Psoriasis, Inflammation, Anxiety & Depression: What the Science Is Teaching Us About the Brain–Body Connection

A 2025 review by Keenan & Granstein in Acta Physiologica offers a powerful and evolving perspective on mental health: anxiety and depression are not “just in the mind.” They are deeply connected to immune signaling, inflammation, and neurobiological pathways that link the skin, brain, and nervous system.

For those of us practicing modern psychiatry, this research reinforces something we are learning more clearly each year — mental health is systemic.

The Article’s Unique Perspective

Keenan and Granstein (2025) explore how proinflammatory cytokines (such as IL-6, TNF-α, and IL-1β) and neuropeptides (including substance P and CGRP) play roles in:

Psoriasis
Depression
Anxiety

Psoriasis has long been understood as an inflammatory autoimmune skin condition. However, this review highlights how the same inflammatory mediators active in psoriasis are also implicated in mood and anxiety disorders.

This is not coincidence. It is biology.

Cytokines & Mood

Proinflammatory cytokines can:

Cross the blood–brain barrier
Alter serotonin and dopamine pathways
Affect glutamate signaling
Activate the HPA axis
Increase neuroinflammation

Understanding Glucose Metabolism Disorders & Inflammation

So the result can cause symptoms that look like depression and anxiety — low mood, fatigue, sleep disruption, irritability, brain fog, and heightened stress reactivity.

This helps explain why:

Patients with psoriasis have higher rates of depression and anxiety.
Patients with chronic inflammatory conditions often report mood symptoms.
Traditional antidepressants sometimes only partially address symptoms when inflammation is a driving factor.

Psychiatry Is Expanding: The Brain–Body Model

For decades, psychiatry focused primarily on neurotransmitters. Today, we are integrating:

Immunology
Endocrinology
Gut-brain signaling
Metabolic health
Stress physiology

This article reinforces the concept of psychoneuroimmunology — the dynamic communication between the nervous system, immune system, and endocrine system.

At CareSync Psych, we believe in treating the whole-person, no just mental health.

Mental health is not separate from:

Autoimmune conditions
Hormonal shifts
Metabolic dysfunction
Chronic stress
Inflammatory load

The brain and body are in constant dialogue.

Why This Matters for Anxiety & Depression Treatment

Understanding inflammation’s role opens doors to more comprehensive treatment planning, including:

Lifestyle interventions that reduce inflammatory burden
Nutrition strategies that support immune regulation
Sleep optimization
Stress-response regulation
Thoughtful medication selection
Targeted lab evaluation when clinically appropriate

This does not mean inflammation causes all cases of depression or anxiety. However, it does mean that being to narrow or ignoring the body misses part of the story.

Anxiety Treatment at CareSync Psych

A Whole-Person Approach in Psychiatry

At CareSync Psych in Lakeland, Florida, we embrace this evolving science. We practice psychiatry with a brain-body framework, integrating:

Evidence-based medication management
Therapy and psychoeducation
Metabolic and lifestyle considerations
Personalized treatment planning

We are licensed to provide psychiatric care in:

Florida (FL)
Iowa (IA)

Telehealth available throughout Florida and Iowa.
Arizona (AZ) and Washington (WA) licensure pending.

If you are struggling with anxiety, depression, autoimmune symptoms, or stress-related flares, know this:

Your symptoms are not a personal failure. They may reflect complex biological signaling — and that means there are multiple pathways toward healing.

The Future of Mental Health Care

Research like Keenan & Granstein (2025) continues to move psychiatry forward. We are no longer separating skin from brain, immune system from mood, or stress from physiology.

The future of mental health care is integrative.

And it is already here.

CareSync Psych
Psychiatric Medication Management | Therapy | Brain-Body Mental Health
Lakeland, FL
Serving Florida & Iowa via telehealth
Arizona & Washington pending licensure

If you’re searching for:

Psychiatric provider in Lakeland FL
Anxiety treatment in Florida
Depression care in Iowa
Integrative psychiatry near me
Brain-body mental health care

We’re here to help.

Glucose and Neuroinflammation

Glucose and Hypometabolism

Cerebral glucose hypometabolism refers to a reduction in the brain’s ability to metabolize glucose, the primary source of neuronal energy. Because neurons have limited capacity for energy storage, consistent glucose supply is essential for proper cognitive, emotional, and behavioral function. When metabolism slows, neurons become less active, leading to impaired neurotransmission, synaptic plasticity, and overall brain performance — even before structural damage occurs.

