OCD threshold levers — the serotonergic / glutamatergic / circuit instantaneous operating-point correction, decomposed into DNA-grounded levers (L3-dominant with L1 strong and L2 sparse and a mixed corrective sign; the pathological loop-lock named, out of reach — the fourth PARTIAL fit in the series, and a new E0 mode)

OCD is the fourth partial fit. The reachable surface is the instantaneous CSTC excitability, where the mainstay routes genuinely but partially help. The dominant loop-lock is a pathological stabilisation, out of reach. The levers do not unstick the loop; intrusive thoughts are a symptom, not a moral failing.

Obsessive-compulsive disorder is, before it is anything else, a disorder of a stuck loop. The serotonergic, glutamatergic and circuit accounts each describe a real, treatable piece of its instantaneous excitability surface — a deficient serotonergic tone, a hyperactive glutamatergic drive, an excess dopaminergic drive, a thin inhibitory arm — but every one of them sits on top of a single dominant fault that none of them resolves: a pathological, self-sustaining, over-consolidated CSTC loop-lock, the obsession-compulsion cycle that cannot let go, reinforced by the transient anxiety-relief each compulsion delivers. That lock is the discriminant — it is what makes OCD OCD, and it is a pathological stabilisation, not a set-point. This chapter applies the same piece of inherited technology the bipolar, epilepsy, depression, schizophrenia, autism, ADHD, addiction and Alzheimer's levers chapters used — the threshold-shift intervention logic from the analgesic reproducibility package (Zenodo 10.5281/zenodo.20733420), whose three abstract levers are L1 change the inward (excitatory) current, L2 change the outward (potassium / inhibitory) current, L3 change the up-stream drive — and it produces the fourth PARTIAL fit in the series, and a new mode. OCD is the ninth distribution pattern, and the first whose inhibitory arm is sparse. Of eight lever genes, four sit on the up-stream serotonergic/dopaminergic-drive lever (L3, mixed sign: SLC6A4 the serotonin transporter, HTR2A and HTR1B the serotonin receptors — restored, the SSRI first-line; DRD2 the D₂ receptor — reduced, antipsychotic augmentation), three on the inward glutamate-excitatory lever (L1, reduced: SLC1A1 the EAAT3 transporter — the most replicated OCD gene — GRIN2B and GRIK2), and one on the inhibitory-restore lever (L2, restored, a single sparse node: GABRA1). The corrective sign is mixed: serotonergic tone pushed up (restore), dopaminergic drive pushed down (reduce), glutamatergic drive pushed down (reduce), inhibition pushed up (restore) — the SSRI / clomipramine direction, the antipsychotic-augmentation direction, the glutamate-modulator direction, and an inhibitory-restore direction, all as directions, never doses. Unlike Alzheimer's purely-symptomatic surface, these levers are the actual mainstay and investigational routes of OCD care, and they genuinely (partially) help. Yet the fit is the fourth partial fit, for a precise and new reason. The reachable surface is the instantaneous CSTC excitability operating point; the dominant OCD fault is the LOCK pathological-stabilisation axis — the over-deep basin, the over-wide hysteresis, that holds the compulsive loop in place — and it is out of reach for a reason that compounds both prior partial fits and adds a third. It is a gain/loss, not a fold (the ADHD lesson: a lever that moves a fold has no handle on a basin depth). It is a consolidated/learned plasticity (E0-layer) variable, not an instantaneous operating point (the addiction lesson). And it is, beyond both, a pathological STABILISATION — an over-deep basin / hysteresis, an E0 stabilisation that is the third distinct E0 mode, distinct from addiction's E0 gain and Alzheimer's E0 decay: addiction builds a trace the levers cannot erase, Alzheimer's loses a substrate the levers cannot rebuild, OCD freezes a maladaptive attractor the levers cannot unstick — completing the trio. So even a drive lever that nudges the instantaneous operating point cannot unstick the loop. The LOCK axis is named with four real genes — DLGAP3/SAPAP3 the corticostriatal scaffold of the canonical OCD model, SLITRK5 and PTPRD the synaptic-adhesion molecules, and BTBD3 the circuit-patterning gene — carried with their own promoter reads alongside but not reached. So the fit is graded [L] partial, the fourth non-clean fit in the series. Each gene is placed by reading its own promoter switch stiffness — γ = −mean nearest-neighbour stacking free energy (SantaLucia 1998) over its promoter window, turned into |h_sp| = spinodal(γ) with the frozen engine read-only — and five of the twelve reads (SLC6A4, HTR2A from the depression cache, DRD2 from addiction, GRIN2B from autism, GABRA1 from epilepsy) are carried over verbatim, with the seven new genes live GRCh38 strand-aware reads. The DNA reads carry a decoupling that is orthogonal to reach and to priority: the stiffest promoter in the set is an out-of-reach loop-lock gene (DLGAP3), the softest is a reachable lever (GABRA1), and the four out-of-reach genes span the whole stiffness range rather than clustering — so promoter stiffness predicts neither which axis a gene is on, nor whether it can be reached, nor where it ranks. Two fail-closed disciplines ride along, and the forbidden-claim scanner adds two classes specific to this topic: a cure / miracle class (it rejects cure / permanently-stop-the-intrusive-thoughts / eliminate-the-compulsions / miracle-cure / one-weird-trick framing) and a moral-framing / stigma class (it rejects just-stop-worrying / lack-of-willpower / character-flaw / moral-failing / attention-seeking / not-a-real-illness framing), both negation-guarded. The firewall is absolute: the promoter |h_sp| is a gene's own switch stiffness, never a basin depth, a hysteresis width, the strength of the compulsive lock, a receptor occupancy, a synaptic serotonin / dopamine / glutamate level, a drug's potency, a dose, or a clinical effect. efficacy = 0; not medical advice; the reachable levers nudge the operating point but do not unstick the loop; a deep-brain-stimulation dynamics intervention is the handle the threshold levers are not; OCD is a treatable medical condition and intrusive thoughts are a symptom, not a moral failing; the hard problem stays open.

