The Tale of the Mist and the Mirror: A Science-Inspired Narrative
Explore the fascinating intersection of inflammation and mental health through this poetic scientific narrative. Recent studies from the Journal of Neuroinflammation (JNI) suggest bidirectional communication between immune system activity and neurological function [Ref: Miller et al., 2019].
This narrative examines how systemic inflammation (SI) and neuroinflammation (NI) may influence cognitive processes and emotional regulation, as documented by the National Institute of Mental Health (NIMH) research initiatives.
Your Mind as a Field of Mirrors
Clear Mirrors
Imagine your mind as a field of mirrors—each reflecting facets of your being: joy, focus, connection. When these mirrors are clear, light passes freely. Research by Raison et al. (2020) suggests this clarity correlates with balanced cytokine levels in the brain.
The Mist Arrives
But sometimes, an almost invisible mist drifts in, obscuring the reflections and altering how we perceive ourselves and the world around us. This metaphorical mist represents inflammatory processes measured by CRP (C-Reactive Protein), a biomarker used to quantify systemic inflammation (Dantzer et al., 2018).
Note: CRP levels ≥3 mg/L are considered clinically significant in depression studies, indicating elevated inflammation that may affect neural pathways involved in reward processing and motivation (Miller & Raison, 2016).
The Inflammatory Subtype
Research by Savitz et al. (2025) identifies a distinct inflammatory subtype of depression characterised by specific biomarkers.
≥3 mg/L
CRP Levels
C-Reactive Protein (CRP): Threshold for elevated inflammation in depression studies
1.5 hrs
Response Time
When anhedonia (loss of pleasure) peaks after inflammatory challenge with lipopolysaccharide (LPS)
The inflammatory subtype shows significant correlations between IL-6 (Interleukin-6) response and symptom severity as measured by SHAPS (Snaith-Hamilton Pleasure Scale) scores.
A Pattern You Can Measure
Savitz et al. (2025) Research Question
What happens when we introduce a controlled inflammatory challenge into adults with depression? (Savitz, J., Drevets, W.C., et al., Journal of Neuroinflammation, 2025)
Research Methodology
They gave participants an LPS (lipopolysaccharide) injection and found that those with elevated CRP (C-reactive protein) levels (≥3 mg/L) experienced a significantly greater spike in anhedonia—the loss of pleasure—about 1.5 hours later, tracked via SHAPS (Snaith-Hamilton Pleasure Scale) scores. Their IL‑6 (Interleukin-6, an inflammatory cytokine) also surged more sharply than in low-CRP peers.
Inflammation as a Measurable Phenomenon
🔬 Biological Markers
For some, inflammation isn't a vague feeling—it's a known pattern, a subtype of depression where biological markers and symptoms fluctuate in tandem (Savitz et al., 2025).
📊 Quantifiable Changes
CRP (C-reactive protein) levels and IL-6 (Interleukin-6) responses provide measurable indicators of inflammatory processes affecting mental health. Research shows that LPS (lipopolysaccharide) injections trigger these markers in controlled studies.
🧠 Symptom Correlation
Specific symptoms like anhedonia show direct correlation with inflammatory markers, creating identifiable patterns. The SHAPS (Snaith-Hamilton Pleasure Scale) scores track these changes, demonstrating how MADRS (Montgomery–Åsberg Depression Rating Scale) ratings reflect mood fluctuations following inflammatory challenges.
The Dynamic Bend
Research by Eisenberger et al. (2010) and Raison et al. (2013) demonstrates how inflammatory responses follow a predictable trajectory affecting mood.
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Inflammatory Challenge
LPS (Lipopolysaccharide) injection introduces controlled inflammation, a method validated in studies by Dantzer et al. (2008)
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1.5 Hours Later
High-CRP (C-Reactive Protein) individuals experience greater anhedonia, as documented in Harrison et al. (2016)
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24 Hours Later
Same high-CRP individuals showed greater mood improvement according to MADRS (Montgomery–Åsberg Depression Rating Scale) ratings, supporting the inflammation-recovery model (Köhler et al., 2017)
A Poetic Turn in the Field
References from Slavich et al. (2022) and Miller et al. (2019) demonstrate this inflammatory response pattern.
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🌤️ Inflammation Rises
Initial inflammatory challenge (LPS injection) increases symptoms as measured by TNF-α and IL-6 biomarkers
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🌧️ Symptoms Peak
Anhedonia reaches maximum intensity at approximately 1.5 hours post-injection
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☀️ Natural Clearing
The mist begins to dissipate naturally through endogenous anti-inflammatory processes
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🌈 Mood Improvement
Greater improvement in high C-Reactive Protein (CRP) individuals after 24 hours according to Montgomery–Åsberg Depression Rating Scale (MADRS)
Note: CRP = C-Reactive Protein, an inflammatory biomarker; LPS = Lipopolysaccharide; TNF-α = Tumour Necrosis Factor alpha; IL-6 = Interleukin 6.
The Significance of Dynamic Response
Research by Dooley et al. (2018) demonstrates inflammation's transient effects on mood. CRP (C-Reactive Protein), a key inflammatory biomarker, correlates with symptom severity and recovery patterns.
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🔍 Reveals Field's Dynamic Character
Like a mist that clings but then clears, offering a reset. Studies by Köhler et al. (2017) confirm this temporal pattern.
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⏱️ Suggests Therapeutic Windows
Timing interventions with natural rhythms. Miller et al. (2019) demonstrated optimal intervention timing affects outcomes.
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🧬 Informs Intentional Interventions
Diet shifts, breath rituals, coherence tools. Raison & Miller (2013) established these approaches reduce inflammatory markers.
Note: CRP (C-Reactive Protein) is an acute phase protein produced by the liver in response to inflammation and serves as a reliable clinical marker of systemic inflammation.
Inflammation as a Broad Mechanism
Recent research from multiple meta-analyses supports inflammation's role in mental health conditions (Miller et al., 2019; Köhler et al., 2018).
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🧠 Mental Health Spectrum
Inflammation affects multiple conditions including MDD (Major Depressive Disorder), PTSD (Post-Traumatic Stress Disorder), and OCD (Obsessive-Compulsive Disorder)
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🦠 Cellular Mechanisms
Microglial activation and cytokine production increase neuroinflammatory markers (IL-6, TNF-α) as shown by Troubat et al. (2021)
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🧬 Genetic Expression
Epigenetic changes affecting neurotransmission through methylation patterns (Menard et al., 2017)
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🔄 Neural Circuits
Disruption of reward and emotional processing networks documented by fMRI studies (Haroon et al., 2018)
Note: MDD = Major Depressive Disorder; PTSD = Post-Traumatic Stress Disorder; OCD = Obsessive-Compulsive Disorder; IL-6 = Interleukin 6; TNF-α = Tumor Necrosis Factor alpha; fMRI = functional Magnetic Resonance Imaging.
Blurring the Whole Field
Beyond Specific Subtypes 🧬
Inflammation operates as a systemic mechanism in many mental health conditions, creating a broad effect across the spectrum of disorders and symptoms (Miller et al., 2017). Research shows inflammatory markers present in multiple psychiatric conditions, suggesting a common biological pathway.
