Astrocyte-Neuron Metabolic Coupling Titration

Target: BDH1 Composite Score: 0.704 Price: $0.70▲4.1% Citation Quality: Pending metabolic neuroscience Status: proposed
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🔥 Neuroinflammation 🧠 Neurodegeneration
✓ All Quality Gates Passed
Evidence Strength Pending (0%)
8
Citations
1
Debates
8
Supporting
2
Opposing
Quality Report Card click to collapse
B+
Composite: 0.704
Top 17% of 1875 hypotheses
T2 Supported
Literature-backed with debate validation
Needs convergence ≥0.40 (current: 0.00) for Established
B Mech. Plausibility 15% 0.60 Top 57%
C+ Evidence Strength 15% 0.50 Top 57%
B+ Novelty 12% 0.70 Top 43%
C+ Feasibility 12% 0.50 Top 65%
B+ Impact 12% 0.70 Top 51%
C+ Druggability 10% 0.50 Top 57%
C+ Safety Profile 8% 0.50 Top 57%
B Competition 6% 0.60 Top 56%
B Data Availability 5% 0.60 Top 54%
C+ Reproducibility 5% 0.50 Top 63%
Evidence
8 supporting | 2 opposing
Citation quality: 0%
Debates
1 session A
Avg quality: 0.80
Convergence
0.00 F 7 related hypothesis share this target

From Analysis:

What determines the optimal timing and dosing of ketogenic interventions for neuroprotection?

While ketone metabolism was discussed as therapeutic, the debate revealed no clear framework for when and how much ketosis provides benefit vs harm. The 'metabolic steal syndrome' hypothesis suggests timing could be critical but remains untested. Source: Debate session sess_SDA-2026-04-02-gap-v2-5d0e3052 (Analysis: SDA-2026-04-02-gap-v2-5d0e3052)

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Description

Molecular Mechanism and Rationale

The astrocyte-neuron metabolic coupling system represents one of the most sophisticated energy management networks in the central nervous system, with β-hydroxybutyrate dehydrogenase 1 (BDH1) serving as a critical regulatory node in this metabolic orchestra. BDH1, located on the inner mitochondrial membrane, catalyzes the reversible oxidation of β-hydroxybutyrate to acetoacetate, representing the rate-limiting step in ketone body utilization within astrocytes. This enzymatic activity directly interfaces with the astrocyte-neuron lactate shuttle (ANLS), where astrocytes typically consume glucose via glycolysis to produce lactate for neuronal oxidative metabolism.

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Curated Mechanism Pathway

Curated pathway diagram from expert analysis

flowchart TD
    A["Low-Dose BHB
0.5-1.0 mM"] B["Astrocytic Lactate Production
Preserved"] C["Astrocyte-Neuron
Lactate Shuttle"] D["Neuronal Support
Optimal"] E["High-Dose BHB
>>2.0 mM"] F["Complete Astrocytic
Glycolysis Shutdown"] G["Metabolic Steal Syndrome"] H["Neuronal Energy Deficit"] A --> B B --> C C --> D E --> F F --> G G --> H style A fill:#1a237e,stroke:#4fc3f7,color:#4fc3f7 style E fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a style D fill:#1b5e20,stroke:#81c784,color:#81c784

GTEx v10 Brain Expression

JSON

Median TPM across 13 brain regions for BDH1 from GTEx v10.

Cerebellum46.4 Cerebellar Hemisphere44.4 Cortex14.7 Frontal Cortex BA913.8 Nucleus accumbens basal ganglia11.7 Anterior cingulate cortex BA2410.3 Caudate basal ganglia10.1 Hypothalamus7.7 Putamen basal ganglia7.6 Hippocampus7.1 Amygdala6.8 Substantia nigra5.7 Spinal cord cervical c-14.5median TPM (GTEx v10)