What the serotonergic, glutamate and circuit accounts establish (a stuck loop, not a set-point)

OCD has been read through three mechanistic accounts, and each one identifies a real, treatable piece of the disorder. The serotonergic account is the oldest and the strongest clinically: serotonin-reuptake inhibitors and clomipramine are the established first-line, OCD characteristically responds to them only at a more sustained, stronger serotonergic course and a longer latency than depression, and that differential response is itself the classic evidence that a serotonergic abnormality is part of the disorder. The glutamatergic account observed that orbitofrontal-striatal circuits are hyperactive in OCD, that this hyperactivity rides an elevated glutamatergic tone, and — strikingly — that the single most replicated OCD candidate gene is SLC1A1, the neuronal glutamate transporter; lowering the glutamate drive is the rationale for the investigational glutamate modulators (riluzole, memantine, N-acetylcysteine). And the dopaminergic account observed that antipsychotic augmentation — adding a D₂ blocker to an SSRI — helps in refractory and tic-related OCD, implicating an excess dopaminergic drive. Three accounts, three pieces of a surface — a deficient serotonergic tone, a hyperactive glutamate drive, an excess dopamine drive — and all three are surfaces a threshold lever could, in principle, move.

But all three accounts share a feature that this chapter is built around: they describe the instantaneous excitability of the loop, and none of them touches the thing that makes the loop a loop. OCD's dominant fault is not a level — it is a dynamic: a pathological, self-sustaining limit-cycle, the cortico-striato-thalamo-cortical circuit settling into an over-consolidated, pathologically stabilised attractor. The obsession raises anxiety; the compulsion transiently relieves it; that relief reinforces the compulsion (a plasticity process, a negative-reinforcement learning); and the loop deepens its own basin until it runs on its own. That self-sustaining lock is a different kind of variable from any set-point. It does not sit at a level a lever can shift; it is a stabilisation — an over-deep basin, an over-wide hysteresis — that holds the cycle in place. OCD is, before it is anything else, a stuck loop. The serotonergic, glutamate and dopamine accounts tell us where the instantaneous surface is; they are silent on whether the lock can be reached at all. That silence is exactly the question the threshold frame is about to make precise — and, as with ADHD, addiction and Alzheimer's, the honest answer is that the frame catches the instantaneous surface and cannot reach the dominant axis. The difference this time is that the reachable surface is not a placebo: it is where the real treatments act, and they genuinely, partially, help.

