Comorbidity–Driven Type

Nerdyssey November 04, 2025

🧠 Overview

“Comorbidity–Driven Type” is a neuropsychological concept used to describe mood states that are driven by multi-system comorbidities — that is, depression, anxiety, or burnout that do not arise from “a single, standalone disorder,” but from the cumulative effect of multiple overlapping brain–body mechanisms over time, eventually becoming systemic stress.

In people who have several comorbid conditions, such as ADHD + Anxiety + chronic insomnia or diabetes + thyroid disorder + Depression, the brain regions that regulate emotion (e.g., amygdala, prefrontal cortex, ACC) must withstand pressure from multiple directions at once. This makes the brain “lose its way” in trying to distinguish which illness is actually generating the suffering.

Individuals in this group often spend a great deal of time seeing multiple specialists, taking multiple medications, or even receiving conflicting diagnoses from different providers. This produces identity confusion (“What exactly is wrong with me?”). As a result, emotional symptoms tend to fluctuate according to physical illness, hormonal changes, medication side effects, and the psychological burden of having to manage life inside a complex, fragmented healthcare system.

The general feeling is: “I’ve become the case manager of my own illnesses.”
They must keep track of drug names, appointments, and medical information, which further intensifies emotional exhaustion and cognitive fatigue. Many people develop secondary depression that does not arise directly from negative thinking, but from “the accumulated fatigue of managing comorbidities.”

Neurobiologically, this condition aligns with the concept of Allostatic Load — a state in which the body and brain must maintain equilibrium under chronic pressure until all regulatory mechanisms begin to lose efficiency: the HPA axis is persistently activated, cortisol remains chronically elevated, and the prefrontal–limbic circuits lose their balance of control.

In daily life, Comorbidity–Driven Type is therefore not just “a depressive disorder,” but rather a global state of fatigue across body–brain–emotion created by a healthcare system that treats people in fragmented parts, with no one holding the picture of “the whole person.” Effective treatment thus tends to require integrated care — bringing together information about physical illnesses, medications, and mental states within one coordinated framework.

In summary, this condition can be described as depression that emerges from the layering of illnesses and treatments themselves, rather than from any single disorder alone. It represents one of the key prototypes of “modern multimorbidity psychiatry,” which focuses on understanding patients as interconnected systems, not just as isolated symptom clusters.

💭 Core Symptoms

The Comorbidity–Driven Type does not present only as “sad mood” or “generalized anxiety.” It is “a state of the brain under pressure from multiple comorbid systems at the same time.”
As a result, symptoms are often diverse, unusual, and change according to bodily state, medication, and psychological exhaustion. They can be summarized into several core axes as follows:

🧩 1. The feeling of “I am a messy, complicated case”

People in this state often feel like they are “a puzzle too complex for any doctor to understand.”
Body and mind seem to be falling apart on multiple fronts at once: chronic headaches, easy fatigue, poor sleep, short attention span, mood swings, etc., to the point that it becomes very difficult to tell what came first and what came after.

  • Many receive different diagnoses at different hospitals, e.g. “Depression” from one psychiatrist, “Generalized Anxiety” from another, and “Hormonal Imbalance” from an internist.
  • This overlapping experience makes them feel like they must become “their own case manager” — making appointments with multiple specialties, organizing their medication schedule, and maintaining health records like a personal research project.
  • Psychologically, this leads to a loss of trust in the system (“No one sees me as a whole person”), identity confusion (“Which illness defines me?”), and chronic emotional fatigue from being “divided into parts” by the medical system.

💊 2. Emotional symptoms that shift with physical illness or concurrent medications

In this condition, mood is not stable but directly “linked” to changes in physical illness or other treatments.
The brain responds to biological changes like a line of dominoes — flare-up of medical illness → mood drops; new medication → mood swings; poor sleep → entire day emotionally ruined.

