What each abnormal finding means, which cascade node it confirms, and how it changes the intervention layer sequence.
See framework disclaimer belowIn regression, abnormal findings are not independent signals. They represent interacting components of a destabilized system — where immune activation, mitochondrial stress, and excitotoxic signaling reinforce each other. Interpretation should focus on convergence, not isolated markers.
This document is for after testing. You have results in front of you and need to know what they mean within the cascade framework — which nodes are confirmed active, how severe the finding is, and how it changes the order in which interventions should be applied.
The interpretation tables below are organized in two stages. Section 2 maps each specific abnormal finding to its cascade interpretation — what the biology is doing. Section 3 translates that into protocol action — what changes about the intervention sequence as a result. Section 4 addresses the most common real-world scenario: multiple channels confirmed active at once, and how to prioritize when everything is pointing in several directions simultaneously.
Some results set a baseline rather than trigger a reorder. Low BDNF confirms that the CREB pathway is suppressed — but the protocol response is to retest at 3 and 6 months, not to reorder the layers. Baseline markers tell you where you are starting from and whether the intervention is working. Distinguishing a routing marker from an outcome marker matters when deciding what to act on first.
The cascade interpretations below reflect the theoretical framework and the peer-reviewed biology underlying it. They are not clinical diagnoses. Abnormal values should always be reviewed with a qualified practitioner before intervention changes are made — particularly when findings involve cortisol patterns, heavy metals, mitochondrial dysfunction, or significant inflammatory markers.
Find your abnormal result in the first column. The cascade interpretation column explains what the biology is doing at the node level. The protocol implication column tells you what changes in the intervention sequence. Results that serve as outcome markers are flagged distinctly.
| Test / finding | Abnormal result | Cascade interpretation | Immediate protocol implication | Channel |
|---|---|---|---|---|
| OAT — TCA cycle markers | Succinic, fumaric, or malic acid elevated (2+ markers) | TCA cycle blocked; mitochondrial respiration impaired; PGC-1α downstream failure confirmed. Cells are running anaerobic glycolysis rather than efficient oxidative phosphorylation. In regression: When TCA markers are elevated alongside active regression — particularly when motor regression is present alongside speech regression — this is not a background metabolic finding. Neuronal maintenance of active synaptic connections is energy-intensive. When ATP production falls below the threshold for sustaining those connections, previously acquired skills become energetically inaccessible. CoQ10 ubiquinol and NMN/NR move to co-foundational Layer 1 regardless of what other channels are confirmed. Order lactate:pyruvate ratio to confirm respiratory chain failure depth. | CoQ10 ubiquinol + NMN/NR move to Layer 1 alongside magnesium. L-carnitine added if carnitine panel confirms deficiency. Add lactate:pyruvate ratio to confirm respiratory chain failure depth. | Mitochondrial |
| OAT — kynurenine metabolites | Quinolinic acid elevated; kynurenic acid low or absent | IDO1 maximally activated; tryptophan fully diverted into neurotoxic kynurenine pathway. SIRT1 fuel (NAD⁺) critically depleted. Quinolinate is actively generating NMDA receptor pressure and oxidative DNA damage. In regression: Quinolinic acid elevation during regression is not merely a SIRT1 fuel problem — it is active NMDA receptor overactivation. QUIN binds NMDA receptors causing calcium influx in neurons, destabilizing the electrical activity required to maintain encoded skills. This is your core regression mechanism: IDO1 → QUIN → excitotoxic pressure → functional skill loss. NAC is urgent not just for oxidative protection but to reduce quinolinate-driven NMDA activation. This finding in a regressing child changes the clinical picture from 'metabolic support needed' to 'active neuroprotection needed immediately.' | NMN/NR urgent — without NAD⁺ repletion no downstream intervention works. NAC immediate to protect against quinolinate-driven oxidative damage. Anti-inflammatory layer (luteolin + omega-3) must run concurrently to reduce IDO1 induction pressure. | MIA / Neuroinflammation |
