroded by class-rotation designs. M9 (alloparenting) assumes children will be cared for by multiple trusted adults - which school + family-only models fail to provide. Educational reform under Cor begins by auditing the design against the mechanism inventory and redesigning to satisfy the resolution conditions of the developing organism.
Governance currently evaluates policy by economic metrics and preference aggregation. Both are defective evaluation axes: economic metrics measure proxies (GDP, employment) rather than organism-level flourishing; preference aggregation treats mismatched preferences as ground truth. Cor provides a human-organism evaluation axis: does this policy satisfy or degrade mechanism resolution conditions for the population? Applied to food policy (M13 resolution conditions vs ultra-processed food availability), urban design (M3 social density, M10 walkability, M7 light-pollution, M4 child play space), work regulation (M6 agency, M7 shift-work protection, M10 movement integration), digital platform regulation (DC2 engagement-based hijacking of M5 and M14), and environmental policy (M7 circadian disruption from light pollution, M8 air quality). A policy that degrades mechanism resolution conditions is costly regardless of its economic or preference-aggregation scores.
Evidence
Places where Cor takes a position instead of reporting a consensus. The framework pulls together fields that do not agree on everything. Where the evidence converges we report the convergence. Where it does not, and we still need a position to stay coherent, that is an interpretive call. They are all listed here.
The framework treats Panksepp's basic-affect architecture (SEEKING, FEAR, RAGE, LUST, CARE, PANIC/GRIEF, PLAY) as the primary structural reference for subcortical motivational systems. Lisa Feldman Barrett's constructionist account of emotion is a serious alternative the framework does not currently adopt. The reasoning: Panksepp's framework integrates more cleanly with comparative neuroscience and the phylogenetic depth principle, and gives the discrete-mechanism handles the application layer needs. The constructionist literature is acknowledged in the Challenges section.
The framework treats inclusive fitness as the loss function the architecture was selected against (foundation P1). It does not treat gene-culture coevolution as a competing framework but as a refinement that operates within the same selection logic. Researchers who treat the two as fundamentally distinct frames may read this as an interpretive bet.
The framework takes the strong-mismatch position: the modern environment is systematically misaligned with the architecture, and that misalignment is the primary driver of widespread non-pathological distress. Weak-mismatch readings - environments are different but the architecture is sufficiently flexible that the mismatch is mostly absorbed - are addressed in the Challenges section but not adopted.
The framework treats the human motivational-emotional architecture as domain-sensitive (domain-specific adaptations exist and can be enumerated), not as the output of a general-purpose learning system. This is a position in an ongoing argument and the framework is not neutral on it.
These are the largest interpretive calls. Smaller calls are noted on the individual mechanism page where they apply.
Evidence
What the framework does not know yet, in priority order. Nothing here is presented as settled when it is not.
Missing. Dedicated empirical depth on Haugen's Facebook Files and on companion-AI harm. The companion-AI reference (Muldoon & Parke 2025, New Media & Society, DOI 10.1177/14614448251395192) has now been located and catalogued as a work; extractions from it remain to be added in v1.
Why it matters. DC2 (Market Proxy Exploitation) grounds A1 AI alignment and A6 platform regulation. It currently rests on Schüll (gambling) and Moss (food), which is narrow. Companion AI is the highest-risk contemporary case and does not yet have primary-source grounding in Cor.
Current approach. Muldoon & Parke 2025 catalogued and cited in DC2's derivation (resolved 2026-05-29). Deeper empirical grounding (Haugen Facebook Files; further companion-AI studies) remains v1 corpus work.
Missing. Cor specifies resolution conditions per mechanism (for example M3: reliable intimate co-regulators typically ~5+; M10: varied daily movement typically ~9-15km/day; M7: dark-cued sleep onset), but operationalizing 'matched' as a measurable state across all 14 mechanisms - with inter-rater and test-retest reliability - is unfinished.
Why it matters. The measurement-protocol gap limits A4 personal assessment from becoming a validated instrument and blocks quantitative A6 policy evaluation against mechanism resolution conditions.
Current approach. A public-facing tool built on the framework will prototype the measurement protocol for A4 individual-level audits. Formal psychometric validation is independent research downstream of the core framework.
Missing. A1 proposes 'matched / mismatched' as a fourth evaluation axis alongside helpful, harmless, and honest. What is missing is a concrete set of test cases - what a 'matched' response to a specific user query looks like versus a 'mismatched' one - scored in a way that a red-team or evaluation harness can apply systematically.