  • For example, in someone with a thyroid disorder + depression, when thyroid hormones drop, mood often becomes noticeably darker, even while taking antidepressants.
  • People with chronic illnesses such as diabetes or SLE often have “low mood days” when physical symptoms flare, because the amygdala and ACC are simultaneously activated by pain signals and stress.
  • Adjusting multiple medications (e.g. antidepressant + antihypertensive + painkiller) can also influence serotonin, dopamine, and norepinephrine, leading to unpredictable mood changes.
  • It is therefore common to hear patients say: “I don’t know if I’m truly depressed or if the meds are making me numb.” — which is a key marker of the Comorbidity–Driven Type.

🧠 3. Cognitive Overload / Decision Fatigue

The brain is pushed beyond its limit by the constant need to “think about how to manage illness and treatment” every day. Blood tests, treatment planning, booking appointments, reading lab reports — all of this gradually becomes a full-time job without the person ever intending it.

  • The dorsolateral prefrontal cortex (DLPFC) works far more than usual, eventually resulting in mental fatigue.
  • Some people spend hours thinking, “Should I adjust my meds?”, “Which doctor should I see next?”, “Do I have to fast before this test?”
  • The brain enters a state of decision fatigue — having no energy left to make even minor decisions, such as whether to eat now, or whether to reply to a message.
  • This accumulated fatigue pulls mood downward and may eventually develop into depressive inertia (emotional inertia, difficulty initiating any action despite desire to improve).

🧍‍♀️ 4. The feeling of “being alone inside the healthcare system”

Even though they are frequently in hospitals and seeing doctors, these individuals often feel “more alone than those who are not in treatment,” because no one holds the picture of “the whole person.”
Each doctor looks only at their own piece — cardiology looks at the heart, endocrinology looks at the thyroid, psychiatry looks at mood — but no one integrates all of this together.

  • Patients must repeat their history over and over until they are exhausted and may feel: “Everyone sees me as data, not as a person.”
  • This fosters emotional detachment toward the healthcare system — they don’t fully trust doctors, yet they are too afraid to stop medication.
  • Some develop medical trauma from experiences of being dismissed or labeled as “overthinking,” even though their symptoms actually arise from the interaction of comorbid conditions.

💧 5. Chronic depression / anxiety / burnout that lingers

Even when one particular illness is treated successfully, the feelings of fatigue, emptiness, and lack of energy often remain.
This is because the autonomic nervous system (ANS) has been chronically activated to the point it becomes “stuck in stress mode.”
Patients often say: “Even when my body gets better, I don’t feel like my life has improved.”

  • The predominant mood pattern is often low-grade depression — not necessarily severe, but persistent and long-lasting.
  • The limbic circuits and prefrontal cortex show poor functional coordination (functional disconnection).
  • Accumulated exhaustion narrows the brain’s perspective, leading to beliefs like “Nothing can be fixed,” or “I’m a case that will never get better.”

🔍 6. A self-image of “I am fundamentally abnormal”

Self-stigma is central to this condition. Patients begin to internalize the belief that “I am too complex to be understood.”
They see themselves more as “a set of illnesses” than as “a living person,” for example:

“I am ADHD with depression and low thyroid,”
rather than
“I am a human being fighting multiple conditions.”

  • Over time, this way of seeing themselves becomes encoded in the medial prefrontal cortex (mPFC), which is involved in self-schema, embedding the pattern of “I am the problem; I am the abnormality.”
  • This directly affects self-worth and recovery — even when physical symptoms improve, the internal identity remains stuck in the story of “I am a case that will never be normal.”
  • This is one of the reasons why the Comorbidity–Driven Type often requires integrative psychotherapy that helps restore a self-image based on “being human” rather than “being a bundle of diagnoses.”

📋 Diagnostic Criteria

Note: These criteria are a clinical conceptual framework for understanding the pattern of mood and comorbidity.
They are not a formal medical diagnosis according to DSM or ICD.

A. Presence of at least 2 comorbid disorders or conditions

The foundation of this type is multimorbidity — the coexistence of multiple systemic conditions in one person, such as:

  • Psychiatric disorders (Major Depression, GAD, Bipolar Disorder, ADHD, ASD, etc.)
  • Chronic medical illnesses (diabetes, thyroid disease, heart disease, SLE, chronic pain, IBS, fibromyalgia)
  • Or a combination of physical and mental disorders.