The inherited technology, applied a ninth time — the L3-dominant, L1-strong, L2-sparse pattern

The handle is not invented here. It is the same threshold-shift intervention logic the bipolar, epilepsy, depression, schizophrenia, autism, ADHD, addiction and Alzheimer's chapters inherited from the analgesic reproducibility package (Zenodo 10.5281/zenodo.20733420). Its premise is general: an operating point is set by a balance of currents and the drives that bias them, so there are exactly three levers on it. L1 — change the inward, excitatory current. L2 — change the outward, repolarising (or inhibitory) current. L3 — change the up-stream drive that sets where the operating point sits. The frame applies unchanged because the OCD excitability substrate, the eight prior levers chapters, and the analgesic package all share the same R19 substrate — the engine's supercritical pitchfork ṣ = g·s − s³ + h, whose spinodal fold IS the switching barrier. Nothing about the engine is touched; the module re-emerges the frozen tree read-only, confirms it byte-unchanged, and registers as the eighteenth atlas citizen (OCD-T3c-L).

OCD is the ninth distribution pattern across the series, and its reachable surface has two properties none of the others did. Of eight lever genes, four sit on L3 (the up-stream serotonergic/dopaminergic drive), three on L1 (the glutamate-excitatory current), and one on L2 (the inhibitory-restore axis). The first distinctive property is that the L2 arm is sparse — a single, weak inhibitory node, where addiction had two and Alzheimer's had three. OCD's GABAergic biology is thin (reduced cortical GABA is reported and a benzodiazepine is an adjunct, but the inhibitory-restore arm is genuinely sparse), and that sparseness is itself a finding the frame records rather than papers over. The second distinctive property is that the corrective sign is mixed: on L3 the serotonergic nodes are restored (tone pushed up — the SSRI direction) while the dopaminergic node is reduced (drive pushed down — the augmentation direction); on L1 the glutamate drive is reduced (the glutamate-modulator direction); on L2 inhibition is restored (pushed up). A lever map that pushes serotonergic tone up, dopaminergic and glutamatergic drive down, and inhibition up — a split corrective sign within a single disorder, the second in the series after Alzheimer's — is the structural signature of a disorder whose instantaneous surface is a balance gone wrong in several directions at once. The pipeline is reused at the level of code, not analogy: five of the twelve reads — SLC6A4 and HTR2A from the depression cache, DRD2 from the addiction cache, GRIN2B from the autism cache, and GABRA1 from the epilepsy cache — are carried over verbatim, because γ is a strand-symmetric property of the sequence and does not change between problems; the seven new genes (HTR1B, SLC1A1, GRIK2, DLGAP3, SLITRK5, PTPRD, BTBD3) are fetched fresh (GRCh38, strand-aware).

The fourth partial fit and a new mode: why the dominant axis is a stabilisation lock

This is the result that makes OCD a structurally distinct chapter in the series, and the fourth that does not produce a clean fit. The module says so in a partial-fit witness that grades the fit [L] partial and records it as the fourth partial fit and a new mode. The reachable side is genuine and broad: the lever frame reaches the instantaneous CSTC excitability operating point across all three levers — the L3 serotonergic/dopaminergic drive, the L1 glutamate-excitatory current, and the L2 sparse inhibitory restore — exactly where the established and investigational OCD pharmacology acts, and (the point that distinguishes OCD from Alzheimer's) where it genuinely, partially, helps. But the dominant OCD fault is the LOCK pathological-stabilisation axis, and it sits out of reach for a reason that compounds both prior partial fits and adds a third on top. The first sense is the ADHD lesson, inherited intact: the lock is a gain/loss, not a fold — an instantaneous lever moves an operating point, and no operating-point shift sets the depth of a basin or the width of a hysteresis loop. The second sense is the addiction lesson: the lock is a consolidated/learned plasticity variable — the loop deepens its own basin through the negative-reinforcement of compulsive relief, a plasticity (E0) process, not an instantaneous operating point a lever can shift at all. ADHD's gain was at least instantaneous; addiction's gain was a learned trace; OCD's lock is a learned trace that has become an attractor.