Why it matters. A1's matched/mismatched evaluation proposal is currently a framework, not an evaluation instrument. Without concrete scorable test cases, the matched/mismatched axis is a conceptual contribution to alignment evaluation rather than a working protocol that labs can run against model outputs.
Current approach. A1's evaluation-criteria field carries the resolution-check and proxy-gradient tests as conceptual criteria. Operational red-team-scorable test cases are the next step of the alignment evaluation work.
Missing. M14 is sex-differentiated, with distinct female (VMH-centered) and male (POA-centered) neural architectures carrying different emphasis on commitment cues versus variety cues. Cross-cultural tests of these specific claims are thin, and the ovulatory-shift literature in particular has an active replication debate.
Why it matters. M14 is the most culturally contested mechanism and the one most likely to be challenged on grounds of cultural construction. A weak empirical cross-cultural base makes the mechanism vulnerable to legitimate challenge even though the core neuroarchitecture is well-supported.
Current approach. Haselton/Buss Error Management Theory and Buss sexual strategies work are the current evidence base. Ovulatory-shift-specific claims are explicitly flagged as contested in extraction caveats to preserve the nuance.
Missing. The Maier & Seligman 2016 reformulation of learned helplessness (default passivity with vmPFC-DRN override) is well-supported in rodent models, but the human neurobiological translation - fMRI studies of controllability in humans - is thinner. Karasek's decision-latitude work provides strong human-level evidence but at a different level of analysis.
Why it matters. M6 is critical as a cascade-break point in Cor's applied framework (A2 clinical practice, A3 environment design, A6 work regulation). Strong rodent evidence combined with weaker human-specific neural evidence leaves the mechanism vulnerable to challenge at the human-specificity level.
Current approach. The rodent-level circuit claims are treated as settled; the human-level circuit mapping is treated as well-supported rather than definitively established. The distinction is preserved in the mechanism description.
Missing. BT1 (Panksepp-Barrett Resolution) is defended conceptually - subcortical affective circuits are real, and folk emotion categories are constructed overlays on top of them. What is missing is a crisp empirical discriminator test that would adjudicate specific cases where the Panksepp and Barrett frameworks make divergent predictions.
Why it matters. Bridge theses are load-bearing for Cor's epistemic credibility. If a bridge is only conceptually defensible and cannot be tested against a concrete prediction, critics can characterize the resolution as rhetorical rather than substantive.
Current approach. BT1 is presented as a level-of-analysis distinction: Panksepp's cross-species deep-brain-stimulation results ground the primary-process claim; Barrett's cross-cultural folk-category variation grounds the tertiary-process claim. The discriminator gap is explicitly acknowledged in the bridge-thesis narrative.
Missing. Boyd & Richerson's gene-culture coevolution constraint requires that 'matched' include cultural scaffolding, not just ancestral surface forms. But operationalizing which cultural configurations count as matched versus mismatched requires a criterion that does not collapse into either ancestral essentialism (only hunter-gatherer life counts) or cultural relativism (everything counts).
Why it matters. Without this distinction sharpened, P3 (Systematic Mismatch) can be attacked as either too permissive (all cultures are matched by definition) or too restrictive (only hunter-gatherer configurations count).
Current approach. The constraint is treated as 'matched must lie within the envelope of culturally-scaffolded human variation historically observed.' The criterion is acknowledged to be not fully sharp and flagged for sharper operationalization in future theoretical work.
Missing. The five-level M14 proxy gradient (real partner → attenuated real → partial proxy → pure proxy soft → pure proxy hard) is architecturally derived but lacks clinical validation metrics. Which clinical presentations map to which proxy level, and what are the dose-response clinical consequences of sustained use at each level, remain open questions.
Why it matters. A1 AI alignment risk analysis and A2 clinical practice both depend on being able to locate specific proxy products on the gradient with some reliability.
Current approach. The gradient is used as a theoretical organizing device. Clinical validation is flagged as a priority research program for A2 clinical applications.
Missing. Cor's forcing-convergence layer currently covers 5 of 15 mechanisms (M1, M2, M3, M11, M14) with explicit multi-literature convergences. The remaining 10 mechanisms (M4, M5, M6, M7, M8, M9, M10, M12, M13, R1) have supporting extractions populating their evidence junctions but do not yet have explicit convergence rows forcing them from multi-stream replication.
Why it matters. Convergences are the forcing-set level of Cor's evidence pyramid. A mechanism without an explicit convergence is an admission that the evidence does not yet force it from multi-stream convergence, even when Tier-1 status is warranted on single-literature grounds.
