uniting patients, researchers & clinicians to advocate & research 30+ neuroinflammation-linked conditions with overlapping symptoms, causes & responses.
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The prevalence of depression and anxiety in children and adolescents has nearly doubled since the COVID-19 pandemic. Global rates are astounding:
- 25.2% for depression
- 20.5% for anxiety
The skyrocketing number of pediatric psychiatric cases suggests traditional treatment approaches are inadequate, such as:
- psychotherapies
- psychotropic medications
These approaches offer:
- poor adherence
- tolerability issues
- treatment resistance
- low efficacy (response rates below 50-70%)
Youth are especially vulnerable to side effects such as:
- suicidal ideation
- severe withdrawal symptoms
\ A Role For Inflammation?
Emerging evidence suggests that neuroinflammation, driven by elevated proinflammatory cytokines (e.g., IL-6, TNF-α), is a key factor in treatment-resistant cases. We argue that this is especially true in cases of sudden-onset, post-infectious triggers (e.g., PANS, Long COVID) or immune dysregulation. Further research is needed to develop protocols and guide clinical adoption.
Please share this so we can amplify this message.
Read our publication here:
buff.ly/GLXdK2r
On a related note, our health tracking platform, unhide, is available for children and adolescents! Visit unhidenow.org to learn more.
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Having a chronic inflammatory condition increases your risk for depression. Many assume this is because the patients are sad about their health circumstances.
Immunopsychiatrists would argue that the chronic inflammation is altering their mental health (in a subset of people).
The following paper supports that concept.
A survey of 113 studies and 4 meta-analyses found that genetic variations in the following inflammation-related genes reduce patients' ability to respond to traditional antidepressants:
- Phospholipase A2
- TNF-alpha
- IL-1beta
- MCP-1
- IL-10
- CRP
- IL-6
This likely explains why chronic inflammatory conditions increase your risk of psychiatric conditions such as depression.
Read the full study here: buff.ly/6XXb3hE
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This is a friendly reminder that a staggering 67% of individuals with Long COVID develop a form of dysautonomia(1).
This translates to 38 million Americans who have likely developed dysfunction of the autonomic nervous system (dysautonomia) following a SARS-CoV-2 infection. However, the actual number of patients formally diagnosed with dysautonomia is likely much lower, as many physicians fail to recognize the clinical presentations.
The symptoms associated with dysautonomia in those with long COVID include:
- Orthostatic hypotension (drop in blood pressure when standing)
- Sensory disturbances or paresthesias (tingling or numbness)
- Heartbeat irregularities (e.g., tachycardia or palpitations)
- Gastrointestinal issues (e.g., bowel dysfunction)
- Brain fog or cognitive disturbances
- Dizziness or light-headedness
- Shortness of breath (dyspnea)
- Bladder dysfunction
- Sleep disturbances
- Chest pain
- Fatigue
Also, if you are reading a scientific publication about Long COVID and the researchers do not describe POTS or dysautonomia, it's because they were not screening for it.
Help us raise awareness that millions with Long COVID may be experiencing disruptions in the function of their autonomic nervous systems.
Literature Cited:
1. Larsen, N., Stiles, L., et al. Front. Neurol. 2022; 13: 1012668.
buff.ly/tx9T5XD
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This paper revealed the shocking prevalence of neuropsychiatric conditions in patients with mast cell activation syndrome (MCAS).
Here are the numbers...
ALT Colorful clay model of a human brain with distinct lobes in yellow, pink, purple, blue, and orange, shown beside the Brain Inflammation Collaborative logo to represent research and collaboration on brain inflammation.
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Inappropriate MC activation can make the blood-brain barrier (BBB) leaky. The BBB describes the barrier-like properties of blood vessels in the brain. This could allow pro-inflammatory cytokines and antibodies into the brain.