🔬 Pathophysiology

Glucose metabolism in the brain occurs primarily through aerobic glycolysis, producing ATP to fuel neuronal signaling. When this process falters — whether due to mitochondrial dysfunction, neuroinflammation, insulin resistance, or oxidative stress — regions of the brain exhibit hypometabolism on FDG-PET (fluorodeoxyglucose positron emission tomography) scans.

Mechanisms contributing to cerebral hypometabolism include:

Mitochondrial dysfunction: decreased ATP synthesis impairs neuronal signaling.
Neuroinflammation: cytokines disrupt insulin and glucose pathways.
Brain insulin resistance: glucose uptake is blunted despite normal peripheral insulin levels.
Oxidative stress: damages neuronal membranes and enzymes critical for metabolism.

🧩 Clinical Correlations

Cerebral glucose hypometabolism is observed across neuropsychiatric and neurodegenerative disorders, with distinct regional patterns:

Condition	Commonly Affected Regions	Clinical Correlates
Alzheimer’s Disease	Posterior cingulate, parietotemporal cortex	Early memory loss and executive dysfunction
Frontotemporal Dementia	Frontal and anterior temporal lobes	Behavioral disinhibition, apathy
Major Depressive Disorder	Dorsolateral prefrontal cortex, anterior cingulate	Impaired concentration, emotional regulation
Schizophrenia	Frontal and temporal regions	Executive dysfunction, cognitive impairment
Bipolar Disorder	Frontal, limbic circuits	Mood instability, impulsivity
Traumatic Brain Injury	Site-specific	Cognitive slowing, emotional dysregulation

In psychiatry, hypometabolism often reflects neural circuit inefficiency rather than cell loss. For instance, decreased glucose utilization in the prefrontal cortex may explain poor emotional regulation in depression or executive dysfunction in schizophrenia.

⚕️ Integrative and Metabolic Psychiatry Perspective

At CareSync Psych, cerebral glucose hypometabolism underscores the mind-body connection — illustrating how metabolic and psychiatric processes intertwine. Emerging research links metabolic dysfunction (e.g., insulin resistance, obesity, chronic inflammation) with neuropsychiatric symptoms, suggesting that improving systemic metabolism may also enhance brain energy and mood stability.

Therapeutic approaches that can help restore cerebral metabolism include:

Lifestyle interventions: balanced nutrition, exercise, restorative sleep.
Nutritional psychiatry: ketogenic or low-glycemic diets supplying ketones as alternate brain fuel.
Pharmacologic supports: metformin, GLP-1 receptor agonists, and mitochondrial antioxidants (e.g., CoQ10).
Psychotherapy and mindfulness: reducing stress-driven cortisol spikes that impair glucose utilization.

🌿 Clinical Implications and Future Directions

FDG-PET imaging remains the gold standard to detect regional hypometabolism.
Metabolic psychiatry is reframing depression, anxiety, and cognitive decline as partly bioenergetic disorders.
Addressing glucose dysregulation early may prevent progression of cognitive and emotional disorders.
Future research aims to integrate metabolic biomarkers into psychiatric diagnostics and personalized treatment plans.

🧾 References (APA 7th Edition)

Butterfield, D. A., & Halliwell, B. (2019). Oxidative stress, dysfunctional glucose metabolism, and Alzheimer disease. Nature Reviews Neuroscience, 20(3), 148–160. https://doi.org/10.1038/s41583-019-0132-6
Cunnane, S. C., Trushina, E., Morland, C., Prigione, A., Casadesus, G., Andrews, Z. B., … & Mattson, M. P. (2020). Brain energy rescue: An emerging therapeutic concept for neurodegenerative disorders of ageing. Nature Reviews Drug Discovery, 19(9), 609–633. https://doi.org/10.1038/s41573-020-0072-x
Mosconi, L., Berti, V., Glodzik, L., Pupi, A., De Santi, S., & de Leon, M. J. (2010). Pre-clinical detection of Alzheimer’s disease using FDG-PET, with or without amyloid imaging. Journal of Alzheimer’s Disease, 20(3), 843–854. https://doi.org/10.3233/JAD-2010-091504
Rasgon, N. L., & McEwen, B. S. (2016). Insulin resistance—a missing link no more. Molecular Psychiatry, 21(12), 1648–1652. https://doi.org/10.1038/mp.2016.163
Tomasi, D., & Volkow, N. D. (2019). Associations between brain activation, glucose metabolism, and psychiatric symptoms in major depressive disorder. Molecular Psychiatry, 24(12), 1672–1680. https://doi.org/10.1038/s41380-018-0262-9
Zhang, X., Chen, W., Li, J., Zhang, Y., & Xu, Y. (2021). Brain glucose hypometabolism and psychiatric disorders: A review of mechanisms and therapeutic perspectives. Frontiers in Psychiatry, 12, 700–714. https://doi.org/10.3389/fpsyt.2021.700714

Understanding Ehlers-Danlos Syndrome

March 16, 2017Body Health Chronic Pain Ehlers-Danlos Syndrome (EDS)hEDS

Ehlers-Danlos Syndrome: The Overlooked Impact on Mind and Body

Living with Ehlers-Danlos Syndrome (EDS) often means more than just joint hypermobility or fragile skin—it means navigating a long, complex journey through the healthcare system while managing pain that others can’t always see. Recent research highlights just how misunderstood EDS remains, and why supporting both body and mind is essential in care.