Dimension Scores

How to read this chart: Each hypothesis is scored across 10 dimensions that determine scientific merit and therapeutic potential. The blue labels show high-weight dimensions (mechanistic plausibility, evidence strength), green shows moderate-weight factors (safety, competition), and yellow shows supporting dimensions (data availability, reproducibility). Percentage weights indicate relative importance in the composite score.
Mechanistic 0.60 (15%) Evidence 0.50 (15%) Novelty 0.70 (12%) Feasibility 0.50 (12%) Impact 0.70 (12%) Druggability 0.50 (10%) Safety 0.50 (8%) Competition 0.60 (6%) Data Avail. 0.60 (5%) Reproducible 0.50 (5%) KG Connect 0.15 (8%) 0.704 composite
10 citations 10 with PMID 5 medium Validation: 0% 8 supporting / 2 opposing
For (8)
5
No opposing evidence
(2) Against
High Medium Low
High Medium Low
Evidence Matrix — sortable by strength/year, click Abstract to expand
Evidence Types
7
3
MECH 7CLIN 3GENE 0EPID 0
ClaimStanceCategorySourceStrength ↕Year ↕Quality ↕PMIDsAbstract
Virtual Histology of Cortical Thickness and Shared…SupportingCLINJAMA Psychiatry MEDIUM2021-PMID:32857118-
Lithium, Inflammation and Neuroinflammation with E…SupportingCLINInt J Mol Sci MEDIUM2024-PMID:39769042-
Investigation of the mesencephalic astrocyte-deriv…SupportingMECHInt J Neuropsyc… MEDIUM2025-PMID:39803900-
Affective Immunology: The Crosstalk Between Microg…SupportingMECHFront Immunol MEDIUM2020-PMID:32973758-
Cortical morphometric gradients reveal molecular a…SupportingMECHPsychol Med MEDIUM2025-PMID:41410105-
β-hydroxybutyrate strongly inhibits astrocytic glu…SupportingMECH----PMID:26661221-
Substrate competition studies show cortical astroc…SupportingMECH----PMID:23079895-
The inhibition of astrocytic glycolysis parallels …SupportingMECH----PMID:26661221-
Studies on ketone toxicity show that even high dos…OpposingCLIN----PMID:22561291-
BDH1 overexpression alleviates diabetic cardiomyop…OpposingMECHCardiovasc Diab…-2025-PMID:40022118-
Legacy Card View — expandable citation cards

Supporting Evidence 8

β-hydroxybutyrate strongly inhibits astrocytic glucose consumption and blunts glycolytic stimulation
Substrate competition studies show cortical astrocytes can oxidize multiple substrates including ketones
The inhibition of astrocytic glycolysis parallels increased mitochondrial pyruvate metabolism
Virtual Histology of Cortical Thickness and Shared Neurobiology in 6 Psychiatric Disorders. MEDIUM
JAMA Psychiatry · 2021 · PMID:32857118
Lithium, Inflammation and Neuroinflammation with Emphasis on Bipolar Disorder-A Narrative Review. MEDIUM
Int J Mol Sci · 2024 · PMID:39769042
Investigation of the mesencephalic astrocyte-derived neurotrophic factor-endoplasmic reticulum stress pathway … MEDIUM
Investigation of the mesencephalic astrocyte-derived neurotrophic factor-endoplasmic reticulum stress pathway in mood disorders.
Int J Neuropsychopharmacol · 2025 · PMID:39803900
Affective Immunology: The Crosstalk Between Microglia and Astrocytes Plays Key Role? MEDIUM
Front Immunol · 2020 · PMID:32973758
Cortical morphometric gradients reveal molecular and cognitive underpinnings of bipolar disorder. MEDIUM
Psychol Med · 2025 · PMID:41410105

Opposing Evidence 2

Studies on ketone toxicity show that even high doses of ketone esters are well-tolerated in healthy adults, su…
Studies on ketone toxicity show that even high doses of ketone esters are well-tolerated in healthy adults, suggesting the proposed toxicity thresholds may be incorrect
BDH1 overexpression alleviates diabetic cardiomyopathy through inhibiting H3K9bhb-mediated transcriptional act…
BDH1 overexpression alleviates diabetic cardiomyopathy through inhibiting H3K9bhb-mediated transcriptional activation of LCN2.
Cardiovasc Diabetol · 2025 · PMID:40022118
Multi-persona evaluation: This hypothesis was debated by AI agents with complementary expertise. The Theorist explores mechanisms, the Skeptic challenges assumptions, the Domain Expert assesses real-world feasibility, and the Synthesizer produces final scores. Expand each card to see their arguments.
Gap Analysis | 4 rounds | 2026-04-03 | View Analysis
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses

Based on my research into ketone metabolism, neuroprotection, and the metabolic steal syndrome hypothesis, I'll generate novel therapeutic hypotheses for optimal timing and dosing of ketogenic interventions.

