The Rhythm Your Immune System Needs

and What Happens When Your Gut Loses It

Why Food Sensitivities, Brain Fog, and Post-Viral Fatigue Are the Same Broken System

By Dr. Justin Dearing | The Dearing Clinic

Key Takeaways

• ‍Your immune system operates on a circadian rhythm orchestrated by the autonomic nervous system, with immune cells deploying during the day under sympathetic control and pulling back at night under parasympathetic control.‍
• Food sensitivities, mast cell activation, brain fog, and post-viral fatigue are different intensity levels of the same broken system — not separate conditions, but expressions of a dysregulated gut-brain-immune axis.‍
• Mast cell hyperreactivity is controlled by the nervous system, not the foods themselves. When your nervous system is locked in sympathetic dominance, mast cells become hypervigilant and react to increasingly more triggers.
• ‍Post-viral illness (like long COVID) hijacks the tryptophan-kynurenine pathway, diverting tryptophan away from serotonin production toward neurotoxic quinolinic acid, creating a self-reinforcing inflammatory cycle that affects mood, energy, and brain function.‍
• Disrupted short-chain fatty acid (SCFA) production is the most common gut issue — more than gluten sensitivity. When upstream bacteria are depleted, the anti-inflammatory SCFA production chain stalls, leading to intestinal permeability and immune hyperreactivity.‍
• IgG food sensitivity testing is often misinterpreted and leads patients to eliminate foods unnecessarily. The real problem is the gut terrain (permeability, bacterial imbalances), not the specific foods flagged on panels.‍
• qEEG brain mapping and functional testing (GI-MAP, Neural Zoomer) reveal the actual mechanisms driving symptoms, allowing for targeted interventions like neurofeedback, vagal tone training, and personalized microbiome restoration rather than generic protocols.‍
• There are no cookie-cutter protocols — restoration typically takes six months and must be sequenced according to each patient's specific dysbiosis, whether it's kynurenine pathway distortion, SCFA depletion, fungal overgrowth, or H. pylori virulence.

A growing body of peer-reviewed research confirms something we’ve been working with clinically for years: your immune system follows a daily rhythm, and that rhythm is orchestrated by the autonomic nervous system.

A 2024 review in Immunology documented that nearly all immune cells autonomously express clock-regulating genes, governing everything from migration and phagocytic activity to cytokine signaling and metabolism (Ding et al., 2024). A practical guide published in the Journal of Clinical Investigation the same year described how the central pacemaker in the hypothalamus converts light cues into synchronized oscillations through hormonal secretion and autonomic neural activity, which then entrain peripheral clocks in immune cells throughout the body (Mok et al., 2024). A 2020 NIH workshop summary specifically identified the relationship between circadian rhythms in autonomic tone and neuroimmune reflexes as a high-priority area for translational research.

White blood cells rise and fall on a predictable schedule. Immune cells deploy from bone marrow during the day under sympathetic signaling, then pull back at night under parasympathetic control. The immune system isn’t just reactive. It’s timed.

This is meaningful validation. But it’s still a partial picture.

In my office, this rhythm breakdown doesn’t present as a research finding. It presents as the person who reacts to foods that used to be fine. The executive with brain fog that won’t lift eighteen months after COVID. The chronic fatigue patient who’s been through every elimination diet and supplement protocol and still can’t stabilize. These are all expressions of the same axis falling out of rhythm.

From Sniffles to MCAS: The Gain Is the Problem

You eat a meal and get mild congestion. Maybe some flushing. You ignore it. Scale that up: rotating food reactions, hives without clear triggers, GI distress after meals that never used to be a problem. Scale it further and you reach mast cell activation syndrome, where the immune system’s threshold for reaction has dropped so low that nearly everything provokes a response.

This isn’t a spectrum of different diseases. It’s the same mechanism at different intensity levels. And the intensity is set by the brain.

Mast cells cluster around autonomic ganglia and vagal nerve pathways. Their degranulation is modulated by the autonomic nervous system through vagal signaling and sympathetic ganglia. A 2023 paper in Cellular & Molecular Immunology described the insular cortex as a site of immune and interoceptive integration, where peripheral inflammation sends afferent signals through the vagus nerve to the brainstem and ultimately to the insula and anterior cingulate cortex. When the brain perceives ongoing threat, it turns up immune surveillance. Mast cells become hypervigilant.