Example: A 30-year-old woman with ADHD + Anxiety + Endometriosis + Chronic Fatigue → every system contributes to her emotional circuitry.

B. Clear relationship between mood and the layering of comorbidities

Mood fluctuations do not arise in isolation, but are directly linked to “the collision of illnesses” or the impact of treatments:

  • Depression when physical illness flares up
  • Anxiety from having to control multiple diseases simultaneously
  • Burnout from frequent hospital visits and repeated medical procedures
  • Worsening mood after medication changes, even if the primary illness appears improved

In some cases, mood improves almost immediately when the treatment structure is reorganized, such as reducing the number of medications, or changing to a more coordinated, integrated scheduling of appointments.

C. Evidence that mood symptoms are driven by “the overall picture” rather than a single disorder

This is the key aspect that distinguishes this from a “single-disorder” framework. For example:

  • When a particular disorder (e.g. ADHD) is well treated but mood remains low → the main driver is likely the total burden of comorbidities.
  • When medication is reduced to only a few necessary ones and mood improves → this suggests polypharmacy was a major trigger.
  • When integrated care is implemented and depressive symptoms decrease, even without changing medication → this indicates that the previous systemic overload has been relieved.

D. Significant distress or impairment in functioning

The person shows clear interference in daily life, for example:

  • Markedly reduced concentration due to fatigue and medication effects
  • Inability to work at full capacity because of frequent appointments or medical procedures
  • Deterioration of relationships due to anxiety and emotional instability
  • Persistently low self-esteem (chronic low self-esteem)

Some spend more than 50% of their waking time on “managing their health,” which can be considered a key marker of Comorbidity–Driven Depression.

E. Symptoms are not better explained by a standalone depressive or anxiety disorder

This is the clear dividing line between Comorbidity–Driven Type and typical MDD or GAD.
If mood improves significantly once the comorbidity structure is reorganized (e.g., medication rationalization, team-based care, improved balance of sleep–nutrition–medication),
it suggests that “depression is not the primary, independent illness,” but rather a downstream consequence of the overall comorbidity burden.

✳️ Summary of the conceptual diagnostic framework

“A person who meets criteria for Comorbidity–Driven Type is someone with depression–anxiety–burnout driven by the combined pressure of multiple systemic illnesses, rather than a single isolated disorder. Mood improves markedly when the structure of care and the burden of comorbidities are addressed in an integrated manner.”

🧩 Subtypes or Specifiers

In the NeuroNerdSociety series, Comorbidity–Driven Type can be divided into specifiers to serve as “sub-links” to other posts, for example:

(1) Neurodevelopmental-Stacked Type

Occurs in people who already have ASD / ADHD / SLD / DCD.

  • Depression/anxiety flare when additional comorbidities arise, such as chronic insomnia, physical illness, or PTSD.
  • Often involves a combination of masking / camouflaging + executive dysfunction + sensory overload stacked together.

(2) Chronic-Illness Burden Type

Chronic physical illness forms the base, such as diabetes, cancer, kidney disease, heart disease, SLE, fibromyalgia.

  • Depression/anxiety emerge from pain, fatigue, reduced quality of life, and frequent medical visits.
  • Mood patterns typically rise and fall in parallel with physical symptoms and treatment intensity.

(3) Poly-Diagnosis Overload Type

The person has multiple psychiatric diagnoses from different places (e.g. previously diagnosed with MDD, Bipolar II, PTSD, BPD, ADHD).

  • They receive treatments based on multiple theories and multiple protocols overlapping at once.
  • Patients are often confused about “what they really are” and feel hopeless about the system.

(4) Iatrogenic / Treatment-Interaction Type

Here, emotional deterioration arises primarily from:

  • Drug–drug interactions
  • Medication side effects (e.g. SSRIs causing emotional blunting, steroids causing mood swings)
  • The “collision” of treatment approaches across specialties

When treatment is reorganized — medications reduced or changed, and care made more coherent — mood improves significantly.