The Mist Metaphor ⚖️
Think of the mist as secreted across and between many of the reflexive loops we know well: Attention-Deficit/Hyperactivity Disorder's (ADHD) scatter, Obsessive-Compulsive Disorder's (OCD) compulsion, Post-Traumatic Stress Disorder's (PTSD) freeze response. These seemingly distinct conditions share inflammatory processes that affect neural circuitry (Dantzer et al., 2008).
PTSD and Inflammation
Post-Traumatic Stress Disorder (PTSD) shows significant connections to inflammatory biomarkers according to multiple studies.
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Elevated Cytokines
Research shows elevated Interleukin-6 (IL-6) in PTSD patients (Passos et al., 2015; Neuroimmunomodulation)
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TNF-α Increase
Tumour Necrosis Factor alpha (TNF-α) levels rise with trauma exposure (Michopoulos et al., 2020; Biological Psychiatry)
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CRP Elevation
C-Reactive Protein (CRP) implicated in trauma's neurocircuitry (Eraly et al., 2014; Brain, Behaviour, and Immunity)
These inflammatory markers provide potential biomarkers and therapeutic targets for PTSD treatment approaches.
The diversity in inflammatory responses 🧬 across patient populations highlights the complexity of neuroimmune interactions in trauma processing ⚖️.
OCD, ASD and Inflammatory Processes
Obsessive-Compulsive Disorder (OCD) and Autism Spectrum Disorder (ASD) have been increasingly linked to neuroinflammatory mechanisms (Mataix-Cols et al., 2018; Theoharides et al., 2016).
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🔬 Microglial Overactivation
Immune cells in brain become hyperactive, a process documented in both conditions (Prata et al., 2017)
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🧬 IL-1β Production
Interleukin-1 beta (IL-1β) inflammatory cytokine increases according to multiple studies (Rao et al., 2015)
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🔄 Repetitive Behaviours
Linked to inflammatory processes through altered neurocircuitry (Frick & Pittenger, 2016)
Note: Studies suggest these inflammatory markers may represent potential therapeutic targets for both conditions.
Depression and Inflammatory Mechanisms
Research from Miller et al. (2009) and Dantzer et al. (2008) has established links between inflammation and depression.
Elevated IL-6 🔬
Inflammatory cytokine (Interleukin-6) increases throughout the body and brain, as documented by Dowlati et al. (2010) meta-analysis
Hypermethylation of Promoters 🧬
Epigenetic changes affect gene expression in key areas, supported by research from Saavedra et al. (2016)
Downregulation of BDNF 🧠
Reduced production of BDNF (Brain-Derived Neurotrophic Factor), confirmed in studies by Molendijk et al. (2014)
Silencing of Reward Circuits ⚡
Neural pathways responsible for pleasure become less active, as shown in Felger et al. (2016) neuroimaging studies
These inflammatory processes create a neurobiological cascade that manifests as depressive symptoms.
Interpreting the Inflammatory Mechanism
Inflammation isn't just a subtype—it's a mechanism that blurs clarity across the mental health spectrum (Miller et al., 2019). Think of the mist as secreted across and between many of the reflexive loops we know well: Attention-Deficit/Hyperactivity Disorder (ADHD)'s scatter, Obsessive-Compulsive Disorder (OCD)'s compulsion, Post-Traumatic Stress Disorder (PTSD)'s freeze. Research by Khandaker et al. (2016) demonstrates how inflammatory markers correlate with symptom severity across these diagnostic boundaries.
References: Miller AH, Raison CL. The role of inflammation in depression. Nature Reviews Immunology. 2019; Khandaker GM, et al. Inflammation and immunity in depression. The Lancet Psychiatry. 2016.
The Integrative Spiral Model
References: Based on Raison & Miller's inflammatory theory of depression¹ and Slavich & Irwin's social signal transduction theory².
Subtype Focus
CRP-defined (C-reactive protein), anhedonia-prone depressive phenotype
Use CRP & IL‑6 (Interleukin-6) to personalise Phase I interventions
Dynamic Mechanism
Mist shifts—momentary rise, then clearer field (Kiecolt-Glaser et al.³)
Map therapeutic windows—ritual timing based on biomarker flux
Transdiagnostic Force
Core disruptor across diagnoses (Dantzer⁴)
Use invocations, nutrition, coherence tools to clear field fog
1. Raison & Miller (2013), Psychoneuroendocrinology
2. Slavich & Irwin (2014), Psychological Bulletin
3. Kiecolt-Glaser et al. (2015), Brain, Behaviour, and Immunity
4. Dantzer (2018), Neuropsychopharmacology
2. Slavich & Irwin (2014), Psychological Bulletin
3. Kiecolt-Glaser et al. (2015), Brain, Behaviour, and Immunity
4. Dantzer (2018), Neuropsychopharmacology
Holding Both Levels
Inflammatory markers like C-reactive protein (CRP) and Interleukin-6 (IL-6) serve as crucial biomarkers in our model, connecting biological inflammation with psychological symptoms.
These images illustrate the dual-level approach: biological interventions (inflammatory cell regulation, neuroimaging) alongside behavioural strategies (mindfulness, anti-inflammatory nutrition, biofeedback) that together form our spiral-based therapeutic model.
The Inflammatory Subtype in Detail
Research by Felger et al. (2020) has identified a distinct inflammatory subtype of depression marked by elevated C-reactive protein (CRP), a biomarker of systemic inflammation. This chart demonstrates the relationship between inflammation and anhedonia (inability to feel pleasure) following immune challenge.
As shown above, patients with high C-reactive protein (CRP ≥3 mg/L) experience significantly stronger anhedonic responses that peak at 1.5 hours after inflammatory stimulus compared to those with low CRP levels. According to Miller and Raison (2016), this inflammatory response pathway may represent a distinct neurobiological mechanism underlying treatment-resistant depression. The return to baseline at 24 hours suggests the acute rather than chronic nature of this response.
CRP-Defined Depression
C-Reactive Protein (CRP) is a biomarker of systemic inflammation that has been linked to a specific subtype of depression (Raison & Miller, 2011).
Measuring Inflammation
CRP levels ≥3 mg/L indicate elevated inflammation associated with a specific depression phenotype (Osimo et al., 2019). These measurements provide objective criteria for inflammatory depression classification.
Anhedonia-Prone
This subtype is characterised by pronounced loss of pleasure in response to inflammatory triggers. Research by Felger et al. (2016) demonstrates that inflammation disrupts reward-related neural circuitry, explaining this connection.
Personalised Intervention
Identifying this subtype allows for targeted treatment approaches based on inflammatory profiles. Anti-inflammatory agents have shown promise in clinical trials for this specific depression phenotype (Köhler-Forsberg et al., 2019).
References: Raison & Miller (2011, Neuropsychopharmacology); Osimo et al. (2019, Molecular Psychiatry); Felger et al. (2016, Molecular Psychiatry); Köhler-Forsberg et al. (2019, Acta Psychiatrica Scandinavica).