| OAT — gut dysbiosis markers | Arabinose elevated (yeast); HPHPA elevated (Clostridia) | Active gut dysbiosis confirmed. Yeast producing arabinose; Clostridia producing HPHPA which inhibits dopamine metabolism. LPS translocation active; propionate excess suppressing mitochondrial function from a second direction. | Antifungal or antimicrobial support before any probiotic. C. butyricum after clearance. Gut becomes Layer 1 — do not advance other layers while active dysbiosis is driving LPS load. | Gut / LPS |
| K:T ratio | Elevated (>0.06; threshold is lab-dependent) | IDO1 actively diverting tryptophan. Functional NAD⁺ insufficiency confirmed — not a deficit of absolute NAD⁺ but of regeneration rate under inflammatory load. Neuroinflammation is sustaining IDO1 induction in a self-reinforcing loop. In regression: In a stable presentation, elevated K:T means the IDO1 loop is running and NAD⁺ is insufficient. In a regression state, the same K:T elevation also confirms that quinolinic acid production is outpacing QPRT conversion — meaning neurotoxic NMDA pressure is active. The urgency of NMN/NR jumps from 'important' to 'immediate.' Anti-inflammatory layer is not optional: without reducing IDO1 induction pressure, NMN/NR cannot keep pace with consumption. | NMN/NR to Layer 1 urgently. Anti-inflammatory layer (luteolin, omega-3) essential to reduce the IDO1 induction pressure. Without anti-inflammatory support, NMN/NR alone cannot keep pace with IDO1-driven NAD⁺ consumption. | MIA / Neuroinflammation |
| hsCRP | Elevated >1.0 mg/L without acute infection | Chronic systemic NF-κB activation confirmed. Rule out acute infection first — hsCRP is non-specific. When chronic, this is the most accessible single indicator that the inflammatory arm of the cascade is active. | Rule out acute infection. If chronic: full anti-inflammatory layer (luteolin, omega-3, curcumin) becomes priority. Pair with ESR — both elevated together provides stronger confirmation than either alone. | MIA / Neuroinflammation |
| Cytokines IL-6 + TNF-α | Both elevated | Active M1 microglial state confirmed. NF-κB driving cytokine production; A1 astrocyte conversion likely ongoing. The neuroinflammatory self-sustaining loop is in active maintenance — not an acute event. | Luteolin 200–400mg + omega-3 EPA:DHA 2:1 at 2–3g/day move to Layer 1. Curcumin phospholipid complex 1g/day as adjunct NF-κB suppressor. Quercetin can substitute if luteolin is unavailable. | MIA / Neuroinflammation |
| Zonulin + LBP | Both elevated | Active gut barrier disruption with systemic LPS translocation confirmed simultaneously from two directions. Gut is a real-time ongoing upstream trigger — not historical. Every systemic intervention is being continuously undermined. | Gut repair is Layer 1, non-negotiable. Zinc carnosine 75mg + L-glutamine 5g + DGL for barrier repair. C. butyricum for microbiome reseeding. Remove dietary LPS-promoting factors (refined carbohydrates, alcohol, processed seed oils). | Gut / LPS |
| GI-MAP — calprotectin | Calprotectin >100 mcg/g stool | Active intestinal inflammation confirmed. Neutrophil activation; LPS translocation risk high; dysbiosis severe. Calprotectin >200 mcg/g warrants gastroenterology review to rule out inflammatory bowel disease before proceeding. | Do not start probiotic protocol until gut inflammation is addressed. Gastroenterology referral if >200 mcg/g. Anti-inflammatory gut support (DGL, omega-3, butyrate) before probiotic reseeding. | Gut / LPS |
| GI-MAP — pancreatic elastase | Elastase <200 mcg/g stool | Pancreatic enzyme output suppressed — the gut signature of elevated SST. Somatostatin directly inhibits pancreatic secretion. Malabsorption of nutrients confirmed; all oral supplement bioavailability is reduced. | Digestive enzyme support at meals immediately (lipase, protease, amylase). SST/HPA channel is co-active — add salivary cortisol + IGF-1. All supplement dosing must account for malabsorption until elastase normalizes. | SST / HPA Axis |
| Salivary cortisol — diurnal pattern | Flat, inverted, or chronically elevated curve | HPA axis dysregulated. Flat or inverted = adrenal exhaustion with SST tonically elevated. Chronically elevated = active stress-driven SST elevation. In either case, cAMP/CREB is suppressed around the clock — not intermittently. | Sleep and circadian optimization is non-negotiable Layer 1. Melatonin 0.5–1mg at consistent time. Phosphatidylserine 100–200mg evening. Eliminate blue light after sunset. Consistent wake time is the most important single sleep intervention. | SST / HPA Axis |