The third sense is new, and it is what makes OCD a distinct mode. The lock is not merely a gain, and not merely a learned accrual — it is a pathological stabilisation: an over-deep basin, an over-wide hysteresis, that freezes a maladaptive attractor in place. This is an E0 stabilisation, and it is the third distinct E0 mode in the series. Addiction met the E0 plasticity layer as gain — the layer builds a trace the instantaneous levers cannot erase. Alzheimer's met the same layer as decay — the degeneration deletes a substrate the levers cannot rebuild. OCD meets it as stabilisation — the loop freezes an attractor the levers cannot unstick. Three disorders, three modes of the same E0 layer: accumulation, loss, and lock-in. And a stabilisation is, in its own way, as far out of reach of a threshold lever as a gain or a decay, because a lever shifts a set-point, and no set-point shift flattens a basin that has grown too deep. So a drive lever that perfectly nudges the instantaneous serotonergic, dopaminergic and glutamatergic tone still leaves the self-sustaining loop running — which is precisely why OCD's response to the mainstay treatments is partial and slow, and why a dynamics intervention (deep-brain stimulation of the CSTC loop, or the exposure-response-prevention that re-plasticises the loop through extinction) can reach refractory cases the levers cannot. The partial grade is the finding, not a failure: it marks exactly where the cross-cutting threshold logic does and does not apply, and it refuses to manufacture a clean fit on a biology whose core is a pathological lock rather than a threshold. The module captures all of this in a domain-restriction witness (INSTANT = reached across L1/L2/L3 with a mixed sign, reachable-but-partial; LOCK = named but not reached) and an out-of-reach-targets section that lists the four loop-lock genes by name — making the partiality concrete, axis-structured and gene-named rather than a vague hedge, and completing the E0 trio (addiction gain → Alzheimer's decay → OCD stabilisation).

L3 is the core — four serotonergic/dopaminergic-drive levers (the mainstay as directions)

The largest reachable lever is the up-stream serotonergic/dopaminergic drive, and it carries four genes — the transporter and receptors that set the tone of the loop's drive, the surface where the established mainstay of OCD care has always acted. SLC6A4 is the serotonin transporter SERT, the molecular target of the SSRIs and clomipramine that are the established serotonergic first-line for OCD — inhibiting it raises synaptic serotonin, the canonical restore-a-deficit move, and OCD's characteristic need for a more sustained, stronger serotonergic course and a longer latency than depression is part of why this lever is the clinical core. HTR2A is the 5-HT_2A serotonin receptor and HTR1B the 5-HT_1B autoreceptor — receptor-level nodes on the same serotonergic drive, each with OCD candidate-gene support, the 5-HT_1B autoreceptor additionally implicated by pharmacological provocation. On all three serotonergic nodes the corrective sign is restore: serotonergic tone is pushed up. The fourth L3 gene reverses the sign. DRD2 is the D₂ dopamine receptor, the target of the antipsychotic augmentation (risperidone, aripiprazole, haloperidol) used for SSRI-refractory and tic-related OCD — and here the direction is reduce: an excess dopaminergic drive is pushed down. These map the real-world OCD pharmacology onto the drive lever as directions on a lever, never as doses, drugs, or recommendations — with the serotonergic restore and the dopaminergic reduce pulling in opposite directions, the source of the mixed sign.

The crucial discipline is the one the whole frame turns on: a promoter read places a gene on a lever; it says nothing about whether raising or lowering that gene's activity is the therapeutic direction, or how far is too far, or in whom. Every one of the four serotonergic/dopaminergic-drive links is graded [O] cited biology, never derived from the substrate. And the drive levers carry the central honesty of this chapter built in — but with a twist that distinguishes OCD from Alzheimer's. A drive-tone lever modulates the instantaneous tone of the loop's drive, which is a real and reachable handle, and here it is not merely symptomatic theatre: the SSRI first-line and the augmentation direction are the actual treatments, and they genuinely reduce obsessions and compulsions in a large fraction of patients. But they reach the operating point, not the lock: restoring serotonergic tone makes the loop easier to interrupt, yet it does not by itself unstick the self-sustaining attractor, which is exactly why response is partial, why it takes weeks, and why a substantial refractory fraction remains. So the drive levers are real, actionable directions on the reachable instantaneous axis that genuinely (partially) help, and they are explicitly not a claim to have reached the loop-lock. A direction, never a dose; the agents are named as a sign on a lever, never as something to obtain or titrate. efficacy = 0.