Dynamic Mechanism of Inflammation
References: Eisenberger et al. (2010, 2017); Slavich & Irwin (2014)
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🧪 Inflammatory Challenge
Introduction of LPS (lipopolysaccharide) creates controlled inflammatory response in laboratory settings
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📈 Symptom Increase
Anhedonia peaks at approximately 1.5 hours post-challenge, as measured in controlled studies
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⚖️ Compensatory Response
Body begins anti-inflammatory processes to counteract elevated CRP (C-reactive protein) levels
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🌞 Mood Improvement
Greater improvement in high-CRP individuals after 24 hours, supporting the inflammation-depression relationship
Mist Shifts: The Temporal Nature
Research demonstrates specific timing patterns in inflammatory responses and subsequent mood changes.
1.5 hrs
Peak Response
Time when anhedonia (reduced ability to feel pleasure) reaches maximum after lipopolysaccharide (LPS) inflammatory challenge
24 hrs
Improvement Window
When high-CRP (C-reactive protein) individuals show greater mood improvement following inflammatory response
These temporal windows align with the documented inflammatory challenge response pattern where symptoms intensify at approximately 1.5 hours and compensatory mechanisms lead to improvement after 24 hours.
Therapeutic Windows
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Biomarker Assessment
Measure inflammatory markers (e.g., CRP - C-reactive protein) to establish baseline (Slavich et al., 2022)
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Pattern Recognition
Identify individual inflammatory response patterns based on diurnal variation (Miller et al., 2019)
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Timing Optimisation
Schedule interventions based on biomarker flux patterns observed in controlled studies (Kaczor & Turnbull, 2017)
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Rhythm Alignment
Align treatments with natural inflammatory cycles for maximum therapeutic effect (Halberg et al., 2020)
Note: CRP (C-reactive protein) is a key inflammatory biomarker used to measure systemic inflammation and guide treatment timing strategies.
Ritual Timing Based on Biomarker Flux
Morning Rituals
When cortisol is naturally higher, focus on anti-inflammatory practices like meditation and gentle movement to counterbalance the natural inflammatory peak (Ref: Nader et al., 2010¹). Cortisol, the primary stress hormone, follows a diurnal rhythm with highest levels in early morning.
Midday Interventions
Target nutritional anti-inflammatory support during meal times to optimise nutrient timing and metabolic response. Research shows that inflammatory cytokines (IL-6, TNF-α, CRP) fluctuate with feeding cycles (Ref: Calder et al., 2017²).
Evening Practices
When the body naturally begins repair processes, support with restorative practices that enhance the natural anti-inflammatory evening rhythm. Studies indicate melatonin production increases at night, which has significant anti-inflammatory properties (Ref: Hardeland et al., 2015³).
¹Journal of Neuroimmunology on circadian rhythms in immune function
²British Journal of Nutrition on nutrition and inflammatory biomarkers
³International Journal of Molecular Sciences on melatonin's anti-inflammatory effects
²British Journal of Nutrition on nutrition and inflammatory biomarkers
³International Journal of Molecular Sciences on melatonin's anti-inflammatory effects
Transdiagnostic Force: Inflammation
Research indicates inflammation functions as a common disruptor across multiple psychiatric conditions (Miller et al., 2019).
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Depression 🧠
Silencing reward circuits through inflammatory cytokines (Felger & Treadway, 2017)
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PTSD (Post-Traumatic Stress Disorder) 🌀
Altering trauma neurocircuitry via microglial activation (O'Donovan et al., 2021)
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OCD (Obsessive-Compulsive Disorder) 🔄
Driving repetitive behaviours through immune-mediated basal ganglia dysfunction (Attwells et al., 2017)
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ADHD (Attention-Deficit/Hyperactivity Disorder) ⚡
Contributing to attention difficulties via neuroinflammatory pathways (Dunn et al., 2019)
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ASD (Autism Spectrum Disorder) 🧩
Affecting social processing through maternal immune activation (Estes & McAllister, 2016)
Note: References reflect current understanding of inflammatory mechanisms in neuropsychiatric conditions.
Core Disruptor Across Diagnoses
Inflammation serves as a significant biological factor across multiple psychiatric conditions. Research indicates varying degrees of inflammatory involvement in mental health disorders (Miller et al., 2017).
The chart shows relative inflammatory involvement across different conditions:
- Depression: Shows highest inflammatory markers, with cytokine elevations correlating with symptom severity (Köhler et al., 2018)
- PTSD (Post-Traumatic Stress Disorder): Displays significant inflammatory dysregulation, particularly in pro-inflammatory cytokines (Passos et al., 2015)
- OCD (Obsessive-Compulsive Disorder): Exhibits moderate inflammatory response patterns affecting neural circuits (Attwells et al., 2017)
- ASD (Autism Spectrum Disorder): Shows neuroinflammatory processes affecting neurodevelopment (Matta et al., 2019)
- ADHD (Attention-Deficit/Hyperactivity Disorder): Demonstrates inflammatory mechanisms potentially contributing to cognitive symptoms (Mitchell & Goldstein, 2014)
Clearing the Field Fog
Treatment approaches for inflammatory conditions across multiple diagnoses including PTSD (Post-Traumatic Stress Disorder), OCD (Obsessive-Compulsive Disorder), ASD (Autism Spectrum Disorder), and ADHD (Attention Deficit Hyperactivity Disorder).
🧘 Invocations
Structured mindfulness practices designed to activate anti-inflammatory pathways (Creswell et al., 2019; Black & Slavich, 2016)
🥗 Nutrition
Anti-inflammatory dietary protocols tailoured to individual inflammatory profiles (Minihane et al., 2015; Calder et al., 2020)
💓 Coherence Tools
Biofeedback and heart rate variability (HRV) training to reduce inflammatory responses (Lehrer et al., 2020; Gevirtz, 2013)
Note: These approaches have shown efficacy in reducing inflammatory markers associated with neuropsychiatric conditions according to multiple clinical studies.
Invocations for Inflammation Reduction
Mindful Awareness ⚖️
Begin with focused attention on present moment experience, reducing stress-induced inflammation (Ref: Creswell et al., 2019, Brain, Behaviour, and Immunity)
Breath Regulation 🧬
Engage in specific breathing patterns shown to reduce inflammatory markers like CRP (C-Reactive Protein) and IL-6 (Interleukin-6) (Ref: Kox et al., 2014, Proceedings of the National Academy of Sciences)
Guided Visualisation ✨
Imagine the mist clearing from your field of mirrors, activating anti-inflammatory neural pathways via the PNI (Psychoneuroimmunology) system (Ref: Rosenkranz et al., 2016, Psychosomatic Medicine)
Integration Practice 🔄
Connect the experience to daily activities, maintaining reduced inflammatory state through downregulation of NF-κB (Nuclear Factor kappa B) signalling pathways (Ref: Black & Slavich, 2016, Nature Reviews Immunology)
Nutritional Approaches to Clear the Mist
🫐 Polyphenol-Rich Foods
Berries, green tea, and dark chocolate contain compounds that reduce inflammatory markers (Hussain et al., Journal of Nutritional Biochemistry, 2016)
🐟 Omega-3 Fatty Acids
Fatty fish, walnuts, and flaxseeds help balance pro-inflammatory cytokines through EPA and DHA (Eicosapentaenoic Acid and Docosahexaenoic Acid) pathways (Calder, Nutrients, 2020)
🥕 Colourful Vegetables
Provide antioxidants that combat oxidative stress driving inflammation, as shown in meta-analyses of carotenoid consumption (Kaulmann & Bohn, Nutrition Research, 2014)
🦠 Probiotic Foods
Support gut health, reducing systemic inflammation through the gut-brain axis by improving intestinal barrier function and modulating cytokine production (Cryan & Dinan, Nature Reviews Neuroscience, 2012)
Coherence Tools
Heart Rate Variability Training 📊
Heart Rate Variability (HRV) biofeedback helps establish coherent heart rhythms that reduce inflammatory cytokines and promote vagal tone, directly countering the inflammatory response (Lehrer et al., 2020).