| Hair cortisol | Elevated (>20–30 pg/mg; lab-dependent) | Sustained chronic HPA load confirmed over the preceding 3 months — not a transient stress response. SST has been chronically elevated long-term. This is the critical distinction from salivary cortisol alone, which cannot confirm chronicity. | Chronic load confirmed — stress reduction and sleep optimization are non-negotiable prerequisites before any other intervention. Reassess hair cortisol at 3 months as primary treatment response marker alongside BDNF. | SST / HPA Axis |
| IGF-1 | Low for age (use pediatric reference range) | Functional SST excess confirmed via GH suppression — a second independent confirmation of elevated SST tone separate from the HPA axis findings. When both cortisol pattern and IGF-1 are abnormal, SST is doubly confirmed from two mechanistic directions. | SST reduction layer moves up in priority. Low-dose forskolin 5mg under practitioner supervision — after HPA stabilization, not before. Address fasting insulin if HOMA-IR is also elevated. | SST / HPA Axis |
| DHEA-S | Low for age; especially with flat cortisol curve | HPA exhaustion pattern confirmed. Adrenal axis in conservation phase after chronic activation — downregulating both cortisol and DHEA-S. Chronic SST elevation sustained without the cortisol spike that would otherwise signal HPA activation. | Adrenal recovery must precede SIRT1 restoration. Phosphatidylserine 100–200mg evening. Sleep optimization non-negotiable. Reduce all identifiable HPA stressors. Do not advance the protocol until adrenal markers begin recovering. | SST / HPA Axis |
| Glutamate / GABA ratio | Elevated glutamate or depressed GABA relative to reference | E/I imbalance confirmed. SST interneuron loss has reached the architectural level — this is structural, not just signaling suppression. Glypican-silent synapses are likely active. The cascade has entered the connectivity disruption stage. | Magnesium glycinate for NMDA modulation. L-theanine for glutamate modulation. Butyrate for GABA upregulation via gut-brain axis. Reduce all SST drivers. Upstream channel work is even more urgent when E/I imbalance is confirmed. | SST / HPA Axis |
| Actigraphy / PSG — sleep architecture | SWS <15% of total sleep; fragmented architecture | Glymphatic clearance impaired during the primary clearance window. Quinolinic acid, cytokines, and metabolic debris accumulate nightly rather than being cleared. Morning inflammatory burden is elevated before the day begins. | Melatonin timing becomes Layer 1, non-negotiable. Magnesium glycinate for GABA-mediated sleep onset. Circadian repair before all other interventions — no other layer has traction while nightly inflammatory accumulation continues. Reassess at 3 months. | SST / HPA Axis |
| GPL-TOX / Glyphosate | Multiple compounds positive; glyphosate quantifiable | Environmental toxin burden actively driving oxidative stress, IDO1 activation, and gut microbiome disruption simultaneously from a separate upstream direction. These effects compound all other active channels — they do not add linearly, they multiply. | Detox sub-layer before Layer 1: NAC + sulforaphane + glycine 2–4g/day. Activated charcoal (away from supplements by 2 hours). Dietary glyphosate reduction non-negotiable — supplementation cannot compensate for continuous re-exposure. | Environmental / Oxidative |
| RBC heavy metals | Mercury, lead, or arsenic elevated | Heavy metal burden suppressing SIRT1 catalytic activity directly; elevating inflammatory cytokines; impairing glutathione synthesis. SIRT1 cannot be meaningfully restored while significant metal burden remains. | NAC + glutathione support immediately. Sulforaphane to restore GSH enzyme synthesis capacity. Professional chelation consultation if Hg or Pb significantly elevated — DMSA/DMPS chelation only under physician supervision with mineral monitoring. | Environmental / Oxidative |