L1 strong, L2 sparse — glutamate drive reduced, a single inhibitory-restore node (the mixed sign)

What broadens OCD's reachable surface beyond the drive lever is a strong inward glutamate arm; what marks it as distinct is that the inhibitory arm is sparse. The inward lever L1 carries three glutamate genes, and here the direction is reduce. SLC1A1 is the neuronal glutamate transporter EAAT3 — and it is not a minor node: it is the single most replicated OCD candidate / linkage gene (the 9p24 signal), encoding the transporter that clears synaptic glutamate, and the principal target of the glutamate-modulator rationale (raising clearance lowers the hyperactive drive). GRIN2B is the NMDA NR2B subunit (the memantine-class direction) and GRIK2 the kainate GluK2 subunit — both glutamate-receptor nodes with OCD candidate-gene support. Because the fault on this lever is an excess — the orbitofrontal-striatal hyperactivity rides an elevated glutamate tone — the corrective push is downward, the same direction as the dopaminergic node and the opposite of the serotonergic ones. The outward lever L2 carries just one gene, and here the direction is restore. GABRA1 is the GABA_A α₁ subunit — the most abundant synaptic GABA_A subunit, carrying fast phasic inhibition; reduced cortical GABA is reported in OCD and a benzodiazepine (clonazepam) is an adjunct, so restoring inhibitory tone to damp the hyperactive loop is the direction. But it is a single, sparse, weak node — OCD's inhibitory-restore biology is genuinely thin, and the frame records that sparseness rather than inflating it.

That combination — a strong L1 and a sparse L2 — is the structural fingerprint of OCD's reachable surface, and it is worth stating plainly what it means and what it does not. It means the reachable surface is dominated by drive and excitation: the loop is driven (L3) and hyperactive (L1), and the levers that reach it are mostly drive-rebalancing and excitation-reducing, with only a thin inhibitory handle. It does not mean the fit is any less partial: a broad, multi-directional reachable surface still does not touch the dominant fault, because that fault is not on any of the three instantaneous levers at all. Like addiction and Alzheimer's, OCD recruits L1 (and a sparse L2); unlike Alzheimer's, the agents on these levers are the actual mainstay/investigational routes that genuinely (partially) help. Each of the four ionic links is graded [O] cited biology, never derived; the glutamate-reduce and GABA-restore directions are genuine handles on the instantaneous network excitability, and they are explicitly not a handle on the loop-lock. The strong glutamate arm widens what the frame reaches and (with the dopaminergic node) sets the mixed sign; the sparse inhibitory arm is a finding in its own right; neither lets the frame reach the stabilisation.

The out-of-reach LOCK axis: SAPAP3, SLITRK5, PTPRD, BTBD3 — an E0 stabilisation

The dominant OCD fault is the LOCK pathological-stabilisation axis — the over-deep basin, the over-wide hysteresis, that holds the self-sustaining compulsive loop — and it is exactly the axis the instantaneous levers cannot reach. The module names it with four real genes, each carried with its own promoter read alongside but explicitly not a lever. DLGAP3 encodes SAPAP3, the postsynaptic-density scaffold at corticostriatal synapses whose knockout produces compulsive overgrooming in mice — the canonical animal model of OCD-like behaviour, and the clearest molecular handle on the loop-fixation that exists. SLITRK5 is a corticostriatal synaptic-adhesion molecule whose knockout also produces OCD-like overgrooming and corticostriatal dysfunction. PTPRD is a presynaptic synaptic-adhesion receptor-phosphatase implicated by OCD genome-wide association, organising the synapse formation that consolidates the loop. And BTBD3 is a regulator of dendritic orientation and activity-dependent circuit patterning, also implicated by OCD GWAS. Together these four are the circuit-fixation machinery: the scaffolds, adhesion molecules and patterning regulators whose action wires and stabilises the compulsive loop into a self-sustaining attractor.