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The Diagnostic Odyssey

For many with hypermobile EDS (hEDS), the road to diagnosis is long and winding. Halverson et al. (2023) found that patients often endure years of misdiagnoses and comorbidities before receiving an accurate EDS diagnosis. Many are initially told they have fibromyalgia, chronic fatigue syndrome, or even psychosomatic conditions. This “diagnostic odyssey” delays effective treatment and increases emotional distress.

The consequences of misdiagnosis include:

Unnecessary treatments or procedures.
Dismissal of symptoms as “in the patient’s head.”
Psychological harm, including mistrust of healthcare providers.
Worsening of both physical and mental health symptoms.

Pain in EDS: More Than Meets the Eye

Pain is one of the most disabling symptoms of EDS, and it’s not just mechanical. Research by Malfait et al. (2021) highlights that EDS pain is multifactorial, involving:

Musculoskeletal pain from joint instability, sprains, and micro-injuries.
Neuropathic pain due to nerve compression or damage.
Central sensitization, where the nervous system becomes hypersensitive to pain signals, amplifying even mild discomfort.

This complexity makes pain in EDS hard to treat with standard approaches, often leaving patients in a cycle of trial-and-error medications, physical therapy, and alternative treatments.

The Mental Health Impact

Both misdiagnosis and chronic pain shape the mental health of people with EDS:

Anxiety & Depression – Rates are significantly higher among those with chronic, uncontrolled pain.
Medical Trauma – Being repeatedly dismissed or misdiagnosed can create PTSD-like responses to healthcare visits.
Cognitive Strain – Chronic pain and fatigue contribute to “brain fog,” memory lapses, and difficulty concentrating.
Isolation – Limited mobility, stigma, and disbelief from others can lead to social withdrawal.

EDS shows us how physical and psychological health are inseparable. Treating only the joints or only the anxiety misses the full picture.

Toward a Whole-Person Approach

To improve care for patients with EDS, treatment must be multidimensional:

Medical – Accurate diagnosis, management of comorbidities (like POTS or mast cell activation), and targeted therapies for connective tissue.
Pain Management – Using multimodal approaches, including medication, physical therapy, nerve blocks, and mindfulness-based strategies.
Mental Health Care – Psychotherapy to address medical trauma, coping skills for chronic pain, and support for mood disorders.
Lifestyle & Integrative Care – Nutrition support, pacing strategies, gentle strengthening exercises, and sleep optimization.

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Conclusion

Ehlers-Danlos Syndrome is far more than a “bendy joint” condition—it is a whole-body, whole-mind disorder that demands compassionate, integrated care. By acknowledging the diagnostic challenges and the complex pain mechanisms, providers can better support patients not just in surviving with EDS, but in finding ways to thrive.

Halverson, C. M., Cao, S., Perkins, S. M., & Francomano, C. A. (2023). Comorbidity, misdiagnoses, and the diagnostic odyssey in patients with hypermobile Ehlers-Danlos syndrome. Genetics in Medicine Open, 1(1), 100812. https://doi.org/10.1016/j.gimo.2023.100812
Malfait, F., Colman, M., Vroman, R., De Wandele, I., Rombaut, L., Miller, R. E., … & Syx, D. (2021). Pain in the Ehlers–Danlos syndromes: Mechanisms, models, and challenges. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 187(4), 429-445. https://doi.org/10.1002/ajmg.c.31967

References

Halverson, C. M., Cao, S., Perkins, S. M., & Francomano, C. A. (2023). Comorbidity, misdiagnoses, and the diagnostic odyssey in patients with hypermobile Ehlers-Danlos syndrome. Genetics in Medicine Open, 1(1), 100812. https://doi.org/10.1002/ajmg.c.31935

Malfait, F., Colman, M., Vroman, R., De Wandele, I., Rombaut, L., Miller, R. E., … & Syx, D. (2021). Pain in the Ehlers–Danlos syndromes: Mechanisms, models, and challenges. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 187(4), 429-445. https://doi.org/10.1002/ajmg.c.31950