| GSH:GSSG ratio | Reduced GSH <80% of total glutathione | Antioxidant system overwhelmed. FOXO axis depleted. DNA damage accumulating faster than it can be repaired. The oxidative burden has exceeded available buffering capacity — qualitatively different from mild depletion. | NAC 600–900mg twice daily is the most urgent single intervention — provides cysteine precursor for glutathione synthesis. Sulforaphane to restore GSH enzyme capacity. If severely low, consider liposomal glutathione in addition to NAC. | Environmental / Oxidative |
| Micronutrient panel | Multiple deficiencies (B6, B12, zinc, magnesium, selenium) | Co-factor depletions limiting enzymatic function across all cascade nodes. Every supplement intervention will underperform until foundational co-factors are in place — this is a pre-Layer 0 finding that must be addressed first. | B6 25–50mg; B12 methylcobalamin 1000mcg; methylfolate 400–800mcg; zinc 10–15mg elemental; selenium 50–100mcg. Magnesium and B6 have ASD-specific RCT data — highest priority within co-factors. | Multi-channel |
| Vitamin D (25-OH-D) | <40 ng/mL | VDR-mediated NF-κB suppression impaired. Near-universal in ASD; strongly correlated with severity. Even modest deficiency permits unchecked NF-κB activation — among the highest-yield, lowest-cost interventions in the entire protocol. | Vitamin D3 2000–5000 IU + K2 (MK-7) 90–180mcg daily. Retest at 3 months. Target 50–70 ng/mL. K2 is essential at therapeutic D3 doses to direct calcium appropriately. | Multi-channel |
| BDNF (serum) — outcome marker | Low (<20 ng/mL; lab-dependent) | CREB pathway output suppressed — downstream readout of both the SST/cAMP arm and the SIRT1/NF-κB arm suppressing the learning circuit simultaneously. Does not trigger a layer reorder — it confirms the cascade has reached output level and sets the treatment response benchmark. In regression: In a regression state, low BDNF is not just a baseline measurement — it is the molecular explanation for the skill loss. BDNF is required not only for acquiring new skills but for maintaining synaptic connections that encode previously learned ones. The lower the BDNF at baseline, the more severe the pathway suppression. A 3-month BDNF retest is the single most important follow-up test in regression: even a modest rise (e.g. 14 → 22 ng/mL) is strong evidence that the circuit is capable of recovering, and should be presented to the practitioner as the primary biological signal of treatment response. | Use as outcome marker only. Retest at 3 and 6 months — rising BDNF is the primary objective biological signal that the cascade is responding. Omega-3 + structured aerobic exercise are most evidence-supported BDNF-promoting interventions alongside upstream channel work. | Multi — CREB output |
| Regression — loss of acquired speech, language, motor skills, or social connection | Skills previously present are gone or significantly diminished. May have appeared abruptly (following illness, fever, or immune event) or gradually over weeks to months. | Regression is not a distinct biological channel — it is the downstream behavioral signature of CREB/BDNF pathway failure severe enough that previously encoded skills can no longer be maintained. The cascade has reached the output level. Both the SST arm and the SIRT1/neuroinflammation arm are typically active simultaneously when regression is present — CREB is being suppressed from two independent directions at once. When regression followed a febrile illness, vaccination, or gut event, that event was likely the acute trigger that tipped a cascade already underway. The trigger is not the root cause; the upstream channels active before the event are. | BDNF baseline is urgent — this is the primary outcome marker for recovery. Address all confirmed upstream channels using standard routing above, but expect slower response timelines (3–6 months for measurable BDNF movement). If regression followed an immune event: add Zonulin + LBP to confirm active gut trigger. If motor regression accompanies speech regression: add plasma lactate:pyruvate ratio — mitochondrial dysfunction is more likely co-active. Do not interpret regression as permanent architectural damage — rising BDNF confirms the circuit is capable of recovering. For full test battery, see 07B — Regression test battery. For communication scripts, see 07D — Regression script. | Multi — CREB failure |
This table translates confirmed channel findings directly into protocol layer changes. When a channel is confirmed active, specific layers are reordered — some elevated to Layer 1, some triggering a new pre-layer, and some confirming a layer that would otherwise be delayed becomes immediately relevant.
