• Feb 18, 2026

Trauma-Informed Metabolic Recovery: Introducing Metabolic Type E

Metabolic Type E: trauma-responsive metabolic fragility, kynurenine pathway activation, estrogen dominance, functional hypothyroidism, and MCAS. Healing begins with safety, glucose, and nervous system regulation.

Trauma is biological overwhelm—especially when the body lacks energy. Those with metabolic fragility are more vulnerable to this collapse, and trauma itself drives metabolic failure.  This cycle defines Metabolic Type E: a state of trauma-responsive metabolic dysfunction marked by kynurenine pathway activation, estrogen dominance, chronically elevated cortisol, low brain serotonin, high gut serotonin, and functional hypothyroidism.

The Kynurenine Pathway: Stress’s Hidden Consequence

Under chronic stress or trauma, cortisol and inflammation activate tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO), shifting tryptophan away from serotonin and into the kynurenine pathway.  This produces:

  • Quinolinic acid (QUIN) – neurotoxic, excitotoxic

  • Kynurenic acid (KYNA) – neuroprotective, but often insufficient 

Result: reduced brain serotonin, mood imbalances, brain fog, and increased seizure or anxiety risk. This pathway links depression, PTSD, and cognitive decline to metabolic dysregulation.

Endotoxemia, Estrogen, and Thyroid Disruption

Endotoxemia (LPS from gut bacteria) fuels inflammation, further activating kynurenine metabolism.  Estrogen dominance amplifies this:

  • Increases gut permeability → more endotoxin

  • Stimulates serotonin production in the gut

  • Promotes mast cell degranulation → histamine release

  • Suppresses mitochondrial function

This trifecta—estrogen, endotoxin, cortisol—impairs T4-to-T3 conversion via:

  • Inflammatory cytokines (IL-6, TNF-α) suppressing deiodinase enzymes

  • Elevated cortisol increasing reverse T3 (rT3)

  • Estrogen raising thyroid-binding globulin (TBG), reducing free T3 

Patients feel hypothyroid despite "normal labs."

Mast Cell Activation Syndrome (MCAS): The Inflammatory Amplifier

MCAS is not just allergy—it’s a metabolic-immune loop deeply influenced by:

  • Estrogen dominance: Estrogen directly triggers mast cell degranulation, releasing histamine. In turn, histamine stimulates further estrogen production, creating a self-sustaining loop.

  • Cortisol dysregulation: Chronic stress elevates cortisol, which can both suppress and paradoxically prime mast cells.

  • Serotonin imbalance: While brain serotonin is low in Metabolic Type E, gut serotonin is often high, and serotonin itself can activate mast cells, worsening gut permeability and systemic inflammation.

  • Endotoxemia: LPS from gut bacteria activates mast cells directly, fueling neuroinflammation and kynurenine pathway activation. 

This creates a triad of dysfunction: trauma → HPA axis disruption → estrogen dominance + endotoxemia → MCAS flare → increased histamine → further estrogen release → metabolic stall.

Anxiety & ADHD: Metabolic, Not Mental

Chronic anxiety and ADHD in Metabolic Type E stem from:

  • Low brain serotonin, high gut serotonin

  • Dopamine instability due to estrogen and cortisol

  • Neuroinflammation from quinolinic acid

  • Thyroid dysfunction impairing neurotransmitter turnover

Stimulants often worsen the cycle by increasing cortisol and adrenaline.

Collagen & Gelatin Sensitivity: A Critical Clarification

Many with Metabolic Type E report weepiness, low mood, or depressive episodes after consuming collagen or gelatin. This is not due to glycine, which does not compete with tryptophan at the blood-brain barrier. Instead, it’s the other large neutral amino acids (LNAAs)—like leucine, isoleucine, and valine—that flood the bloodstream and outcompete tryptophan, reducing its brain uptake.

When tryptophan is blocked from the brain, it’s shunted into the kynurenine pathway, generating neurotoxic metabolites. 

If you tolerate collagen or gelatin:

  • Pair it with fruit or honey to stimulate insulin, which clears competing amino acids and improves tryptophan transport

  • This supports gut health without triggering mood crashes

If you have MCAS:

  • Collagen and gelatin may trigger histamine release or oxalate production

  • Avoid or test cautiously—many report flares in histamine, fatigue, or joint pain

Better alternative: free glycine (2–3g at night)

  • Provides glycine for gut healing, detox, and sleep

  • Does not interfere with tryptophan

  • May even support serotonin production

Fueling Recovery: The Role of Glucose & Tryptophan

To rebuild brain serotonin:

  • Pair tryptophan-rich foods (egg, dairy, turkey) with glucose sources (fruit, juice, honey)

  • Insulin from glucose lowers competing amino acids, increasing tryptophan’s brain access

  • This is essential during metabolic crisis—never pair tryptophan with protein-only or collagen-rich meals

Microglial Priming & Brain Inflammation: The Trauma-Brain Connection

In Metabolic Type E, trauma doesn’t just affect mood—it primes microglia, the brain’s immune cells, setting the stage for chronic neuroinflammation. 