None of these is a lever, and the reason is the tripled one from the partial-fit section: the lock is a gain/loss, not a fold (no instantaneous lever sets the depth of a basin), it is a consolidated/learned plasticity variable (it deepens through the negative-reinforcement of compulsive relief, a plasticity process, not an instantaneous operating point), and it is a pathological stabilisation — an E0 stabilisation, an over-deep basin / hysteresis that is the third distinct E0 mode after addiction's E0 gain and Alzheimer's E0 decay. This is the precise point the chapter builds toward: addiction's out-of-reach axis was the E0 plasticity layer met as accumulation, Alzheimer's as loss, and OCD's as lock-in — the three completing a trio of E0 modes. A lever shifts a set-point; it does not flatten a basin that the loop's own reinforcement has deepened, just as it could not erase a trace the plasticity had written or rebuild a substrate the degeneration had removed. So the honest move — and the one this chapter makes — is for the threshold frame to name the loop-lock out of reach rather than pretend a drive or ionic lever can unstick a self-sustaining attractor. It is worth being exact about the real therapeutics here: the interventions that do reach the lock are dynamics interventions, not threshold levers — deep-brain stimulation of the CSTC loop for the most refractory cases, and the exposure-response-prevention that re-plasticises the loop through extinction learning. They belong to the dynamics of the out-of-reach axis, not to the instantaneous lever surface this chapter reaches, and they are exactly where a future B-ii (E2/E0 lock-dynamics) layer would act. Each of the four genes is graded [F] NOT REACHED for the lever frame (axis-structured, not dose-structured), with its promoter γ read carried alongside as [V] structural context only.

The DNA grounding: a promoter's own switch stiffness, and a decoupling orthogonal to reach and priority

What places each of the twelve genes — the four serotonergic/dopaminergic levers, the three glutamate levers, the one GABA lever, and the four out-of-reach loop-lock genes — is not a list but a read. For every gene, the module takes its promoter window (transcription start −2000 to +500 bases, Homo sapiens) and computes γ = −mean of the nearest-neighbour base-stacking free energies along that window (the SantaLucia 1998 nearest-neighbour thermodynamics), then turns that γ into the promoter's switch stiffness through the frozen engine's own functions: |h_sp| = spinodal(γ) = 2(γ/3)^1.5 and barrier = γ²/4. The reads span a real range. The four L3 serotonergic/dopaminergic levers, stiffest to softest, are the serotonin transporter SLC6A4 at γ ≈ 1.516 (|h_sp| ≈ 0.719), the D₂ receptor DRD2 (γ ≈ 1.481, |h_sp| ≈ 0.694), the 5-HT_1B autoreceptor HTR1B (γ ≈ 1.475, |h_sp| ≈ 0.689), and the 5-HT_2A receptor HTR2A (γ ≈ 1.321, |h_sp| ≈ 0.584). The three L1 glutamate levers read the kainate subunit GRIK2 at γ ≈ 1.490 (|h_sp| ≈ 0.700), the EAAT3 transporter SLC1A1 (γ ≈ 1.485, |h_sp| ≈ 0.697) and the NMDA NR2B subunit GRIN2B (γ ≈ 1.361, |h_sp| ≈ 0.611); the single L2 GABA lever reads GABRA1 at γ ≈ 1.246 (|h_sp| ≈ 0.536, the softest in the whole set). And the four out-of-reach loop-lock genes do not sit in one place: the corticostriatal scaffold DLGAP3 reads γ ≈ 1.590 (|h_sp| ≈ 0.772, the stiffest in the whole set), the adhesion phosphatase PTPRD reads γ ≈ 1.451 (|h_sp| ≈ 0.673), the patterning gene BTBD3 reads γ ≈ 1.416 (|h_sp| ≈ 0.648), and the adhesion molecule SLITRK5 reads γ ≈ 1.293 (|h_sp| ≈ 0.566, near the soft end).