All of these are “tags/specifiers” meant to link to other sub-posts.
They are not formal medical diagnoses.

🧬 Brain & Neurobiology

In Comorbidity–Driven Type, the brain does not have a single, isolated deficit.
Instead, it works extremely hard to “maintain balance” amid pressure from physical illness, mental illness, and medication effects,
leading to what is called Allostatic Load — a state in which the biological system expends more energy than the body can recover.

Rather than being only “a depressive disorder,”
this is “a state of the brain operating in multi-system survival mode.”

1️⃣ Allostatic Load & Stress System Dysregulation

“Allostasis” refers to the body’s ability to adapt in order to maintain internal balance (homeostasis).
When this adaptive process is triggered repeatedly without adequate rest — for example, managing chronic illness, controlling medications, coping with anxiety, and enduring chronic pain all at once —
the brain–endocrine–immune axis enters a state of allostatic overload.

  • The HPA Axis (Hypothalamus–Pituitary–Adrenal) becomes overactive → cortisol is secreted at high levels continuously,
    keeping the body in a state of arousal even when there is no immediate threat.
  • Chronically elevated cortisol can cause atrophy in the hippocampus (involved in memory and stress regulation) over time.
  • The amygdala becomes hyper-responsive → general stress is interpreted as threat.
  • The prefrontal cortex, which normally regulates emotions and decision-making, starts to weaken (hypofunction)
    → leading to rumination, depression, and difficulty controlling emotions.
  • Patients often experience insomnia, chronic fatigue, brain fog, mood instability, and weakened immunity — all signs that the brain is “running out of energy” from excessive attempts to maintain balance.

2️⃣ Neuroinflammation (Brain-Level Inflammation)

Over the past decade, numerous studies have indicated that chronic low-grade inflammation is a key mechanism linking chronic physical illness with depression.

  • Conditions such as diabetes, SLE, IBS, chronic pain, obesity, autoimmune disorders
    increase levels of cytokines (IL-1β, IL-6, TNF-α, CRP) in a persistent way.
  • These cytokines can cross the blood–brain barrier (BBB) or signal through the vagus nerve
    to activate the limbic system, leading to sickness behavior — depressive mood, fatigue, and social withdrawal.

  • In the brain, inflammation leads to:

    • Over-activation of microglia (the brain’s immune cells) → release of neurotoxic mediators.
    • Suppression of dopamine and serotonin function → causing anhedonia (loss of pleasure), apathy, and emotional blunting.
    • Reduced neurogenesis in the hippocampus, progressively impairing stress-regulation mechanisms.

The net effect is that the brain remains in a state of chronic inflammatory activation —
like an engine running overheated while still being forced to keep working.

3️⃣ Network-Level Dysregulation

The human brain does not work in isolated modules, but as interlinked networks.
In Comorbidity–Driven Type, three major networks become dysregulated simultaneously:

  • Default Mode Network (DMN) — involved in self-reflection, past–future thinking, and internal narrative.
    • When DMN is overactive → rumination and self-blame increase.
    • Often associated with chronic depression.
  • Salience Network (SN) — detects important stimuli and potential threats (insula + ACC).
    • In people with multiple comorbidities, the SN becomes hypervigilant, reacting to minor cues as if they were major threats.
  • Executive Control Network (ECN) — supports decision-making and behavioral control.
    • Suppressed by chronic stress and medication, leading to executive dysfunction: forgetfulness, slow decision-making, poor self-control.

When these three networks fail to coordinate,
the brain “loses rhythm” in switching between modes, for example:

  • from task-focus mode → relaxation mode → social mode

This results in cognitive fatigue and the feeling of “I can’t think, even about simple things.”

4️⃣ Neurotransmitter & Drug-Interaction Imbalance

People with many comorbidities are often prescribed multiple medications (polypharmacy)
such as antidepressants + anxiolytics + antihypertensives + painkillers + thyroid medications.
As a result, the brain’s neurotransmitter systems (dopamine, serotonin, norepinephrine, acetylcholine, GABA, glutamate)
are impacted in multiple directions at once.