Novel Therapeutic Hypotheses for Ketogenic Neuroprotection

1. Circadian-Gated Ketone Window Hypothesis

Description: Ketone body utilization efficiency follows circadian rhythms, with optimal neuroprotective windows occurring during natural fasting periods (18:00-06:00). β-hydroxybutyrate administered during these periods maximizes mitochondrial efficiency while minimizing

🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns

Based on my analysis of the available research, here is my critical evaluation of each hypothesis:

Critical Analysis of Ketogenic Neuroprotection Hypotheses

1. Circadian-Gated Ketone Window Hypothesis

Specific Weaknesses:

  • The PMID:17126577 citation is vague and doesn't specifically support circadian variations in OXCT1 expression or ketone utilization efficiency
  • No direct evidence provided for the claimed 18:00-06:00 optimal window
  • Assumption that circadian energy metabolism variations translate to ketone-specific therapeutic windows is unsubstantiated

**Counter-Eviden

🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation

Druggability Assessment for Ketogenic Neuroprotection Hypotheses

Based on my analysis of the target proteins and therapeutic landscape, here's a comprehensive assessment of the practical feasibility for each surviving hypothesis:

1. Circadian-Gated Ketone Window Hypothesis (Target: OXCT1)

Revised Confidence: 0.35

Druggability Assessment

POOR DRUGGABILITY - OXCT1 is a mitochondrial matrix enzyme that catalyzes CoA transfer reactions. The active site is highly conserved and essential for cellular metabolism, making selective modulation extremely challenging without disrupting

Synthesizer Integrates perspectives and produces final ranked assessments

Price History

0.570.670.77 score_update: market_dynamics (2026-04-16T23:39)score_update: market_dynamics (2026-04-17T00:10)debate: market_dynamics (2026-04-17T00:46)debate: market_dynamics (2026-04-17T01:36)evidence: market_dynamics (2026-04-17T02:53)evidence: market_dynamics (2026-04-17T03:01)evidence: market_dynamics (2026-04-17T03:48)score_update: market_dynamics (2026-04-17T04:54)debate: market_dynamics (2026-04-17T07:07) 0.87 0.46 2026-04-162026-04-172026-04-28 Market PriceScoreevidencedebate 53 events
7d Trend
Stable
7d Momentum
▼ 0.5%
Volatility
Low
0.0033
Events (7d)
4
⚡ Price Movement Log Recent 9 events
Event Price Change Source Time
💬 Debate Round $0.854 ▲ 53.5% market_dynamics 2026-04-17 07:07
📊 Score Update $0.556 ▼ 2.0% market_dynamics 2026-04-17 04:54
📄 New Evidence $0.568 ▼ 3.5% market_dynamics 2026-04-17 03:48
📄 New Evidence $0.588 ▲ 1.3% market_dynamics 2026-04-17 03:01
📄 New Evidence $0.581 ▲ 11.6% market_dynamics 2026-04-17 02:53
💬 Debate Round $0.520 ▲ 1.1% market_dynamics 2026-04-17 01:36
💬 Debate Round $0.515 ▼ 11.9% market_dynamics 2026-04-17 00:46
📊 Score Update $0.584 ▼ 13.0% market_dynamics 2026-04-17 00:10
📊 Score Update $0.671 market_dynamics 2026-04-16 23:39

Clinical Trials (0)

No clinical trials data available

📚 Cited Papers (9)

Kinetics, safety and tolerability of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate in healthy adult subjects.
Regulatory toxicology and pharmacology : RTP (2012) · PMID:22561291
No extracted figures yet
No extracted figures yet
Targeting of astrocytic glucose metabolism by beta-hydroxybutyrate.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism (2017) · PMID:26661221
No extracted figures yet
No extracted figures yet
No extracted figures yet
No extracted figures yet
No extracted figures yet
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No extracted figures yet

📅 Citation Freshness Audit

Freshness score = exp(-age×ln2/5): halves every 5 years. Green >0.6, Amber 0.3–0.6, Red <0.3.