Microglia become activated by:

  • Chronic cortisol elevation

  • Endotoxemia (LPS)

  • Estrogen dominance

  • Psychological trauma

Once primed, they overproduce quinolinic acid (QUIN)—a neurotoxic kynurenine metabolite—within 24 hours of activation.  QUIN acts as an NMDA receptor agonist, driving excitotoxicity, oxidative stress, and neuronal damage—particularly in brain regions linked to mood and memory (hippocampus, anterior cingulate cortex). 

Research shows depressed and suicidal individuals have significantly higher microglial QUIN expression in these areas—direct evidence of trauma-induced brain inflammation. 

While QUIN is neurotoxic, kynurenine itself has a surprising role: it exerts anti-inflammatory effects on microglia, reducing pro-inflammatory cytokines like TNF-α and IL-6.  This suggests the balance between kynurenine and QUIN—driven by enzyme activity (KMO)—is critical. 

The takeaway?
Metabolic support isn’t just about hormones and energy—it’s about calming the brain’s immune response.  Glucose, thyroid support, and lowering estrogen/endotoxin reduce microglial activation and shift kynurenine metabolism toward protection, not destruction.

Chronic Narcissistic & Scapegoat Abuse: A Metabolic Emergency

Those enduring chronic narcissistic abuse or scapegoating are in a state of biological siege. The relentless gaslighting, control, and emotional exploitation create continuous HPA axis activation, driving:

  • Chronically elevated cortisol

  • Gut barrier breakdown (leaky gut)

  • Endotoxemia

  • Estrogen dominance

  • Kynurenine pathway overactivation

This is not just psychological trauma—it’s metabolic depletion.  The body burns through energy reserves simply to survive the environment, with no chance to rest, repair, or replenish.

Survivors often develop C-PTSD with profound metabolic symptoms: fatigue, brain fog, hormone imbalances, food sensitivities, severe gut dysfunction, and mood crashes—especially after collagen, fasting, or low-carb diets.

You are not broken.
You are under-resourced.

Your body is signaling the need for safety, glucose, and nourishment—not more endurance.

What You Can Do Now

  • Fuel consistently: Eat glucose-rich foods (fruit, juice, honey) every 2–3 hours to lower cortisol

  • Avoid metabolic stressors: No fasting, keto, or collagen if it worsens mood

  • Support liver and thyroid: Crucial for detoxifying estrogen and endotoxin

  • Prioritize safety: Healing begins when the nervous system feels resourced 

Your symptoms are real. They are not weakness—they are biological responses to ongoing trauma.

Healing Is Possible: Your Metabolic Recovery Journey

This is not a life sentence.

Metabolic Type E can be restored. The kynurenine pathway does not have to stay chronically activated.  Trauma-responsive metabolic fragility is not permanent—it’s a signal, not a destiny.

When the body is fueled with glucose, cortisol drops.
When the nervous system senses safety, survival mode begins to quiet.
And when survival isn't the priority, the body can finally redirect resources into healing, repair, and resilience.

You don’t have to white-knuckle through anxiety, brain fog, or hormonal chaos. These are not character flaws—they are metabolic symptoms that respond to metabolic support.

👉 In my 6-week Safe & Nourished Trauma-Informed Metabolic Reclamation Plan, we go deep into a step-by-step approach to restoring balance—for all metabolic types, including Type E. This is where theory becomes practice: daily guidance, food frameworks, nervous system tools, and community support to help you rebuild from the ground up.

This isn’t about willpower.
It’s about resourcing.

And you are worth it.

👉 Begin your journey with the free 7-day Body Wisdom trauma-informed mini-course—designed for those in survival mode, ready to reclaim safety and energy.


Scientific references supporting the mechanisms in Metabolic Type E:

Kynurenine Pathway & Stress

  • Gibney et al. (2014) – Chronic stress increases kynurenine, not acute stress, due to sustained TDO activation Tandfonline

  • Van der Kolk – HPA axis dysregulation in PTSD links cortisol to immune and metabolic disruption Reddit/CPTSD 

Microglia, Quinolinic Acid & Depression

  • Sathyasaikumar et al. (2011) – Microglia produce quinolinic acid, elevated in depression and suicide PMC

  • Steiner et al. (2011) – Severe depression linked to increased microglial quinolinic acid in brain tissue Biomed Central 

Estrogen, Histamine & MCAS

  • Gannage (2025) – Estrogen stimulates mast cell degranulation; histamine increases estrogen, creating a feedback loop Integrative Medicine 

Glucose, Insulin & Tryptophan Uptake

  • Tagliamonte et al. (1975) – Insulin enhances tryptophan transport into the brain ScienceDirect

  • Kumar (2025) – Carbohydrates boost insulin, clearing competing amino acids and increasing brain tryptophan DrKumarDiscovery 

Thyroid, Inflammation & T4-to-T3 Conversion

  • Jonklaas et al. (2019) – Inflammation suppresses deiodinase activity, impairing T4-to-T3 conversion Oxford Academic

Restorative Medicine (2018) – Inflammatory conditions reduce tissue T3, causing hypothyroid symptoms despite normal TSH Restorative Medicine




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