The high-histamine food list gets longer because the food was never the root signal. A nervous system locked in sympathetic dominance is.

Antihistamines, DAO support, and mast cell stabilizers all help manage symptoms, and they should be used. But without addressing the nervous system commanding the heightened reactivity, you’re adjusting the volume while something keeps turning the dial back up.

When a Virus Flips the Switch

This becomes even clearer in post-viral illness. COVID didn’t just cause acute respiratory disease. It created a wave of patients whose gut-brain-immune axis got fundamentally rewired.

A 2024 systematic review and meta-analysis published in Neuroscience (Almulla et al.) analyzed 14 studies across 1,167 participants and found a significant increase in the kynurenine-to-tryptophan ratio in long COVID patients compared to healthy controls, with a large effect size. A study published in Brain, Behavior, and Immunity (Li et al., 2025) was the first to confirm elevated kynurenine metabolites, including quinolinic acid, in the central nervous system of COVID patients, with levels correlating to neurodegenerative markers. A review in Infection (2024) described the molecular cascade: pro-inflammatory cytokines including interferon-gamma, IL-6, and TNF-alpha upregulate the enzyme IDO-1, which catalyzes the first step of tryptophan catabolism through the kynurenine pathway, diverting tryptophan away from serotonin production and toward neurotoxic and immunosuppressive metabolites.

In plain terms: the inflammatory response hijacks tryptophan, the building block your gut needs to produce serotonin (most of which is made in the gut, not the brain), and shunts it into a pathway that produces quinolinic acid, which is neurotoxic and pro-inflammatory. The pathway feeds itself.

This is why long COVID patients and chronic fatigue patients share so many overlapping symptoms: brain fog, mood disruption, fatigue that doesn’t respond to rest, and gut dysfunction that seems disconnected from diet. The tryptophan-kynurenine shift explains the neurotransmitter piece. The gut inflammatory switch explains why their microbiome can’t recover on its own. And the autonomic dysregulation, measurable on HRV, explains why their nervous system can’t downshift from vigilance mode.

Seeing the Brain Under Siege

When we suspect the nervous system is wound up in this way, we don’t guess. We map it.

Quantitative EEG (qEEG) brain mapping lets us see which networks are most burdened by the inflammatory and autonomic dysfunction. In these patients, the areas that light up are predictable. The insula, the brain’s primary body-monitoring station, is almost always involved. Published research in Biological Psychiatry (2022) documented that peripheral inflammation is associated with increased activation and disrupted connectivity of the insula, dorsal anterior cingulate cortex (dACC), and posterior cingulate cortex (PCC), and that inflammatory markers like CRP and IL-6 negatively correlated with connectivity in these regions in depressed patients with elevated inflammation.

This maps directly onto what we see clinically. The insula and anterior cingulate cortex form the core of the brain’s interoceptive network. They process visceral signals from the gut, the immune system, and the autonomic nervous system. When inflammation burdens these structures, the patient experiences heightened internal alarm. Everything feels threatening. Anxiety becomes persistent. The body’s monitoring system is overloaded with inflammatory noise, and the brain can’t filter signal from static.

We also frequently see posterior brain involvement, particularly around the PCC and structures associated with visual processing and vestibular function. These patients often report dizziness, visual sensitivity, and spatial disorientation alongside their fatigue, brain fog, and anxiety. The anxiety isn’t psychological in origin. It’s neurological. The brain regions responsible for sensing and interpreting the body’s internal state are genuinely overwhelmed.

Once we identify which networks are most affected, we can target them. Infra-slow fluctuation (ISF) neurofeedback allows us to train specific brain regions toward better self-regulation. Transcutaneous vagus nerve stimulation (tVNS) directly addresses vagal tone and parasympathetic signaling, helping restore the autonomic balance that controls mast cell behavior, immune scheduling, and gut-brain communication. These aren’t generic brain exercises. They’re targeted interventions matched to what the qEEG reveals.

The Terrain Nobody’s Measuring

Whether the entry point is mast cell reactivity, post-viral illness, or chronic fatigue, the gut terrain tells us what’s driving immune activation. GI-MAP microbiome analysis changes the conversation entirely.