That range tells a story, and it is the orthogonality the prior partial fits showed, in its cleanest form yet. Stiffness is orthogonal to reach: the stiffest promoter in the entire set is an out-of-reach loop-lock gene (DLGAP3), the softest is a reachable lever (GABRA1), and the four out-of-reach genes span the whole range — the stiffest (DLGAP3) and the near-softest (SLITRK5) are both out of reach, with reachable levers in between. Reachable and out-of-reach genes are interleaved across the entire stiffness range — so promoter stiffness predicts neither which axis a gene is on nor whether it can be reached nor where it ranks. That interleaving is itself the cleanest demonstration of the firewall: if stiffness drove anything, this arrangement could not occur. These are read on the same R19 substrate, with the same engine, that the bipolar, epilepsy, depression, schizophrenia, autism, ADHD, addiction, Alzheimer's and analgesic packages used — one substrate, one pipeline, now nine problems. And the γ read is a property of the gene's promoter sequence, blind to whether the gene is on or off and to gain / loss / expression level — that is all it is, and it is the reason the next section's ranking can carry γ alongside every target without ever letting it touch the score.

Ranking targets, the OCD unmet-need signature, and the firewall that adds two guards

The last component prioritises, and it prioritises targets, never drugs or doses. The OCD ranking spans all twelve genes (the eight levers and the four out-of-reach loop-lock genes), precisely so the partiality is visible in the ranking itself. A burden-weighted score combines three declared, cited weights — clinical burden (0.40), unmet need (0.35), and genetic-evidence / druggability (0.25) — on cited 1–5 tiers. The OCD signature is a new variation on the partial-fit signature, expressed through the unmet-need ceiling. The deepest-unmet tier (U = 5) is held entirely by the four out-of-reach loop-lock genes (DLGAP3, SLITRK5, PTPRD, BTBD3): the refractory loop-lock is the dominant fault and has no molecular therapy — deep-brain stimulation is the only option for the most refractory — so its unmet need is at the ceiling, and it is flagged not actionable. The leading actionable target is the glutamate transporter SLC1A1 at #1 (score 4.65) — the single most replicated OCD candidate gene and the most druggable molecular handle, the glutamate-modulator direction — with the serotonin transporter SLC6A4 at #2 (4.30, the SSRI first-line, its unmet lowered by an established but only partially effective route). The highest-scoring non-actionable target, the corticostriatal scaffold DLGAP3, sits at #3 (4.10). OCD's unmet-need floor is set at 3, above ADHD's floor of 2, because even the established serotonergic route is only partially effective, with a large residual / refractory fraction even under adequate pharmacotherapy and exposure-response-prevention.

The consequence is a ranking that itself encodes the partial fit, with a new twist. Unlike Alzheimer's — where the highest-scoring targets were out of reach — OCD's strongest druggable target (SLC1A1) is reachable; what is out of reach is the deepest-unmet tier (the loop-lock), and even the strongest reachable lever only partially helps because it nudges the operating point and does not unstick the loop. Where the unmet need is at its ceiling the target is unreachable (the lock), and where the target is reachable the benefit is partial (no unsticking of the loop) — the signature of a disorder whose treatments genuinely help while the dominant axis runs untouched. This also produces the firewall made visible, as decoupling. The γ read is carried alongside each target as structural context but is never folded into the score: the stiffest promoter in the set, the out-of-reach scaffold DLGAP3 (|h_sp| ≈ 0.772), sits at priority #3, not the top; and the top-priority target, the reachable transporter SLC1A1, has only the fourth-stiffest read. If promoter stiffness drove the ranking, neither target could sit where it does.