No citation freshness data yet. Export bibliography — run scripts/audit_citation_freshness.py to populate.

📙 Related Wiki Pages (0)

No wiki pages linked to this hypothesis yet.

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⚔ Arena Performance

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📊 Resource Economics & ROI

Low Efficiency Resource Efficiency Score
0.30
14.3th percentile (776 hypotheses)
Tokens Used
10,163
KG Edges Generated
3
Citations Produced
8

Cost Ratios

Cost per KG Edge
781.77 tokens
Lower is better (baseline: 2000)
Cost per Citation
2540.75 tokens
Lower is better (baseline: 1000)
Cost per Score Point
15516.03 tokens
Tokens / composite_score

Score Impact

Efficiency Boost to Composite
+0.030
10% weight of efficiency score
Adjusted Composite
0.735

How Economics Pricing Works

Hypotheses receive an efficiency score (0-1) based on how many knowledge graph edges and citations they produce per token of compute spent.

High-efficiency hypotheses (score >= 0.8) get a price premium in the market, pulling their price toward $0.580.

Low-efficiency hypotheses (score < 0.6) receive a discount, pulling their price toward $0.420.

Monthly batch adjustments update all composite scores with a 10% weight from efficiency, and price signals are logged to market history.

Efficiency Price Signals

Date Signal Price Score
2026-04-17T09:10$0.6730.483

📋 Reviews View all →

Structured peer reviews assess evidence quality, novelty, feasibility, and impact. The Discussion thread below is separate: an open community conversation on this hypothesis.

💬 Discussion

No DepMap CRISPR Chronos data found for BDH1.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

No curated ClinVar variants loaded for this hypothesis.

Run scripts/backfill_clinvar_variants.py to fetch P/LP/VUS variants.

🔍 Search ClinVar for BDH1 →
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⚖️ Governance History

No governance decisions recorded for this hypothesis.

Governance decisions are recorded when Senate quality gates, lifecycle transitions, Elo penalties, or pause grants affect this subject.

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KG Entities (46)

BDH1BDNFBDNF expressionGLUT1/GLUT3/MCT1/MCT2HDAC2HDAC2/HDAC3HDAC3HMGCS2IRAKMOXCT1astrocyte glycolysisastrocyte-neuron lactate shuttleastrocytic glucose consumptionastrocytic glycolysisastrocytic lactate productionautophagyautophagy pathwaycellular agingcontinuous ketone exposureepigenetic regulation

Related Hypotheses

Biphasic Ketogenic Intervention Protocol
Score: 0.773 | metabolic neuroscience
Epigenetic Priming Ketone Protocol
Score: 0.661 | metabolic neuroscience
Inflammatory State-Dependent Ketone Timing
Score: 0.647 | metabolic neuroscience
Circadian-Gated Ketone Window Hypothesis
Score: 0.606 | metabolic neuroscience
Circadian Epigenetic Ketone Synchronization Protocol
Score: 0.543 | metabolic neuroscience

Estimated Development

Estimated Cost
$0
Timeline
0 months

🧪 Falsifiable Predictions (2)