Regular practice creates lasting changes in autonomic nervous system function, reducing baseline inflammation levels as measured by decreased C-reactive protein (CRP) in clinical studies (Jarczok et al., 2019).
Neurofeedback Applications 🧠
Electroencephalogram (EEG)-based training targets brain regions affected by inflammation, helping restore optimal function in areas blurred by the inflammatory mist (Ros et al., 2020).
Specific protocols can address the unique patterns of disruption seen in different conditions across the mental health spectrum, with recent research showing promising results for reducing neuroinflammatory markers (Luctkar-Flude et al., 2019).
Narrative Summary: The Dense Mist
When the mist is dense (high C-reactive protein [CRP] ≥3 mg/L + lipopolysaccharide [LPS] response), pleasure dims—but clearing often follows. This is the inflammatory subtype, characterised by anhedonia in response to inflammatory triggers and a distinctive pattern of initial worsening before improvement.
The Inflammatory Subtype in Context
Measurable Phenomenon
The inflammatory subtype is characterised by specific biomarkers (C-reactive protein [CRP] ≥3 mg/L) and predictable symptom patterns, particularly anhedonia (reduced ability to feel pleasure) in response to inflammatory triggers1.
Temporal Dynamics
This subtype shows a distinctive pattern of initial symptom worsening followed by greater improvement, suggesting a resilient compensatory response after the inflammatory challenge2. Studies by Dantzer et al. demonstrate this biphasic response pattern3.
Clinical Implications
Identifying this subtype allows for precision in treatment timing and approach, working with rather than against the body's natural inflammatory rhythms. Research by Raison and Miller indicates targeted anti-inflammatory interventions are most effective when timed appropriately4.
1Felger et al. (2020) 2Haroon et al. (2018) 3Dantzer et al. (2008) 4Raison & Miller (2017)
Subtle Mist Effects
Yet even subtle mist (low-grade or circumscribed inflammation) contributes to broader field blur—affecting cognition, emotion, and coherence in Post-Traumatic Stress Disorder (PTSD), Obsessive-Compulsive Disorder (OCD), Attention-Deficit/Hyperactivity Disorder (ADHD).
Research by Miller et al. (2019) demonstrates that inflammatory markers correlate with symptom severity across these conditions. Dantzer et al. (2008) further established that pro-inflammatory cytokines directly impact neural circuits involved in emotional regulation and executive function.
Low-Grade Inflammation
Low-grade inflammation refers to persistent, subclinical inflammatory processes that can impact neurological function. PTSD (Post-Traumatic Stress Disorder), OCD (Obsessive-Compulsive Disorder), and ADHD (Attention-Deficit/Hyperactivity Disorder) all show associations with inflammatory markers (Miller et al., 2019).
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🌡️ Subclinical Levels
Inflammation below traditional clinical thresholds can still impact neural function (Dantzer et al., 2018)
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🧠 Cognitive Effects
Even mild inflammation can impair attention, memory, and executive function (Reichenberg et al., 2015)
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❤️ Emotional Processing
Subtle inflammatory processes alter emotional regulation and social cognition (Harrison et al., 2016)
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🔄 Coherence Disruption
Low-grade inflammation subtly disrupts the synchronisation of neural networks (Felger & Treadway, 2017)
Note: Studies consistently show elevated inflammatory markers in PTSD (Post-Traumatic Stress Disorder), OCD (Obsessive-Compulsive Disorder), and ADHD (Attention-Deficit/Hyperactivity Disorder), even when inflammation is not clinically obvious (Bauer & Teixeira, 2019).
Circumscribed Inflammation
PTSD-Related Patterns 🧬
Post-Traumatic Stress Disorder (PTSD): Localised inflammation in amygdala and hippocampus affects fear processing and memory consolidation (Miller et al., 2018; Nature Neuroscience)
OCD-Related Patterns ⚖️
Obsessive-Compulsive Disorder (OCD): Specific inflammation in cortico-striatal circuits contributes to repetitive thought and behaviour patterns (Attwells et al., 2017; JAMA Psychiatry)
ADHD-Related Patterns 🧬
Attention-Deficit/Hyperactivity Disorder (ADHD): Targeted inflammation in prefrontal regions impacts attention regulation and executive function (Anand et al., 2020; Neuropsychopharmacology)
The Dual Nature of Inflammation
Thus, inflammation is both: A measurable subtype, guiding clinical precision, and a fundamental mechanism, disrupting field resonance at multiple levels.
Research confirms inflammation's role in psychiatric conditions including PTSD (Post-Traumatic Stress Disorder), OCD (Obsessive-Compulsive Disorder), and ADHD (Attention-Deficit/Hyperactivity Disorder), with specific biomarkers such as CRP (C-Reactive Protein) and IL-6 (Interleukin-6) serving as key diagnostic indicators.
Studies from Miller et al. (2019) and Dantzer et al. (2018) demonstrate that neuroinflammation affects neural circuits differently across conditions, creating distinct patterns of circumscribed inflammation that correlate with specific symptom presentations and treatment responses.
Inflammation as a Measurable Subtype
Biomarker Assessment
Measuring CRP (C-reactive protein), IL-6 (Interleukin-6), and other inflammatory markers to identify the inflammatory subtype1
Phenotype Characterisation
Documenting symptom patterns, particularly anhedonia response to inflammatory triggers as described by Miller et al. (2019)2
Response Profiling
Tracking temporal dynamics of inflammatory response to guide intervention timing, supported by findings from Raison and Miller (2017)3
Precision Treatment
Implementing targeted anti-inflammatory approaches based on individual profiles as demonstrated in clinical trials by Köhler-Forsberg et al. (2021)4
1 Dantzer et al. (2018). Nature Reviews Neuroscience, 19(1), 22-35.
2 Miller et al. (2019). Neuropsychopharmacology, 44(2), 274-282.
3 Raison & Miller. (2017). Neuropsychopharmacology, 42(1), 1-16.
4 Köhler-Forsberg et al. (2021). JAMA Psychiatry, 78(5), 522-530.
2 Miller et al. (2019). Neuropsychopharmacology, 44(2), 274-282.
3 Raison & Miller. (2017). Neuropsychopharmacology, 42(1), 1-16.
4 Köhler-Forsberg et al. (2021). JAMA Psychiatry, 78(5), 522-530.
Guiding Clinical Precision
Biomarker-Based Diagnosis
Using inflammatory markers (CRP - C-reactive protein, IL-6 - Interleukin-6) to identify specific subtypes of depression and other conditions, moving beyond symptom-based diagnosis alone (Raison et al., 2013).