| Confirmed finding | Channel | Layer reorder | Interventions prioritized |
|---|---|---|---|
| OAT: TCA markers elevated (2+) | Mitochondrial | Layer 3 → Layer 1 | Ubiquinol 200–400mg; NMN/NR 250–500mg; L-carnitine 500–1000mg with meals; magnesium glycinate maintained as foundation. |
| OAT: Quinolinic acid elevated | MIA / IDO1 | Layer 3 → Layer 1–2 | NMN/NR immediately; luteolin + omega-3 to reduce IDO1 induction; NAC for quinolinate-driven oxidative damage. Anti-inflammatory layer must precede SIRT1 activation attempts. |
| OAT: Arabinose + HPHPA elevated | Gut / Dysbiosis | Layer 4 → Layer 1 | Antifungal support (yeast); Clostridia-targeted intervention; C. butyricum only after clearance phase; butyrate support to restore colonocyte function. |
| Zonulin + LBP both elevated | Gut / LPS Active | Layer 4 → Layer 1 | Zinc carnosine 75mg; L-glutamine 5g; DGL; C. butyricum; remove LPS-promoting dietary factors. Systemic layers underperform while LPS continuously re-triggers NF-κB. |
| K:T ratio elevated | MIA / IDO1 | Layer 3 → Layer 1 | NMN/NR 250–500mg; niacinamide as adjunct NAD⁺ support; luteolin + omega-3 to suppress IDO1 induction. Anti-inflammatory layer must run concurrently. |
| Cortisol: flat or inverted curve | SST / HPA | Layer 5 → Layer 1 | Melatonin 0.5–1mg at consistent time; phosphatidylserine 100–200mg evening; eliminate blue light after sunset; consistent wake time. No other layers advance until sleep is stabilizing. |
| IGF-1 low + cortisol abnormal | SST — doubly confirmed | Layer 5 → Layer 2 | All cortisol-normalization steps applied first. Low-dose forskolin 5mg under practitioner supervision after HPA stabilization. Address fasting insulin if HOMA-IR also elevated. |
| DHEA-S low + cortisol flat | SST / HPA — Exhaustion | Layer 5 → Layer 1 | Phosphatidylserine 100–200mg evening; sleep optimization urgent; melatonin; reduce all HPA stressors. Adrenal recovery precedes SIRT1 restoration — do not advance protocol until markers recover. |
| Cytokines IL-6 + TNF-α elevated | MIA / Microglia | Layer 2 urgency elevated | Luteolin 200–400mg + quercetin; omega-3 EPA:DHA 2:1 at 2–3g/day; curcumin phospholipid complex 1g/day. Both anti-inflammatory agents move to highest urgency within their layer. |
| GSH:GSSG ratio low | Environmental / FOXO | Layer 2 → NAC becomes Layer 1 | NAC 600–900mg twice daily becomes co-foundational. Sulforaphane standardized 50–100mcg/day. Antioxidant depletion overrides standard sequencing. |
| GPL-TOX / Glyphosate positive | Environmental | New pre-Layer 1: Detox | NAC; sulforaphane; glycine 2–4g/day; activated charcoal (2 hours from supplements). Detox support runs before and alongside all other layers to prevent re-toxification. |
| RBC metals elevated | Environmental | New pre-Layer 1: Detox | NAC + glutathione support immediately. DMSA/DMPS chelation only under physician supervision. Cannot restore SIRT1 while heavy metal burden directly suppresses it. |
| Micronutrients: multiple deficiencies | Multi-channel | Pre-Layer 0 — address first | B6 25–50mg; B12 methylcobalamin 1000mcg; methylfolate; zinc 10–15mg; selenium 50–100mcg. Co-factor deficiencies limit every other intervention — correct before targeted protocol begins. |
| Vitamin D <40 ng/mL | Multi — NF-κB | Layer 2 — add immediately | Vitamin D3 2000–5000 IU + K2 (MK-7) 90–180mcg daily. Retest at 3 months. Target 50–70 ng/mL. High-yield, low-cost regardless of other findings. |
| BDNF low (baseline) | Multi — CREB output | Outcome marker — no layer change | Retest at 3 and 6 months. Rising BDNF = cascade responding. Omega-3 + structured aerobic exercise most evidence-supported alongside upstream channel work. |
Most children present with two or more channels confirmed active simultaneously. These pattern cards address the most common combinations and how to prioritize when findings are pointing in multiple directions at once.
The gut is the most frequent upstream driver of neuroinflammation in ASD — LPS continuously activating TLR4/NF-κB is the direct ignition source for M1 microglial activation. When both channels are confirmed, addressing gut first is mechanistically required, not a preference.
Sequencing ruleGut repair is Layer 1. Anti-inflammatory layer (luteolin, omega-3) runs concurrently but cannot fully succeed while LPS is still entering systemic circulation. NMN/NR introduced in parallel but has limited effect until IDO1 induction pressure from LPS is reduced. Expect 4–8 weeks of gut repair before neuroinflammatory markers begin to improve.