  • SSRIs / SNRIs may reduce sadness but suppress dopamine → causing emotional flattening.
  • Benzodiazepines reduce anxiety but strongly enhance GABA → leading to cognitive dulling.
  • Pain medications (opioids, gabapentin, pregabalin) dampen reward circuits → the brain becomes less responsive to pleasure.
  • Steroids / thyroid medications stimulate arousal → heightening anxiety and causing insomnia.
  • Each medication can interact with others (drug–drug interactions), destabilizing neurotransmitter release.

The result is a state of chemical instability in the brain,
with periods of numbness, periods of mood swings, and periods of somatic arousal (trembling, palpitations) without clear cause.

From a neurochemical perspective, this is a brain trying to “maintain balance among too many simultaneous chemical forces,”
leading patients to feel “I don’t feel like myself anymore, even though I’m taking everything as prescribed.”

5️⃣ Neural Energy Depletion & Brain Fatigue

The brain of someone with multiple comorbidities must consume large amounts of energy to process multiple bodily systems at once,
especially the frontal lobes and insula, which integrate signals from body and emotion.

  • Inflammation + stress hormones + multiple medications → reduce mitochondrial efficiency in neurons.
  • Neurons produce less ATP (cellular energy) → leading to a sensation of “fatigue without obvious cause.”
  • The reward system (ventral striatum) becomes less responsive to positive stimuli → motivational energy drops.
  • The anterior insula, which links bodily states and emotional awareness, becomes over-active → resulting in psychosomatic fatigue.

Patients often describe this as:

“I’m tired from the inside. My brain feels exhausted in a way I can’t put into words.”

🔬 Neurobiological Summary

“Comorbidity–Driven Type” describes a brain forced to function on behalf of multiple bodily systems simultaneously —
physical illnesses, mental disorders, hormonal changes, and medication effects —
culminating in allostatic overload + neuroinflammation + neurotransmitter chaos + network dysregulation.

Together, these processes generate chronic depression and burnout
even when no single disorder can be identified as the sole primary cause.

⚠️ Causes & Risk Factors

1️⃣ Presence of chronic or multi-system illness (Chronic Multi-System Burden)

Having multiple systemic illnesses is a core foundation of this state:
endocrine diseases, autoimmune conditions, neurological disorders, cardiac diseases, chronic inflammatory syndromes.
Each illness sends stress signals to the brain via the vagus nerve and hormonal pathways, forcing the brain to constantly adjust its mode.

  • Physical illness reduces energy levels → affecting motivation.
  • Treatment of physical illness increases medication load → affecting brain chemistry.
  • The brain must “learn to live with chronic pain or chronic symptoms,” a form of never-ending stress.

Examples such as fibromyalgia, IBS, migraines, autoimmune disorders all have evidence linking them to increased risk of depression and cognitive fatigue.

2️⃣ A “fragmented” healthcare system

In many countries, healthcare is still divided by specialty:
the heart belongs to cardiology, thyroid to endocrinology, emotions to psychiatry —
but no one is responsible for “the whole person.”

  • Patients must retell the same story repeatedly to each doctor.
  • Medication lists and treatment plans may not be fully synchronized.
  • Each doctor brings in their own viewpoint, leading to overlapping or conflicting diagnoses.
  • There is no single care coordinator integrating all dimensions.

As a result, patients carry the burden of information, decision-making, and communication themselves,
developing systemic fatigue and a profound sense of “being alone inside the healthcare system.”
This becomes a major driver of complex burnout and depression.

3️⃣ Polypharmacy (use of multiple medications simultaneously)

  • Each medication can have emotional side effects (e.g., some antihypertensives can suppress serotonin).
  • Some drugs unintentionally potentiate each other → causing neurotransmitter imbalance.
  • Adjustments or switches in medications without a coherent overview can create a cycle of mood instability.

Polypharmacy is thus both “a consequence of comorbidity” and “an additional driver of comorbidity-related burden.”
Some patients find that when they discontinue several medications (under medical supervision), their mood improves markedly,
because the brain can begin to restore its own chemical balance.