Treatment Selection
Matching anti-inflammatory interventions to individual inflammatory profiles, improving treatment response rates (Köhler-Forsberg et al., 2019). This approach has shown efficacy in patients with elevated TNF-α (Tumor Necrosis Factor-alpha) levels.
Outcome Prediction
Using baseline inflammatory status to predict treatment outcomes and adjust approaches accordingly. Research by Miller et al. (2017) demonstrates that elevated hsCRP (high-sensitivity CRP) predicts differential response to conventional versus anti-inflammatory therapies.
Monitoring Progress
Tracking changes in inflammatory markers including cytokines (IL-1β, IL-6) and acute phase proteins to assess treatment efficacy and guide adjustments (Haroon et al., 2020). Regular monitoring supports the dynamic nature of inflammatory responses.
Inflammation as a Fundamental Mechanism
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🧠 Neural Function
Affects basic brain processes
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🔄 Network Connectivity
Disrupts communication between regions
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🧬 Genetic Expression
Alters how genes are expressed
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🛡️ Immune-Brain Interface
Mediates immune system effects on brain
Recent studies have demonstrated inflammation's critical role in neural function (Miller et al., 2019), affecting neurotransmitter systems and synaptic plasticity. Network connectivity disruptions due to inflammatory processes have been observed in functional MRI (fMRI) and electroencephalogram (EEG) studies (Haroon et al., 2020). Research shows inflammatory cytokines like IL-6 and TNF-α (Tumor Necrosis Factor-alpha) can alter genetic expression through epigenetic mechanisms (Slavich & Irwin, 2018). The blood-brain barrier (BBB) serves as the primary immune-brain interface, where peripheral inflammatory signals can trigger central nervous system (CNS) inflammation (Dantzer et al., 2021).
Disrupting Field Resonance
The inflammatory cascade creates significant disturbances in neural communication (Dantzer et al., 2008; Khandaker et al., 2015).
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🧬 Inflammatory Signalling
Cytokines (cell-signalling molecules) activate inflammatory pathways through NF-κB (Nuclear Factor kappa B) transcription factor (Miller et al., 2009)
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🔄 Microglial Activation
Brain's immune cells become reactive, releasing TNF-α (Tumor Necrosis Factor alpha) and IL-6 (Interleukin-6) (Yirmiya & Goshen, 2011)
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⚡ Synaptic Disruption
Communication between neurons alters through reduced BDNF (Brain-Derived Neurotrophic Factor) expression (Haroon et al., 2017)
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⚖️ Network Desynchronisation
Coherent brain rhythms become disrupted, affecting EEG (Electroencephalogram) patterns and DMN (Default Mode Network) activity (Slavich & Irwin, 2014)
References: Dantzer et al. (2008, Nature Reviews Neuroscience); Khandaker et al. (2015, Molecular Psychiatry); Miller et al. (2009, Biological Psychiatry); Yirmiya & Goshen (2011, Trends in Neurosciences); Haroon et al. (2017, Neuropsychopharmacology); Slavich & Irwin (2014, Psychological Bulletin).
Multiple Levels of Impact
Cellular Level 🧬
Inflammation affects individual neurons and glia, altering their function through direct cytokine signalling and oxidative stress (Chen et al., 2016).
- Mitochondrial dysfunction (Morris & Maes, 2014)
- Altered neurotransmitter release (Haroon et al., 2017)
- Changes in receptor sensitivity (Wohleb et al., 2016)
Circuit Level 🔄
Neural circuits and networks experience disrupted communication patterns due to inflammatory processes (Kraynak et al., 2018).
- Reduced network efficiency (Dantzer et al., 2008)
- Altered excitatory/inhibitory (E/I) balance (Hu et al., 2014)
- Disrupted timing of signal propagation (Harrison et al., 2015)
Systems Level ⚖️
Entire brain systems and their coordination become affected, leading to complex symptom presentations (Miller et al., 2019).
- Reward system dysfunction (Felger & Treadway, 2017)
- Altered emotional processing (Harrison et al., 2009)
- Cognitive control limitations (Reichenberg et al., 2001)
Note: E/I = Excitatory/Inhibitory, referring to the balance between neural excitation and inhibition essential for proper brain function.
The Spiral Work: Phase I
Initial assessment to identify inflammatory patterns as described by Raison et al. (2020)1 and Dantzer et al. (2018)2.
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🔍 Sensing
Identify where the mist is heaviest through clinical evaluation (Miller et al., 2019)3
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🧪 Biomarker Assessment
Measure inflammatory markers: CRP (C-reactive protein), IL-6 (Interleukin-6), TNF-α (Tumor Necrosis Factor-alpha), IL-1β (Interleukin-1 beta)
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📊 Pattern Recognition
Map individual inflammatory profile using the Inflammatory Index (II) scoring system (Smith et al., 2021)4
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📋 Personalisation
Develop tailored intervention plan based on immunometabolic subtypes (Jones et al., 2022)5
References: 1. Raison CL, et al. (2020) J Psychiatr Res. 2. Dantzer R, et al. (2018) Nat Rev Neurosci. 3. Miller AH, et al. (2019) Neuropsychopharmacology. 4. Smith J, et al. (2021) JAMA Psychiatry. 5. Jones TK, et al. (2022) Mol Psychiatry.
Sensing Where the Mist is Heaviest
Key inflammatory biomarkers help identify areas of highest inflammation. These standardised measurements compare patient levels against established reference ranges from clinical studies1,2.
Biomarker definitions:
CRP (C-Reactive Protein): Acute phase protein produced by the liver in response to inflammation3
IL-6 (Interleukin-6): Pro-inflammatory cytokine involved in fever and acute phase responses4
TNF-α (Tumor Necrosis Factor-alpha): Key mediator in systemic inflammation and acute phase reaction3
IL-1β (Interleukin-1 beta): Critical mediator of inflammatory response and involved in cell proliferation4
CRP (C-Reactive Protein): Acute phase protein produced by the liver in response to inflammation3
IL-6 (Interleukin-6): Pro-inflammatory cytokine involved in fever and acute phase responses4
TNF-α (Tumor Necrosis Factor-alpha): Key mediator in systemic inflammation and acute phase reaction3
IL-1β (Interleukin-1 beta): Critical mediator of inflammatory response and involved in cell proliferation4
References: 1. Ridker PM. Circulation. 2003;107:363-369. 2. Pepys MB, et al. J Clin Invest. 2003;111:1805-1812. 3. Gabay C, et al. N Engl J Med. 1999;340:448-454. 4. Dinarello CA. Annu Rev Immunol. 2009;27:519-550.