Current approach. The original convergence pass followed a strict rule (≥3 independent literatures each). A follow-up convergence pass should be able to add convergences for M6 (Maier/Seligman + Karasek + Amat/Baratta), M7 (Walker + Roenneberg + Czeisler), M12 (Rozin + Curtis + Schaller), and possibly M10 (Pontzer/Lieberman + Chekroud large-cohort + Schuch meta-analysis).
Missing. The current challenge layer holds 5 challenge extractions (EAAT philosophical critique, social-media-effect-size meta-analyses, Landy disgust-moral meta-analysis). Dedicated challenges from Active Inference (Friston) as a competing framework, substance-specific addiction neuroscience (Volkow/Kreek), and cultural-construction critiques of specific mechanism claims beyond Barrett are not yet in the corpus.
Why it matters. A credible framework must engage its strongest critics. The current challenge layer is thin and leans on methodological critiques rather than framework-level competitors like Active Inference or RDoC.
Current approach. The current challenge layer is treated as sufficient for initial framing. A dedicated challenge-layer expansion is a priority for the next round of work, covering Active Inference, addiction neuroscience, and RDoC comparisons.
Missing. The current evidence_quality categories compress some distinctions that matter for specific epistemic claims - cross-species biological replications, landmark longitudinal cohorts, ethnographic evidence from non-WEIRD populations, and contested findings each carry different epistemic weight but can currently collapse into broader buckets such as 'replicated' or 'clinical'.
Why it matters. Cross-species replication is especially load-bearing for Cor's phylogenetic-priority claims (DA8, ancient affective circuits). Longitudinal cohort depth matters for ACE-dose-response claims. Contested findings should be first-class flaggable to surface scope questions to readers drilling into primary evidence.
Current approach. The broader buckets are used as the machine-readable tag; finer-grained epistemic nuance is preserved in the caveats field per row. Expansion of the first-class tag list is under review.
Missing. The new Restorative Environments domain has no primary extractions yet. A primary-source ingestion queue is defined, each item to be grabbed under v2 standards (full text, fresh extraction, verbatim author_quote, DOI/PMID or physical collection) and never ingested via a review: (1) Ulrich 1984, "View through a window may influence recovery from surgery," Science, the anchor stress-recovery result; (2) Kaplan and Kaplan 1989, The Experience of Nature (Attention Restoration Theory), with Berman, Jonides and Kaplan 2008, Psychological Science, as the experimental test; (3) Miyazaki and Li forest-medicine primaries on phytoncides, NK-cell activity, and cortisol/HRV (strongest primary studies, not review-of-reviews); (4) Hartig et al. 2014, "Nature and health," Annual Review of Public Health, itself a review, so treat as a routing source only under the same rule as the Yong review; (5) Bratman et al. 2015, PNAS, nature walk reduces rumination and subgenual prefrontal activity, a strong mechanism-level primary.
Why it matters. Restorative-environment mismatch is the cleanest non-social mismatch available to Cor: strong evidence, an obvious resolution condition, and a delivery form that need not be literal wilderness. It makes the atlas visibly more than a social-mismatch account. Until the primaries are extracted, the domain is a container without grounding.
Current approach. Domain created as a cross-cutting input-resolution domain with no new mechanism. Evidence-tagging discipline recorded in the domain description (stress-recovery and attention-restoration core well-supported and partly replicated; forest-medicine immune findings thinner and often small-sample, so tag down when in doubt). Queue to be worked as future v2 extraction work.
Missing. Yong, Lim, Tan and Chan 2026 (DOI 10.3390/bs16050650) advance a "social evolutionary mismatch and competition hypothesis": social features of mismatch (increasing population size, fragmented communities, rising socioeconomic inequality, constant exposure to inflated social-status cues) jointly inflate real and perceived competition, driving obsessive status pursuit, hostility, risk appetite, ultralow fertility, and social withdrawal (tang ping, quiet quitting, hikikomori). Open question: is this a distinct convergence Cor is currently missing, or a downstream expression of existing structure, namely C9 (Allostatic Load Accumulation) plus C11 (Reciprocity, Norm Enforcement, and Coalition Architecture) plus M5 status and rank regulation and DC2 market proxy exploitation?
Why it matters. It is the one original theoretical move in an otherwise routing-only review, and it bears directly on whether Cor's convergence layer is complete. Resolving it either surfaces a genuine gap in the forcing-set layer or sharpens the claim that competition intensification is already entailed by existing convergences and mechanisms.
Current approach. Logged as an open derivation question, not added to the locked convergence inventory. Evaluate the theoretical spine first: Sng, Neuberg and Kenrick 2017 (resource competition and life-history, density-dependent life-history strategy) as candidate mechanism-level grounding, then test whether the Yong competition construct reduces to C9 plus C11 plus M5 plus DC2 or requires its own forcing convergence.