4️⃣ Life experiences and psychosocial stressors

The lives of people with comorbidities are often filled with hidden chronic stress:

  • Feeling restricted in their capabilities (“I can’t function like other people”).
  • Fear of being a burden to family.
  • Anxiety about medical costs and financial stability.
  • Social stigma (“People see me as ‘the sick person’ all the time”).

These ongoing stresses become constant signals in the brain — activating the amygdala and HPA axis
and keeping the brain in threat mode.
Without adequate recovery time, the parasympathetic nervous system (rest-and-repair mode) is under-activated → leading to burnout of both body and mind.

5️⃣ Personality and core beliefs

People with perfectionistic, highly conscientious, or hyper-responsible personalities are especially vulnerable,
because they tend to blame themselves when they cannot control their body as expected.

  • They hold inner beliefs like “I must be strong,” “I must handle everything.”
  • When the body weakens or illness limits activity, they feel ashamed, inferior, or like they have “failed at life.”
  • These core beliefs push the prefrontal cortex to keep sending “control” signals even when the body is exhausted → leading to chronic fatigue of willpower.
  • Perfectionistic traits are also linked, in some individuals, to lower serotonin function, increasing vulnerability to depression.

🧩 Additional contributing factors

  • Genetic susceptibility:
    Genes related to cortisol regulation, the serotonin transporter (5-HTTLPR), and inflammatory markers may increase risk.
  • Environmental triggers:
    Pollution, sleep deprivation, chronic under-eating, shift work — all can promote neuroinflammation.
  • Socio-cultural factors:
    In cultures that glorify strength and stoicism, chronic illness may be labeled as weakness → increasing self-stigma.
  • Lack of emotional support:
    Absence of friends or family who understand the condition amplifies isolation.

🔚 Summary of causes and risk factors

“Comorbidity–Driven Type does not arise from a single cause,
but from the intersection of biology–healthcare system–medications–society–personality.
Together, these create a state of systemic fatigue and depression (Systemic Depression).

Therefore, solutions must be holistic — not merely increasing or decreasing medication,
but restructuring the entire life and care system to restore balance.”

🩺 Treatment & Management

This section is for general educational purposes
and cannot substitute for diagnosis or treatment by a qualified clinician.

1. See “the whole person,” not just “the list of diagnoses”

  • Compile a complete history of all diagnoses and medications.
  • Ask clinicians/therapists to help create a symptom map:
    which symptoms come from which illness / medication / situation.

2. Reduce diagnostic redundancy

  • Discuss with clinicians how to organize the diagnoses:
    which ones are core drivers, which are secondary or consequences.
  • Focus on the primary drivers instead of trying to extinguish every symptom simultaneously.

3. Manage polypharmacy carefully

Ask clinicians to evaluate:

  • Which medications are truly necessary
  • Which may duplicate effects
  • Which might be worsening mood or causing emotional blunting

The goal is: “use the fewest medications necessary while still achieving good symptom control.”

4. Integrated Care / Team-Based Care

When possible, use a coordinated team, such as:

  • Psychiatrist + medical specialist(s) + psychologist + dietitian + physiotherapist

Have one person act as a central coordinator seeing the whole picture —
for example, a primary care physician or a therapist who helps track symptoms over time.

5. Psychotherapy and living-with-comorbidity skills

  • CBT, ACT, trauma-informed therapy, psychoeducation

  • Train skills such as:

    • Pacing (managing energy use across the day)
    • Self-monitoring (tracking symptoms + meds + events)
    • Structured communication with doctors (preparing a checklist before appointments)

6. Lifestyle & Self-Care (modifying what can be controlled)

  • Sleep hygiene
  • Nutrition that supports brain and immune function
  • Exercise at a level appropriate to physical conditions
  • Connecting with support groups of others with similar comorbidities

7. Preventing hopelessness and managing safety risks

Because people with Comorbidity–Driven Type often feel “my case is unsolvable,”
it is essential to watch for signs of hopelessness / self-harm ideation early.

A safety plan should be developed with professionals, including:

  • Emergency numbers
  • Trusted contacts
  • Specific steps to follow when symptoms worsen

📝 Notes

  • Comorbidity–Driven Type is not a formal DSM or ICD diagnosis.