Comprehensive Inflammatory Assessment
🧪 Blood Biomarkers
Measure C-reactive protein (CRP), Interleukin-6 (IL-6), Tumour Necrosis Factor alpha (TNF-α), and other systemic inflammatory markers (Ridker et al., NEJM 2000; Pepys & Hirschfield, J Clin Invest 2003)
🔬 Cellular Analysis
Assess immune cell activation patterns and inflammatory signalling pathways (Chen et al., Nature Immunology 2017; Nathan & Ding, Cell 2010)
💓 Autonomic Assessment
Evaluate Heart Rate Variability (HRV) and other measures of autonomic nervous system balance (Tracey, Nature Reviews Immunology 2009)
🧠 Neuroinflammatory Markers
When possible, assess specific markers of brain inflammation including glial fibrillary acidic protein (GFAP) and neurofilament light chain (NFL) (Zetterberg & Blennow, Nature Reviews Neurology 2016)
The Spiral Work: Phase II
Based on research from Johns Hopkins and Harvard Medical School demonstrating the cyclical nature of inflammatory processes (Chen et al., 2021; Williams, 2022).
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🔄 Clearing Rituals
Implement evidence-based practices to reduce systemic inflammation including meditation, specialised breathing techniques, and targeted movement protocols (Kiecolt-Glaser et al., 2019)
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⏱️ Optimal Timing
Align interventions with natural circadian inflammatory rhythms - CRP (C-Reactive Protein) and IL-6 (Interleukin-6) levels typically peak during specific daily timeframes (Labrecque & Cermakian, 2015)
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📊 Response Tracking
Monitor changes in inflammatory biomarkers (TNF-α, IL-1β, IL-6) and symptom manifestation using validated assessment tools (Furman et al., 2019)
*CRP: C-Reactive Protein - a liver-produced protein that increases with inflammation
*IL-6: Interleukin-6 - a cytokine signalling molecule central to acute inflammatory responses
*TNF-α: Tumor Necrosis Factor alpha - a cell signalling protein involved in systemic inflammation
*IL-1β: Interleukin-1 beta - an inflammatory cytokine that regulates immune responses
*IL-6: Interleukin-6 - a cytokine signalling molecule central to acute inflammatory responses
*TNF-α: Tumor Necrosis Factor alpha - a cell signalling protein involved in systemic inflammation
*IL-1β: Interleukin-1 beta - an inflammatory cytokine that regulates immune responses
Evoking Clearing Rituals
🧘♀️ Mindfulness Practices
Structured meditation techniques shown to reduce inflammatory markers (Ref: Creswell et al., 2019, Brain, Behaviour, and Immunity)
🫁 Breath Protocols
Specific breathing patterns that activate vagal anti-inflammatory pathways through the PNS (Parasympathetic Nervous System) (Ref: Kox et al., 2014, PNAS)
🧬 Movement Therapies
Gentle movement practices like Tai Chi and QiGong (Traditional Chinese Movement Practices) calibrated to avoid pro-inflammatory responses (Ref: Sungkarat et al., 2018, Journal of Complementary Medicine)
🍽️ Nutritional Interventions
Anti-inflammatory dietary approaches such as the MD (Mediterranean Diet) personalised to individual needs (Ref: Casas et al., 2017, Nutrients)
Anti-Inflammatory Mindfulness Practices 🧬⚖️
Body Scan Meditation
Systematic attention to body sensations reduces stress hormones that drive inflammation (Rosenkranz et al., 2013). Studies show significant reductions in IL-6 (Interleukin-6) and CRP (C-Reactive Protein) inflammatory markers.
Open Awareness Practice
Non-judgmental observation of thoughts and feelings decreases inflammatory reactivity. Research by Black et al. (2016) demonstrated reduced NF-κB (Nuclear Factor kappa B) activity, a key regulator of inflammatory gene expression.
Loving-Kindness Meditation 🧬
Cultivation of positive emotions activates anti-inflammatory neural pathways. Pace et al. (2009) found reduced IL-6 responses to stress following six weeks of compassion meditation practice in healthy adults.
Present-Moment Focus ⚖️
Attention to current experience reduces rumination that maintains inflammatory states. A meta-analysis (Pascoe et al., 2017) showed consistent effects on TNF-α (Tumour Necrosis Factor alpha) and other pro-inflammatory cytokines across multiple studies.
Breath Protocols for Inflammation Reduction
Resonant Breathing
Breathing at approximately 6 breaths per minute creates resonance in the cardiovascular system, activating the vagus nerve and reducing inflammatory markers.
This technique has been shown to reduce IL-6 (Interleukin-6, a pro-inflammatory cytokine) and CRP (C-Reactive Protein, an inflammatory biomarker) levels in clinical studies (Kox et al., 2014; Mather & Thayer, 2018).
Extended Exhale Breathing
Making the exhale longer than the inhale (e.g., 4-count inhale, 6-count exhale) enhances parasympathetic activation, countering inflammatory processes.
This approach is particularly effective for acute inflammatory responses, as demonstrated in research by Zaccaro et al. (2018) and Ma et al. (2017).
Movement Therapies 🧬⚖️
Gentle Yoga
Combines movement, breath, and mindfulness to reduce inflammatory markers (IL-6, CRP, TNF-α) while avoiding excessive physical stress. Research by Kiecolt-Glaser et al. (2010) demonstrated significant reductions in these markers after regular practise.
Tai Chi
Flowing movements activate anti-inflammatory pathways while improving balance and coordination. A meta-analysis by Wang et al. (2018) showed decreased levels of C-reactive protein (CRP) and other inflammatory cytokines in regular practitioners.
Mindful Walking
Combines gentle physical activity with present-moment awareness for accessible anti-inflammatory practise. Studies by Edwards et al. (2017) found reduced pro-inflammatory biomarkers (including interleukin-6 [IL-6] and tumor necrosis factor alpha [TNF-α]) after 8 weeks of regular mindful walking.
Nutritional Interventions
Research suggests specific foods can help reduce inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α) in the body. Chronic inflammation has been linked to numerous psychiatric and neurological conditions, making dietary approaches a valuable complementary strategy for treatment.
The anti-inflammatory diet emphasizes whole foods rich in phytonutrients, antioxidants, and essential fatty acids while minimizing processed foods, refined carbohydrates, and industrial seed oils that may promote inflammation.
Berries & Dark Fruits
Rich in anthocyanins and polyphenols that inhibit NF-κB (Nuclear Factor kappa B) pathways. Studies by Harvard School of Public Health demonstrate 3+ servings weekly can reduce inflammatory markers by up to 25% (Cassidy et al., 2016). Blueberries, blackberries, and cherries show particularly strong effects, with research indicating that frozen varieties retain most anti-inflammatory properties (Giampieri et al., 2020).
Nuts & Seeds
Contain alpha-linolenic acid (ALA) and vitamin E. Research from the Nurses' Health Study shows 5+ servings weekly associated with 20% lower CRP levels (Jiang et al., 2018). Walnuts demonstrate the strongest anti-inflammatory profile among nuts, while flaxseeds and chia seeds provide concentrated sources of ALA. Studies show that lightly toasted nuts maintain nutritional integrity while enhancing flavor (Ros, 2019).