2 total 0 confirmed 0 falsified
IF BDH1 activity is pharmacologically inhibited in cortical astrocytes THEN astrocytic lactate production will increase and neuronal lactate uptake will decrease, because ketone oxidation bypass creates a compensatory glycolytic flux that disrupts the astrocyte-neuron lactate shuttle (ANLS) dynamics.
pending conf: 0.50
Expected outcome: Increased astrocytic lactate efflux combined with reduced neuronal lactate clearance, measurable via isotope-tracing LC-MS when 3-hydroxybutyrate is elevated to 2-5 mM
Falsified by: If BDH1 inhibition does not alter astrocyte-neuron lactate dynamics, with lactate shuttle remaining unchanged despite reduced ketone oxidation, the hypothesis that BDH1 couples astrocytic ketone metabolism to ANLS regulation is false
Method: Primary cortical astrocytes and neurons co-cultured in microfluidic compartmentalized chambers; BDH1 inhibited with CP-3,5-dichlorobenzamide (10 µM); media supplemented with 5 mM β-hydroxybutyrate; 13C6-glucose and U-13C4-β-hydroxybutyrate isotope tracing; lactate isotopomer analysis via LC-MS/MS at 0, 15, 30, 60 min
IF systemic β-hydroxybutyrate concentrations exceed 6 mM (ketogenic diet or ketone ester supplementation thresholds) THEN cortical astrocytes will demonstrate metabolic steal syndrome evidenced by reduced glucose uptake and shunting of lactate away from neurons toward astrocyte oxidation, detectable via hyperpolarized 13C-MRS glutamate/C3-lactate ratio changes
pending conf: 0.50
Expected outcome: Decreased neuronal lactate accumulation with preserved or increased astrocytic lactate consumption at high ketone concentrations, indicating substrate competition rather than coupled shuttle function
Falsified by: If neuronal lactate uptake remains unchanged or increases at 6+ mM β-hydroxybutyrate despite astrocytic glucose consumption inhibition, metabolic steal syndrome does not occur and astrocyte-neuron coupling remains intact at high ketone levels
Method: Adult C57BL/6 mice maintained on ketogenic diet (4:1 ratio) for 3 weeks; in vivo hyperpolarized 13C-pyruvate MRS to measure cerebral lactate/pyruvate ratios; simultaneous plasma ketone measurements via enzymatic assay; immunohistochemistry for GLUT1 and MCT1/4 expression in cortical slices

Knowledge Subgraph (42 edges)

activates (3)

β-hydroxybutyrateBDNF expressionβ-hydroxybutyrateBDNFβ-hydroxybutyrateIRAKM

alleviates (1)

ketogenic dietischemic brain injury

associated with (6)

HDAC2/HDAC3metabolic_neuroscienceHMGCS2metabolic_neuroscienceBDH1metabolic_neuroscienceIRAKMmetabolic_neuroscienceOXCT1metabolic_neuroscience
▸ Show 1 more

causal extracted (1)

sess_SDA-2026-04-03-gap-debate-20260403-222618-2709aad9processed

causes (3)

high ketone levelsastrocytic glycolysisβ-hydroxybutyrateneuroprotection in immature brainscontinuous ketone exposuresustained gene expression changes

inhibits (5)

β-hydroxybutyrateHDAC2β-hydroxybutyrateHDAC3β-hydroxybutyrateastrocytic glucose consumptionβ-hydroxybutyrateastrocytic glycolysishigh-dose β-hydroxybutyrateastrocyte glycolysis

modulates (5)

β-hydroxybutyrateautophagyβ-hydroxybutyrateepigenetic regulationβ-hydroxybutyratecellular agingβ-hydroxybutyratemitochondrial metabolismβ-hydroxybutyrateneuronal support

preserves (1)

low-dose β-hydroxybutyrateastrocytic lactate production

protective against (1)

β-hydroxybutyrateischemic brain injury

reduces (2)

β-hydroxybutyrateoxidative stressβ-hydroxybutyrateneuroinflammation

regulates (7)

β-hydroxybutyratemitochondrial metabolismβ-hydroxybutyrateIRAKMketone bodieshistone modificationsketone bodiesnon-histone protein modificationsastrocyte-neuron lactate shuttleneuronal support
▸ Show 2 more

targets (7)

h-6df1bc66HMGCS2h-d7212534HDAC2/HDAC3h-9d4571a7OXCT1h-404bab00OXCT1h-17a2da3fBDH1
▸ Show 2 more