The most common finding I see, far more often than gluten sensitivity, is a disrupted short-chain fatty acid (SCFA) production chain. Upstream Bacteroidetes species break down dietary fiber and polyphenols into intermediate substrates. Downstream Firmicutes species like Faecalibacterium prausnitzii and Roseburia convert those substrates into SCFAs, primarily butyrate, propionate, and acetate. When upstream bacteria are depleted, the downstream producers starve. The entire anti-inflammatory production line stalls.

SCFAs fuel the cells lining your colon, regulate tight junction integrity, and butyrate specifically modulates regulatory T-cells that keep the immune system from overreacting. When this production chain fails, the gut barrier becomes permeable, immune signaling shifts toward reactivity, and histamine-mediated responses escalate. Over 95% of patients I test show documented intestinal permeability. This SCFA breakdown is the most common driver.

Beyond this, GI-MAP reveals opportunistic overgrowths, H. pylori with virulence factors, parasites missed on standard stool testing, fungal overgrowth, digestive enzyme sufficiency, inflammatory markers like calprotectin, mucosal immune status through secretory IgA, and direct permeability markers. Together, these give us a map of the terrain no food sensitivity panel could provide.

And speaking of food sensitivity panels: IgG testing is among the most over-ordered, misinterpreted tests in functional medicine. IgG to foods often represents normal immune exposure, not pathology. Patients get 25 foods flagged in red, eliminate half their diet, and never improve, because the terrain was always the problem, not the food.

When the gut barrier fails, bacterial fragments and proteins enter systemic circulation and the immune system generates antibodies. Some of those antibodies, through molecular mimicry, cross-react with neural tissue. This is where GI-MAP findings connect to Neural Zoomer antibody panels, which measure antibodies against neuronal structures and myelin proteins. The originating source of elevated neural antibodies almost always traces back to intestinal permeability.

The loop closes: gut permeability drives systemic immune activation, which triggers neuroinflammation, which dysregulates the autonomic nervous system, which commands mast cells to increase their gain, which worsens gut inflammation. Add the tryptophan-kynurenine shift feeding quinolinic acid into the neuroinflammatory fire, and you have a self-reinforcing cycle that no single intervention can break.

There Are No Cookie-Cutter Protocols

I’ve tried. The standard protocol that works for most patients with these patterns does not exist.

A post-viral patient with kynurenine pathway distortion and quinolinic acid dominance needs a fundamentally different first twelve weeks than a patient with MCAS driven by bacterial overgrowth and SCFA depletion. A chronic fatigue patient with suppressed secretory IgA and fungal overgrowth needs a different restoration sequence than someone whose primary driver is H. pylori virulence and upstream Bacteroidetes collapse. The first twelve weeks have to be crafted according to their specific ecology and dysbiosis.

It usually takes about six months to create a durable shift. But the architecture of those six months is different for every patient. A parasite cleanse in an already-stripped ecosystem makes things worse. Keto in someone with compromised mitochondrial function deepens the energy crisis. Going gluten-free when the real issue is upstream bacterial imbalance doesn’t address the mechanism.

A “detox” won’t fix this. A protocol downloaded from a podcast won’t fix this. Measurement and guided sequential restoration will.

HRV monitoring with Oura or WHOOP gives us daily tracking of autonomic function throughout treatment. Our patients typically see HRV improvements of 20 to 45 percent. But HRV alone doesn’t tell you what to fix. Standard blood work wasn’t designed to measure SCFA production, microbial ecology, neural antibodies, or kynurenine metabolites. You need functional testing to see the terrain. And you need an expert who understands how these systems interact to build a sequence your body can actually integrate.

Restoring the Rhythm

Morning movement, focused breathing, and early sunlight exposure remain the most powerful things you can do to anchor circadian rhythm. The research supports it. The clinical outcomes confirm it.

But when the rhythm has been disrupted long enough, when the gut is compromised, neural antibodies are present, the kynurenine pathway is distorted, and the brain’s interoceptive networks are overloaded, you need more than lifestyle changes. You need the systems measured. You need the sequence mapped. And you need targeted interventions, from microbiome restoration to ISF neurofeedback to vagal tone training, delivered in an order that matches your terrain.