Missing. R1 (Touch) is currently the only Tier 3 regulatory input in the inventory. Other candidate regulatory inputs deserve architectural consideration: thermoregulation signaling to M2/M6, gut-brain axis signaling to M3/M8, hydration signaling, and proprioceptive/vestibular input regulation.
Why it matters. R1's inclusion establishes the Tier 3 category - but leaving it as a set of one invites scope questions about why touch and not other regulatory inputs are architecturally load-bearing.
Current approach. R1 is treated as the template for the Tier 3 category. Additional regulatory inputs are candidates for future architectural work but are not added retroactively without explicit review.
Missing. Some extractions imported from prior cleanup passes may be mis-classified at the source_type level - for example, an extraction marked as 'primary' research that on closer reading of the source paper turns out to be a propagation of another researcher's finding through a later author's lens.
Why it matters. The primary/propagation distinction is important for citation-chain auditability - readers tracing an evidence claim back to its source should land on the original research, not a secondary interpretation. Mis-classification creates downstream drift in this chain.
Current approach. Imported source_type labels are trusted pending a content-level audit against the original source papers. Rows where a discrepancy is suspected are flagged for review.
Missing. Jointly-authored works are currently credited to a single primary researcher in the database, with co-authors listed only in the free-text authors field. For example, The Adapted Mind is credited to Tooby but also co-authored by Cosmides; Not by Genes Alone is credited to Boyd but also co-authored by Richerson; Paleolithic Nutrition to Eaton and Konner; The Mismatch Hypothesis to Li, van Vugt, and Colarelli.
Why it matters. Researcher-coverage queries against the primary-researcher field undercount jointly-authored contributors. Cosmides, Richerson, Konner, and van Vugt each show zero distinct work rows under this query even though they are substantive co-authors of pillar works.
Current approach. Joint authorship is handled via the free-text authors field. A dedicated author-join table is a candidate future improvement if per-author granular queries become necessary.
Evidence
The applied and research fields the framework touches, each tied to a primary mechanism. Cross-cutting domains span several.
Learned helplessness research (Maier & Seligman reformulation), decision latitude, vmPFC-DRN circuitry, and the agency-as-override-of-default-passivity framework. Maps to M6; critical cascade-break point for A2 clinical work.
Hrdy's cooperative-breeding thesis, parental-burnout research, the alloparental-network requirement, and the consequences of nuclear-family isolation for child development and parent wellbeing. Maps to M9; relevant to A3, A4, A5.
Research on cumulative physiological cost of chronic activation: McEwen's allostasis framework, Whitehall socioeconomic-gradient work, Felitti ACE dose-response, Sapolsky primate hierarchy-cortisol links. Grounds DC1. Critical for A6 policy and A2 clinical.
Attachment theory, co-regulation research, grief, loneliness epidemiology, and the social-baseline literature. Maps to M3; primary domain for DA2 evidence and for A2, A3, A4, A5 applications.
Research areas where seemingly conflicting frameworks admit a level-of-analysis resolution - notably the Panksepp-Barrett debate on emotion natural kinds vs constructed emotions. Grounds BT1.
Cross-mechanism cascade research: depression cascades, anxiety-insomnia spirals, social isolation cascades, sickness behavior traps, status-defeat cascades, parent burnout, proxy hijacking spirals, and reproductive disruption cascades. Grounds DA3 (cascading) and DA8 (phylogenetic priority). Central for A2 clinical reasoning about which lever to pull first.
Three-domain disgust research (Rozin), behavioral immune system (Schaller, Curtis), pathogen-prevalence cross-cultural psychology, and the moral/social extensions of contamination avoidance. Maps to M12.
Reciprocal altruism research, norm enforcement, altruistic punishment (Fehr & Gächter), reverse dominance (Boehm), and shared intentionality (Tomasello). Maps to M11; grounds social-contract claims in A6 policy.
Research on aversive psychological and physiological outputs as intelligible defensive signals rather than malfunctions - Nesse evolutionary psychiatry, Birkett & Newton-Fisher captive-chimp abnormality, Bowlby environment of evolutionary adaptedness. Grounds DA1. Directly reframes A2 clinical practice.
Research on developmental windows in which specific systems calibrate to environmental inputs within evolved parameters - attachment (Bowlby), HPA axis (Meaney), adolescent circadian shift (Walker), Bucharest early-intervention studies. Grounds DA7. Supports A2 clinical, A5 education.