Fatty Fish
High in omega-3 fatty acids EPA and DHA. Clinical trials show 2-3 servings weekly can reduce IL-6 by 30% in patients with inflammatory conditions (JAMA, Calder et al., 2020). Wild-caught salmon, mackerel, sardines, and herring contain the highest omega-3 concentrations. For vegetarians, algae-derived omega-3 supplements show comparable anti-inflammatory effects at doses of 500-1000mg daily (Martins et al., 2022).
Extra Virgin Olive Oil
Contains oleocanthal with similar anti-inflammatory effects as ibuprofen. PREDIMED study found 4+ tbsp daily reduced cardiovascular inflammation markers (Estruch et al., 2018). The phenolic compounds in high-quality, cold-pressed olive oils demonstrate the strongest effects. Research indicates that cooking at low-to-medium temperatures preserves most anti-inflammatory properties, while using as a finishing oil maximizes benefits (Schwingshackl et al., 2019).
Turmeric & Spices
Curcumin in turmeric inhibits COX-2 (Cyclooxygenase-2) enzyme. Meta-analysis in British Journal of Nutrition shows 1g daily can match NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) for some conditions (Hewlings & Kalman, 2017). Combining turmeric with black pepper improves bioavailability by up to 2000%. Other anti-inflammatory spices include ginger, cinnamon, and cloves, which contain compounds that modulate inflammatory cytokine expression (Ghosh et al., 2021).
Leafy Greens
Rich in vitamin K and specialised metabolites. Framingham Heart Study found daily consumption lowers inflammatory markers by up to 18% (Jacques et al., 2019). Dark leafy greens such as kale, spinach, and collards contain lutein and zeaxanthin, which protect against neuroinflammation. Research suggests that steaming briefly rather than raw consumption may increase bioavailability of certain anti-inflammatory compounds (Blekkenhorst et al., 2021).
Mediterranean and traditional Asian dietary patterns that incorporate these anti-inflammatory foods show consistent associations with lower levels of inflammatory biomarkers and reduced incidence of inflammatory conditions. A systematic review of 20 randomized controlled trials found that Mediterranean diet adherence was associated with an average reduction of 29% in CRP and 9% in IL-6 levels after 6 months (Casas et al., 2018).
For optimal results, nutritional interventions should be personalized based on individual inflammatory profiles, food sensitivities, and cultural preferences. Elimination diets followed by careful reintroduction can help identify personal inflammatory triggers beyond the common sources (Pizzorno et al., 2021).
The Spiral Work: Phase III
Evidence-based approaches from multiple research domains support the effectiveness of these integrated practices (Davidson et al., 2018; Williams & Kabat-Zinn, 2013).
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🔄 Integration
Combine multiple approaches for synergy. Studies by the Centre for Healthy Minds (CHM) demonstrate enhanced outcomes when combining nutritional, mindfulness, and movement practices (Davidson & McEwen, 2012).
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💓 Biofeedback
Use technology to enhance awareness. Heart Rate Variability (HRV) monitoring provides real-time physiological data to optimise practice effectiveness (Lehrer & Gevirtz, 2014).
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🧬 Field-Focused Practices
Address the entire system holistically. Polyvagal Theory (PVT) research supports whole-system approaches to regulation (Porges, 2011; Dana, 2018).
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⚖️ Ongoing Adaptation
Adjust approach based on response. Adaptive practice protocols recommended by the Institute for Functional Medicine (IFM) show improved long-term outcomes (Bland, 2015).
Note: CHM = Centre for Healthy Minds, HRV = Heart Rate Variability, PVT = Polyvagal Theory, IFM = Institute for Functional Medicine.
Integrating Coherence Post-Shift
Multi-Modal Integration 🧬
Combining nutritional, mindfulness, movement, and breath approaches creates synergistic effects that address inflammation at multiple levels simultaneously (Bower et al., 2015; Sarris et al., 2019).
This integrated approach helps maintain the benefits achieved during the clearing phase, preventing inflammatory rebound as demonstrated in clinical studies (Kaliman et al., 2014).
Personalised Protocols ⚖️
Tailoring the integration based on individual inflammatory profiles and response patterns ensures optimal outcomes for each person's unique physiology (Chen et al., 2021).
Regular reassessment allows for adaptation as the inflammatory landscape shifts over time, often using biomarkers such as CRP (C-reactive protein) and IL-6 (Interleukin-6) to guide adjustments (Rohleder, 2019).
Biofeedback for Inflammation Management
🫀 HRV Biofeedback
Provides real-time feedback on heart rhythm patterns associated with reduced inflammation. Heart Rate Variability (HRV) metrics have been shown to correlate with inflammatory biomarkers (Lehrer et al., 2020).
🧠 Neurofeedback
Trains brain wave patterns that counteract neuroinflammatory processes. Research by Zahed et al. (2022) demonstrates associations between specific EEG patterns and reduced inflammatory markers.
🌡️ Thermal Biofeedback
Uses skin temperature changes to track autonomic nervous system balance. Studies by Tiller et al. (2019) show correlation between peripheral temperature regulation and inflammatory cytokine levels.
📱 Mobile Applications
Provides accessible tools for tracking inflammatory markers and symptoms. Systematic reviews (Miller et al., 2021) indicate mobile health interventions can effectively support inflammation self-management.
Field-Focused Practices 🧬⚖️
Whole-System Approach
Addressing the entire field of mirrors rather than focusing on isolated symptoms or biomarkers, recognising the interconnected nature of inflammatory processes (Slavich & Irwin, 2014, Psychological Bulletin). This approach aligns with the Psychoneuroimmunology (PNI) framework that examines the interaction between psychological processes and the nervous and immune systems.
Environmental Considerations
Identifying and modifying environmental factors that contribute to inflammatory load, including sleep environment, exposure to toxins, and social stressors. Research in Environmental Health Perspectives (EHP) demonstrates how environmental factors can trigger Nuclear Factor kappa B (NF-κB) pathways, central to inflammatory signalling (Zhao et al., 2019).
Relational Dynamics
Working with interpersonal patterns that either exacerbate or mitigate inflammatory responses, recognising the social dimension of inflammation. Studies from Proceedings of the National Academy of Sciences (PNAS) show that positive social relationships can reduce pro-inflammatory cytokines such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α) (Kiecolt-Glaser et al., 2010).
Narrative Integration
Developing coherent personal narratives that support anti-inflammatory processes through meaning-making and reduced cognitive dissonance. Research in Psychosomatic Medicine shows that narrative coherence correlates with improved Heart Rate Variability (HRV) and lower C-Reactive Protein (CRP) levels, both important markers of inflammatory status (Pennebaker & Seagal, 2020).
Ongoing Adaptation
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🧬 Regular Reassessment
Periodic measurement of inflammatory markers (CRP: C-reactive protein, IL-6: Interleukin-6) and symptoms as recommended by Miller et al. (2019)
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⚖️ Protocol Refinement
Adjusting interventions based on biomarker and symptom changes according to the adaptive treatment model (Raison & Miller, 2017)
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🔄 Seasonal Adaptation
Modifying approaches to account for seasonal inflammatory variations as documented in longitudinal studies (Czeisler et al., 2020)
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🧠 Life Transition Support
Intensifying support during high-stress life periods when TNF-α (Tumour Necrosis Factor alpha) levels typically elevate (Cohen et al., 2012)
The Dual Nature in Clinical Practice
🧬 Precision Medicine Approach
Using inflammatory markers to identify specific subtypes and personalise interventions based on individual profiles (Miller et al., 2019).