This is what the Rhythm Reset course was built to teach. How these systems connect. Why restoration has to be sequenced. And what it takes to rebuild the terrain everything else depends on.

If your food reactions keep expanding, if your brain fog won’t clear, if you’ve been given labels without anyone measuring the systems underneath them, there is an explanation. It’s mappable. It’s measurable. And it’s restorable.

Frequently Asked Questions (FAQs)

Why do I suddenly react to foods that never bothered me before?‍

It's not the food that changed — it's your nervous system and gut terrain. When your autonomic nervous system is stuck in sympathetic dominance (fight-or-flight mode), it commands mast cells to become hypervigilant. Combined with gut barrier breakdown and disrupted SCFA production, your immune system's threshold for reaction drops dramatically. The expanding list of trigger foods is a symptom of a dysregulated gut-brain-immune axis, not true allergies.

What's the connection between long COVID and chronic fatigue?‍

Both conditions involve the same broken mechanisms: the tryptophan-kynurenine pathway gets hijacked by inflammation, producing neurotoxic quinolinic acid instead of serotonin; the gut microbiome can't recover on its own; and the autonomic nervous system can't downshift from vigilance mode. This explains why symptoms like brain fog, fatigue that doesn't respond to rest, mood disruption, and gut dysfunction overlap so significantly between post-viral illness and chronic fatigue.

Are food sensitivity panels (IgG testing) accurate?‍

IgG testing is one of the most over-ordered and misinterpreted tests in functional medicine. IgG antibodies to foods often represent normal immune exposure, not pathology. Eliminating 20+ foods based on these panels rarely improves symptoms because the root issue is gut permeability and terrain disruption, not the foods themselves. When the gut barrier is compromised, bacterial fragments trigger antibody production — fixing the terrain is what matters, not avoiding specific foods.‍

What is SCFA production and why does it matter?‍

Short-chain fatty acids (SCFAs) like butyrate, propionate, and acetate are produced when gut bacteria break down fiber. SCFAs fuel the cells lining your colon, maintain gut barrier integrity, and regulate immune function. Over 95% of patients tested show disrupted SCFA production chains — when upstream bacteria are depleted, downstream beneficial bacteria starve, the gut barrier becomes permeable, and immune reactivity escalates. This is often the primary driver of food sensitivities and inflammation.

How do you identify what's actually wrong with my system?‍

We use functional testing that standard blood work doesn't measure: GI-MAP microbiome analysis (SCFA production, bacterial overgrowths, parasites, permeability markers, inflammation), qEEG brain mapping (to see which neural networks are burdened by inflammation), Neural Zoomer antibody panels (antibodies against brain tissue), and HRV monitoring (autonomic nervous system function). These tests reveal the terrain and mechanisms driving your symptoms, not just surface-level markers.

Why don't generic protocols work for these conditions?‍

Because the underlying drivers vary dramatically between patients. A post-viral patient with kynurenine pathway dysfunction needs a fundamentally different approach than someone with MCAS driven by bacterial overgrowth. A parasite cleanse in an already-depleted gut ecosystem makes things worse. Keto in someone with compromised mitochondrial function deepens the energy crisis. Restoration must be sequenced according to your specific test results — it typically takes six months, but the architecture of those months is unique to each patient.‍

Can lifestyle changes alone fix this?‍

Morning movement, breathwork, and early sunlight exposure are powerful tools for anchoring circadian rhythm and should absolutely be part of your routine. However, when the gut is severely compromised, neural antibodies are present, the kynurenine pathway is distorted, and brain networks are overloaded with inflammatory signaling, lifestyle changes alone won't break the cycle. You need targeted interventions — microbiome restoration, neurofeedback, vagal tone training — delivered in a sequence that matches your specific terrain.

What kind of improvements can I expect with proper treatment?‍

With personalized, sequenced restoration based on functional testing, patients typically see HRV (heart rate variability) improvements of 20-45%, indicating better autonomic nervous system regulation. Symptoms like expanding food reactions, persistent brain fog, chronic fatigue, anxiety, dizziness, and gut dysfunction begin to resolve as the underlying mechanisms are addressed. It takes about six months to create a durable shift, but outcomes depend on measuring the right systems, targeting the actual drivers, and following a protocol built specifically for your terrain.

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