A fail-closed forbidden-claim scanner guards the whole package, and for OCD it adds two classes specific to the topic. The cure / miracle class rejects cure, permanently-stop-the-intrusive-thoughts, eliminate-the-compulsions, OCD-gone, miracle-cure and one-weird-trick framing outright, because the reachable surface is reachable-but-partial and none of it unsticks the loop — the gravest YMYL risk around OCD is exactly the cure-and-miracle myth that preys on patients and families. The moral-framing / stigma class rejects just-stop-worrying, lack-of-willpower, character-flaw, moral-failing, attention-seeking, so-OCD-about and not-a-real-illness framing, because OCD is a treatable medical condition and intrusive thoughts are a symptom, not a confession or a weakness. Both classes are negation-guarded — a sentence that rejects a frame (‘is not a cure’, ‘does not eliminate the compulsions’, ‘is not a moral failing’) is allowed, a sentence that asserts one fails the build — and each carries a planted self-test that must fire on its own bait, failing the build if it ever does not. The firewall must be stated once more in full: the promoter |h_sp| is a gene's own switch stiffness, and it is never equated with a basin depth, a hysteresis width, the strength of the compulsive lock, a receptor occupancy, a synaptic serotonin / dopamine / glutamate level, a drug's potency, a dose, an in-vivo selectivity, or any clinical effect. This module reproduces bit-for-bit with the engine byte-unchanged.

Discipline: the levers genuinely but partially help — OCD is treatable, intrusive thoughts are not a moral failing

Everything here is an in-silico reading of promoter sequence and a frame for organising targets, not a clinical measure, a diagnosis, or a prescription. The model asserts mechanism directions and target placements — OCD's instantaneous CSTC excitability surface can be engaged through the up-stream serotonergic/dopaminergic-drive lever and, strongly, through the glutamate lever and, sparsely, through a single inhibitory node, with a mixed sign; these serotonergic, dopaminergic, glutamate and GABA genes populate those levers; OCD loads most on L3 but strongly engages L1 and sparsely engages L2; the map reaches the instantaneous operating point across all three levers, and (unlike Alzheimer's) the agents on those levers genuinely, partially help; the dominant pathological loop-lock is named and out of reach — for a new reason, as a gain/loss, a consolidated/learned plasticity variable, and a pathological stabilisation (an E0 stabilisation, the third distinct E0 mode after addiction's gain and Alzheimer's decay); the fit is therefore the fourth [L] partial fit and a new mode — and nothing about which agent acts on any lever, at what dose, in whom, whether any real compound changes anyone's condition, or that anyone should change anything. The agents named as directions (the SSRI / clomipramine, antipsychotic-augmentation and glutamate-modulator arms) are illustrations of a sign on a reachable lever, never a recommendation, and the recorded structure — the dominant axis out of reach, the loop-lock named but unreached — is there precisely because a generic lever placement is not a clinical direction. Real OCD is polygenic and heterogeneous, and its established serotonergic first-line is only partially effective, with its strongest response often needing combined pharmacotherapy and exposure-response-prevention — a limit that is locked, not smoothed over.

Two stricter boundaries close the chapter. First, the reachable levers genuinely but partially help, and do not unstick the loop. The SSRI, augmentation and glutamate-modulator directions act on the instantaneous operating point; they relieve obsessions and compulsions in many patients, and they do not by themselves dissolve the self-sustaining attractor, which is why response is partial and slow and why a refractory fraction remains. The map does not assert that any lever direction cures OCD or permanently stops intrusive thoughts, and the interventions that reach the loop-lock at all — deep-brain stimulation of the CSTC loop, and the exposure-response-prevention that re-plasticises it through extinction — act on the out-of-reach dynamics axis, not the instantaneous lever surface. Second, OCD is a treatable medical condition, and intrusive thoughts are a symptom, not a confession or a weakness. The moral-framing class in the scanner is not decoration: OCD is surrounded by trivialising and willpower-shaming language — ‘just stop worrying’, ‘a bit OCD about my desk’, ‘snap out of it’ — and this chapter rejects all of it. A person's compulsions are not a choice and their intrusive thoughts are not a moral failing; the disorder is a pathological lock in a circuit, not a flaw in a character, and nothing in the mechanism described here licenses treating anyone as weak-willed or culpable. A promoter read and a lever assignment are mechanism boundaries, not a claim about the felt quality of obsession, compulsion, or relief in OCD (Axis-A firewall — consciousness_claim = 0, the hard problem stays open). This is not medical advice, not a diagnosis, not a treatment protocol, and not a cure. medium_efficacy_tested = 0; targets ranked, never drugs or doses; no cure / miracle or moral-framing licence; the reachable levers genuinely but partially help and do not unstick the loop; OCD is a treatable medical condition and intrusive thoughts are a symptom, not a moral failing.