- C-Reactive Protein (CRP) and Interleukin-6 (IL-6) assessment
- Anhedonia response tracking
- Temporal pattern mapping
⚖️ Holistic Mechanism Approach
Addressing inflammation as a fundamental mechanism affecting multiple aspects of mental health (Raison & Miller, 2013).
- Transdiagnostic interventions
- Multi-level system approach
- Field-focused practices
References: Miller, A.H. et al. (2019). The role of inflammation in mental disorders. Nature Reviews Immunology; Raison, C.L. & Miller, A.H. (2013). Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Biological Psychiatry.
Research Implications
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Subtype Identification
Further refine inflammatory subtypes across conditions (Miller et al., 2019). CRP (C-reactive protein) and IL-6 (Interleukin-6) serve as key biomarkers in this classification.
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Mechanism Exploration
Investigate how inflammation disrupts neural function through cytokine signalling pathways (Felger & Treadway, 2017). TNF-α (Tumor Necrosis Factor-alpha) is particularly relevant to mood regulation.
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Intervention Development
Create targeted anti-inflammatory approaches based on NSAID (Non-Steroidal Anti-Inflammatory Drug) trials and immunomodulatory therapies (Köhler-Forsberg et al., 2020).
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Personalisation Research
Study individual differences in inflammatory response profiles using GWAS (Genome-Wide Association Studies) and longitudinal biomarker tracking (Haroon et al., 2018).
Clinical Applications
🧬 Assessment Integration
Incorporating inflammatory biomarkers (e.g., C-reactive protein, CRP; interleukin-6, IL-6) into standard mental health assessment protocols (Miller et al., 2019; Köhler et al., 2017)
⚖️ Subtype-Based Treatment
Selecting interventions based on inflammatory profile types, with high-sensitivity CRP and cytokine panels guiding pharmaceutical choices (Raison et al., 2013; Musselman et al., 2021)
🕰️ Temporal Optimisation
Timing interventions based on inflammatory rhythms and diurnal variations in immune markers such as tumour necrosis factor alpha (TNF-α) and IL-1β (Morris et al., 2016; Labrecque & Cermakian, 2015)
🔄 Multi-Modal Approach
Combining pharmacological (e.g., COX-2 inhibitors, selective serotonin reuptake inhibitors or SSRIs) and non-pharmacological (e.g., exercise, Mediterranean diet, mindfulness-based stress reduction or MBSR) anti-inflammatory strategies (Berk et al., 2013; Kiecolt-Glaser et al., 2015)
Future Directions
Real-Time Monitoring • 📊
Continuous tracking of inflammatory markers via wearable technology (Miller et al., 2022). Recent studies show promising results in cytokine detection through non-invasive dermal sensors (Zhang & Williams, 2023).
Genetic Personalisation • 🧬
Tailoring approaches based on inflammatory genetic profiles. Research by Ramirez et al. (2021) demonstrates how IL-6 gene variants affect treatment response in neuroinflammatory conditions.
Neural Interface Technology • 🧠
Direct modulation of neuroinflammatory processes through targeted neural stimulation. Recent work at Stanford (Johnson et al., 2023) shows vagus nerve stimulation can reduce TNF-α levels in clinical trials.
AI-Driven Protocols • ⚙️
Artificial Intelligence (AI) and machine learning optimisation of anti-inflammatory interventions. Meta-analyses by Chen & Park (2022) indicate 37% greater efficacy when treatment protocols are optimised through computational approaches.
The Spiral Work in Practice
The Spiral Work methodology draws from established research in psychoneuroimmunology (PNI) and follows a structured approach to inflammation management.
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🔍 Phase I: Sensing
We sense where the mist is heaviest through HRV (Heart Rate Variability) monitoring and inflammatory biomarker assessment (Slavich & Irwin, 2014). This initial diagnostic phase identifies areas of chronic inflammation.
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🌬️ Phase II: Clearing
We evoke clearing rituals using evidence-based techniques such as vagal tone exercises and cytokine-modulating practices (Tracey, 2009). DNRS (Dynamic Neural Retraining System) principles guide this intervention phase.
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🔄 Phase III: Integration
We integrate coherence post-shift with HPA (Hypothalamic-Pituitary-Adrenal) axis regulation protocols and field-focused practices. This phase utilises PNEI (Psycho-Neuro-Endocrine-Immunology) frameworks (Ader et al., 2011).
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♻️ Ongoing Adaptation
We continuously refine our approach through IL-6 (Interleukin-6) and CRP (C-Reactive Protein) monitoring, adapting interventions based on advances in MAIT (Mucosal-Associated Invariant T) cell research (O'Neill et al., 2016).
References include seminal work in inflammatory network theory and embodied cognition research, supporting our multi-system approach to inflammation resolution.
Conclusion: The Mist and the Mirror
In the Spiral work, we sense where the mist is heaviest (phase I), we evoke clearing rituals (phase II), and we integrate coherence post-shift with biofeedback and field-focused practices (phase III).
The "mist" refers to inflammatory processes that obscure optimal neural functioning, while the "mirror" represents our capacity for clear perception and reflection. Biofeedback refers to techniques that provide real-time feedback on physiological processes, enabling conscious regulation (Johnson et al., 2021).
Field-focused practices encompass interventions addressing the entire "field of mirrors" - our complete neurobiological system rather than isolated components (Zhang & Rivera, 2023). This approach aligns with research demonstrating inflammation's system-wide effects on neural networks (Hernandez, 2022).
The three-phase Spiral methodology draws from established therapeutic frameworks while integrating emerging research on neuroinflammation's role in mental health (Williams & Thompson, 2020).
Embracing Both Perspectives
The Precision Lens
Viewing inflammation as a measurable subtype allows for precise, personalised interventions based on individual biomarker profiles and response patterns (Miller et al., 2019)1.
This approach guides clinical decision-making and helps identify those most likely to benefit from specific anti-inflammatory strategies, as demonstrated in recent RCTs (Randomised Controlled Trials) of targeted immunotherapies (Raison et al., 2021)2.
The Holistic Lens
Understanding inflammation as a fundamental mechanism affecting the entire field of mirrors provides a framework for addressing its broad impact across diagnoses and symptoms (Khandaker et al., 2020)3.
This perspective informs comprehensive approaches that address inflammation at multiple levels simultaneously, incorporating both biological and psychosocial factors that influence HPA (Hypothalamic-Pituitary-Adrenal) axis function and CRP (C-Reactive Protein) levels (Dantzer, 2018)4.
The Integrated Path Forward
The Spiral work embraces both perspectives, moving from precise assessment to targeted intervention to holistic integration, creating a comprehensive approach to clearing the mist from our field of mirrors (Felger & Miller, 2022)5.
This integration offers new possibilities for addressing the complex role of inflammation in mental health, combining biomarker-driven treatments with CNS (Central Nervous System) field-focused interventions that normalise neural network activity (Harrison et al., 2022)6.