It is a shared language that helps people understand:

“I’m not falling apart because of one illness; it’s because everything is layered on top of everything else.”

  •  This framework helps to:
    • Reduce self-blame (“It’s not because I’m weak — the conditions I’m facing exceed what a typical person’s system can handle.”)
    • Clarify why treatment feels so complex.

    • Open up conversation with doctors:

“Can we try to look at the whole picture together?”

📚 Reference (Academic & Clinical Sources)

Core Diagnostic and Conceptual Frameworks

  • American Psychiatric Association. (2022). Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). Washington, DC.
  • World Health Organization. (2021). International Classification of Diseases, 11th Revision (ICD-11): Mental, Behavioural and Neurodevelopmental Disorders. Geneva: WHO.
  • Kendler, K. S., & Gardner, C. O. (2016). Depression heterogeneity and comorbidity: implications for classification and treatment. Molecular Psychiatry, 21(3), 339–346.
  • Vigo, D., Thornicroft, G., & Atun, R. (2016). Estimating the true global burden of mental illness. The Lancet Psychiatry, 3(2), 171–178.

Neurobiology & Allostatic Load

  • McEwen, B. S., & Gianaros, P. J. (2011). Stress- and allostasis-induced brain plasticity. Annual Review of Medicine, 62, 431–445.
  • Juster, R.-P., McEwen, B. S., & Lupien, S. J. (2010). Allostatic load biomarkers of chronic stress and their links with depression. Psychoneuroendocrinology, 35(7), 1055–1069.
  • Slavich, G. M., & Irwin, M. R. (2014). From stress to inflammation and major depressive disorder: a social signal transduction theory of depression. Psychological Bulletin, 140(3), 774–815.
  • Dantzer, R., O’Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008). From inflammation to sickness and depression: when the immune system subjugates the brain. Nature Reviews Neuroscience, 9(1), 46–56.

Comorbidity & Polypharmacy

  • Fortin, M., et al. (2005). Prevalence of multimorbidity among adults seen in family practice. Annals of Family Medicine, 3(3), 223–228.
  • McIntyre, R. S., et al. (2020). Polypharmacy in psychiatric treatment: challenges and opportunities for patient safety and clinical outcomes. World Psychiatry, 19(2), 231–242.
  • Bair, M. J., Robinson, R. L., Katon, W., & Kroenke, K. (2003). Depression and pain comorbidity: a literature review. Archives of Internal Medicine, 163(20), 2433–2445.

Network Dysregulation & Cognitive Fatigue

  • Menon, V. (2011). Large-scale brain networks and psychopathology: a unifying triple network model. Trends in Cognitive Sciences, 15(10), 483–506.
  • Whitfield-Gabrieli, S., & Ford, J. M. (2012). Default mode network activity and connectivity in psychopathology. Annual Review of Clinical Psychology, 8, 49–76.
  • Proulx, J. D., et al. (2023). Cognitive fatigue and brain network dysregulation in multimorbid patients: a neuroimaging review. Frontiers in Human Neuroscience, 17, 1145612.

Psychosocial & Systemic Factors

  • Bury, M. (1982). Chronic illness as biographical disruption. Sociology of Health & Illness, 4(2), 167–182.
  • Katon, W., & Ciechanowski, P. (2002). Impact of major depression on chronic medical illness. Journal of Psychosomatic Research, 53(4), 859–863.
  • Klasnja, P., et al. (2019). Integrating behavioral health with chronic care management: lessons from system fragmentation. Health Services Research, 54(5), 1110–1128.

🏷 Hashtags

#ComorbidityDrivenType #Multimorbidity #DepressionSubtype #AllostaticLoad #Neuroinflammation #Neurobiology #Polypharmacy #IntegratedCare #ComplexDepression #BrainHealth #MentalHealthEducation #NeuroNerdSociety #PsychiatricComorbidity #StressSystem #CognitiveFatigue #NetworkDysregulation #MindBrainSystem #EmotionalExhaustion

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