When both the SST arm and the SIRT1/neuroinflammation arm are confirmed active, CREB is being suppressed from two independent directions simultaneously. This is the cascade's most treatment-resistant configuration — neither arm can be fully addressed without the other.
Sequencing ruleSleep and circadian optimization is Layer 1 non-negotiable. Anti-inflammatory layer runs in parallel. NMN/NR starts once sleep is stabilizing. BDNF retest at 3 months is the primary progress marker. This pattern typically requires 3–6 months to show measurable improvement — expect a gradual trend, not an acute response.
Environmental burden does not add linearly to other active channels — it multiplies their effect. Glyphosate compounds gut dysbiosis. Heavy metals directly suppress SIRT1. Both elevate oxidative load that further activates IDO1. When environmental is confirmed alongside any other channel, detox support becomes foundational — not optional.
Sequencing ruleDetox sub-layer runs before Layer 1: NAC, sulforaphane, glycine. Ongoing exposure reduction is non-negotiable — no supplement protocol compensates for continuous re-exposure. If metals are significantly elevated, other channel interventions have substantially reduced efficacy until metal burden is meaningfully reduced.
Mitochondrial dysfunction reduces cellular energy available for every repair and detoxification process. When the mito channel is confirmed alongside gut, neuroinflammation, or SST, all other intervention responses are attenuated — the cell cannot mount a repair response without adequate ATP.
Sequencing ruleCoQ10 ubiquinol + NMN/NR move to Layer 1 alongside the primary driver from the other active channel. Carnitine added if deficient. Magnesium is foundational throughout. Mito channel does not take sequencing priority over active gut or extreme HPA pattern, but runs co-foundationally in parallel from the beginning.
Regression is not a channel finding — it is a clinical presentation that signals CREB/BDNF pathway failure has reached the output level. Unlike the other pattern cards, the question is not "which two channels are active" but "which channels are suppressing CREB from both directions simultaneously." In practice, most regression cases involve both the neuroinflammation arm (IDO1-driven NAD⁺ depletion → SIRT1 failure → CREB suppressed) and the SST arm (HPA dysregulation → SST tonically elevated → cAMP/CREB suppressed) — making it functionally equivalent to the double CREB suppression pattern above, but with a confirmed behavioral output that makes the urgency concrete.
What to look for in resultsLow BDNF confirms the output failure. Elevated K:T or quinolinic acid on OAT confirms the neuroinflammation arm. Abnormal cortisol pattern + low IGF-1 confirms the SST arm. If both arms are confirmed and BDNF is low, you are looking at the full double-suppression pattern with behavioral output. If regression followed a gut or immune event, elevated Zonulin + LBP confirm the triggering channel is still active.
Sequencing rule for regressionAddress upstream channels using standard routing — the regression itself does not change the intervention sequence, but it raises the urgency of the BDNF retest timeline. Use 3-month BDNF retesting as the primary progress signal. If motor regression accompanies speech regression, mitochondrial support (CoQ10 ubiquinol, NMN/NR) moves to co-foundational Layer 1 alongside whatever primary channel driver is confirmed. Rising BDNF at 3 months — even modestly — is the most meaningful signal that the circuit is capable of recovering. The goal is not restoration of the lost skills directly; it is restoration of the biological conditions under which skill consolidation can occur again.
When gut, neuroinflammation, SST/HPA, mitochondrial, and environmental channels are all confirmed active, the cascade has reached its self-sustaining state — each arm reinforcing the others. Single-target approaches are most likely to fail here. The loop cannot be broken from any single point.
Priority hierarchy for the full-cascade pattern(1) Environmental detox sub-layer if metals or toxins are significantly elevated — this is the prerequisite that limits all other recovery. (2) Co-factor deficiencies corrected (pre-Layer 0). (3) Gut repair as Layer 1 if active LPS translocation is confirmed — the most common primary driver. (4) Sleep and circadian repair concurrently — without glymphatic clearance, nightly inflammatory accumulation defeats all other progress. (5) Anti-inflammatory layer (luteolin, omega-3) running from the beginning. (6) NAD⁺ repletion (NMN/NR) once layers 1–4 are stabilizing. (7) SIRT1 activation (resveratrol, low-dose forskolin) only after confirmed improvement in upstream markers. Retest BDNF, K:T ratio, and hair cortisol at 3 months to assess whether the loop is responding.