Satiety signaling research, constrained energy expenditure, ultra-processed food effects, and the dietary-intervention trials (SMILES, HELFIMED). Maps to M13; grounds A6 food policy work.
Sickness behavior research, cytokine signaling, inflammation-depression links, and the cascading role of chronic low-grade inflammation. Maps to M8; key hub for DA3 cascading and A2 clinical rethinking.
The mismatch hypothesis literature proper - Eaton & Konner discordance, Li/van Vugt/Colarelli mismatch review, Boyd & Richerson gene-culture coevolution, Henrich WEIRD psychology. Grounds P3. Central to the whole framework and all applications.
Exercise-as-regulator research, Pontzer's constrained-energy model, movement-as-zeitgeber, and the anti-inflammatory and mood-regulatory effects of embedded daily movement. Maps to M10; supports A2 clinical, A3 environment design, A6 policy.
Rough-and-tumble play research, developmental play deprivation, play circuits, and the education-policy consequences of structured-activity substitution. Maps to M4; critical domain for A5 education application.
Research on how industrial proxies (variable-reward apps, ultra-processed food, pornography, AI companions, social-media status metrics) hijack evolved mechanisms by supplying input cues without resolution conditions. Grounds DA4 (open-loop vulnerability) and DC2 (market exploitation). Central to A1 AI alignment and A6 platform regulation.
SEEKING-system research on goal pursuit, reward, engagement, motivation, and the open-loop vulnerabilities that variable-reward applications and proxy cues exploit. Maps to M2; central to DC2 and DA4 application analysis.
Sexual strategies theory, sex-differentiated mate preferences, pair bonding research, LUST circuit neuroscience, and the proxy gradient from real partner to pure proxy. Maps to M14; central to A1 AI alignment risk-pattern analysis.
Restricted contact with natural and restorative environments as an input mismatch. Framed resolution-condition-first, not form-first: the target is the functional restorative property (fractal visual complexity, soft-fascination attention recovery, non-threatening biological motion, restorative soundscape, phytoncide exposure), not "return to nature" and not an innate biophilia drive. Forest exposure is one delivery form; built and urban environments can supply the same properties, which keeps the domain scalable and out of the naturalistic-fallacy trap. Classified cross-cutting because restorative input resolves several existing systems rather than one: threat and vigilance de-arousal with parasympathetic recovery (Ulrich Stress Reduction Theory), directed-attention restoration (Kaplan Attention Restoration Theory), allostatic offloading (DC1 and C9), immune and inflammatory modulation (M8; forest-medicine phytoncide and NK-cell work), and reduced rumination (Bratman). No new mechanism is asserted; nature contact is treated as an environmental input that lets existing systems stand down, consistent with the core thesis that the fix is the environment. Evidence discipline: the stress-recovery and attention-restoration core is well-supported and partly replicated; forest-medicine immune findings are thinner and often small-sample, so tag down at extraction time. Primary-source grounding is pending (see the ingestion-queue gap, G15). Note: the biophilia literature is the umbrella term for this territory, but Cor treats it as an input-resolution domain, not an innate-drive claim.
SCN master clock research, chronotype variation, social jetlag, sleep deprivation consequences, and chronotherapy in psychiatric conditions. Maps to M7; large evidence base and central to A2 clinical and A3 environment design.
Hierarchy physiology, rank vigilance, shame and submission, Whitehall-style socioeconomic gradient research, and the status-defeat cascade. Maps to M5; central to the DC2 platform-regulation case.
Research and applied work on defensive responses to threat cues: fear circuitry, frustration-aggression, panic disorder, PTSD, and the conditions under which safety can be established. Maps to M1; feeds A2 clinical and A3 environment design applications.
C-tactile afferent research (McGlone), skin-to-skin contact trials (Feldman, Charpak kangaroo care), and touch as a regulatory input to M3 rather than a standalone motivational system. Maps to R1.
Evidence
The researchers whose work the framework draws on, grouped by the role they play, and the bibliography behind the whole account.
Evidence
The strongest counter-evidence and live disputes, stated in their own terms.
Papers
The long-form papers. Each one stands alone, so read them in any order.
The AI-alignment wedge: why an optimizer with no model of what resolves a human mechanism cannot be aligned by preference satisfaction alone.
as of 2026-08-11The model, written for the systems that will design our environments and for the people building them.
as of 2026-08-11The framework as a Lakatosian research programme: hard core, protective belt, falsifiers, and boundary conditions.
as of 2026-08-11Start here. What Cor is in plain words, how the atlas was built, what its counts mean, and how to read the framework's epistemic tiers - the ordinal proxy gradient, a cue that fires without supplying what resolves it.
as of 2026-08-11