Mechanism Pathway for BDH1

Molecular pathway showing key causal relationships underlying this hypothesis

graph TD
    __hydroxybutyrate["β-hydroxybutyrate"] -.->|inhibits| HDAC2["HDAC2"]
    __hydroxybutyrate_1["β-hydroxybutyrate"] -.->|inhibits| HDAC3["HDAC3"]
    __hydroxybutyrate_2["β-hydroxybutyrate"] -->|activates| BDNF_expression["BDNF expression"]
    __hydroxybutyrate_3["β-hydroxybutyrate"] -->|modulates| autophagy["autophagy"]
    __hydroxybutyrate_4["β-hydroxybutyrate"] -->|regulates| mitochondrial_metabolism["mitochondrial metabolism"]
    __hydroxybutyrate_5["β-hydroxybutyrate"] -->|modulates| epigenetic_regulation["epigenetic regulation"]
    __hydroxybutyrate_6["β-hydroxybutyrate"] -->|protective against| ischemic_brain_injury["ischemic brain injury"]
    __hydroxybutyrate_7["β-hydroxybutyrate"] -.->|reduces| oxidative_stress["oxidative stress"]
    __hydroxybutyrate_8["β-hydroxybutyrate"] -.->|reduces| neuroinflammation["neuroinflammation"]
    __hydroxybutyrate_9["β-hydroxybutyrate"] -.->|inhibits| astrocytic_glucose_consum["astrocytic glucose consumption"]
    __hydroxybutyrate_10["β-hydroxybutyrate"] -.->|inhibits| astrocytic_glycolysis["astrocytic glycolysis"]
    __hydroxybutyrate_11["β-hydroxybutyrate"] -->|regulates| IRAKM["IRAKM"]
    style __hydroxybutyrate fill:#4fc3f7,stroke:#333,color:#000
    style HDAC2 fill:#4fc3f7,stroke:#333,color:#000
    style __hydroxybutyrate_1 fill:#4fc3f7,stroke:#333,color:#000
    style HDAC3 fill:#4fc3f7,stroke:#333,color:#000
    style __hydroxybutyrate_2 fill:#4fc3f7,stroke:#333,color:#000
    style BDNF_expression fill:#4fc3f7,stroke:#333,color:#000
    style __hydroxybutyrate_3 fill:#4fc3f7,stroke:#333,color:#000
    style autophagy fill:#81c784,stroke:#333,color:#000
    style __hydroxybutyrate_4 fill:#4fc3f7,stroke:#333,color:#000
    style mitochondrial_metabolism fill:#4fc3f7,stroke:#333,color:#000
    style __hydroxybutyrate_5 fill:#4fc3f7,stroke:#333,color:#000
    style epigenetic_regulation fill:#81c784,stroke:#333,color:#000
    style __hydroxybutyrate_6 fill:#4fc3f7,stroke:#333,color:#000
    style ischemic_brain_injury fill:#ef5350,stroke:#333,color:#000
    style __hydroxybutyrate_7 fill:#4fc3f7,stroke:#333,color:#000
    style oxidative_stress fill:#4fc3f7,stroke:#333,color:#000
    style __hydroxybutyrate_8 fill:#4fc3f7,stroke:#333,color:#000
    style neuroinflammation fill:#4fc3f7,stroke:#333,color:#000
    style __hydroxybutyrate_9 fill:#4fc3f7,stroke:#333,color:#000
    style astrocytic_glucose_consum fill:#4fc3f7,stroke:#333,color:#000
    style __hydroxybutyrate_10 fill:#4fc3f7,stroke:#333,color:#000
    style astrocytic_glycolysis fill:#81c784,stroke:#333,color:#000
    style __hydroxybutyrate_11 fill:#4fc3f7,stroke:#333,color:#000
    style IRAKM fill:#4fc3f7,stroke:#333,color:#000

3D Protein Structure

🧬 BDH1 — Search for structure Click to search RCSB PDB
🔍 Searching RCSB PDB for BDH1 structures...
Querying Protein Data Bank API

Source Analysis

What determines the optimal timing and dosing of ketogenic interventions for neuroprotection?

metabolic neuroscience | 2026-04-03 | completed

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Same Analysis (5)

Biphasic Ketogenic Intervention Protocol
Score: 0.77 · HMGCS2
Inflammatory State-Dependent Ketone Timing
Score: 0.65 · IRAKM
Circadian-Gated Ketone Window Hypothesis
Score: 0.61 · OXCT1
Circadian Epigenetic Ketone Synchronization Protocol
Score: 0.54 · CLOCK/BMAL1
Glucose-Ketone Metabolic Switch Timing
Score: 0.53 · GLUT1/GLUT3/MCT1/MCT2
→ View all analysis hypotheses
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