Too much histamine can affect peripheral neurons and also interact with immune and glial cells in the CNS. This could indirectly drive a wide array of issues categorized as:
- neurologic
- psychiatric
- dysautonomia
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Mast cell-derived cytokines like IL-12 can mediate neuroinflammation. IL-12 can do this by altering neurotransmitter systems and activating microglia (the primary immune cells of the CNS).
Let us know what you think of this study by dropping a comment below.
Read the full study here:
buff.ly/r5nfS9H
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A subset of individuals with depression (1), sleep disorders (2), bipolar disorder (3), or mood disorders (1) have all been found to have elevated pro-inflammatory cytokines in their blood.
The study below is yet another example of why immunopsychiatry is an area of active research.
Literature Cited:
1. Felger JC. Curr Neuropharmacol. 2018. PMID: 29173175
2. Zielinski MR, Gibbons AJ. Front Cell Infect Microbiol. 2022. PMID: 35392608
3. Dolsen MR, Soehner AM, Harvey AG. Psychosom Med. Jan 2018. PMID: 28914726
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Thank you again for allowing us to host you in our webinar series and for inspiring this week's Substack article. We admire the academic and clinical contributions you are making in the dysautonomia world!
For those who haven't yet watched Dr. Blitshteyn's @dysclinic recent webinar, it's outstanding.
piped.video/watch?v=gi03hmor…
Thanks to @BrainInflCollab for discussing my papers on #POTS, #MECFS and #LongCOVID as neuroimmune disorders and a possible CNS localization of POTS/dysautonomia to the dorsolateral medulla! 🧠
Read more about these emerging topics here:
tandfonline.com/doi/full/10.…
mdpi.com/2227-9059/13/1/166
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Key brainstem regions help control heart rate, blood pressure, breathing, and the body’s inflammatory “brake” through the vagus nerve.
In this article, we examine neuroimaging and post-mortem findings in COVID-19, a recent neuroimmune hypothesis for POTS, the medulla’s role as an inflammatory thermostat, and how connective tissue laxity or mast cell activation may amplify vulnerability in a subset of patients.
Read more here: buff.ly/Lx71wkY
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New research highlights something many of us already know too well: females with autoimmune diseases are far more likely than males to have their symptoms dismissed as psychiatric or psychosomatic.
In a study of over 6,600 people:
- 43% of females reported a previous psychiatric misdiagnosis vs 33% of males.
- 34% of females reported psychosomatic labels vs 22% of males.
Even after adjusting for other factors, females were:
- ~50% more likely to receive a psychiatric misdiagnosis.
- ~75% more likely to receive a psychosomatic misdiagnosis.
Females also waited longer for a correct diagnosis, often 1 to 2 years, while many males were diagnosed in under 3 months.
Patient partner Shaista Tayabali put it clearly: “The differences between the sexes in misdiagnoses for people with autoimmune diseases are stark… as women, we still often have a harder time having our symptoms believed and therefore addressed accurately.”
If your symptoms persist, evolve, or affect multiple systems, keep advocating for proper investigation. Your experiences are valid and deserve to be heard.
Share this if it resonates.
Full article in the comments.
You have 23 chromosomes from your biological mother and 23 from your biological father, or two copies of every gene.
However, males technically don't have two copies of EVERY gene.
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Read more here: medicalxpress.com/news/2026-…
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After having her daughter at age 27, Sebrina Smith-Henry was constantly thirsty, with dry mouth and skin, body aches, and chronic fatigue. It took about 7 years of symptoms before she received a diagnosis.
Sebrina was in and out of a military hospital while her husband was in service, but she explained, “I had never had a doctor put all the pieces together before then… and you never saw the same doctor twice there.”
It wasn’t until a chance encounter with a nurse that things began to change. Her daughter, then 7, was participating in a clinical study at Duke University Children’s Hospital. The study required long hours at the hospital, and a nurse allowed her to sleep in a guest room.
After waking up 8 hours later, the nurse checked her vitals and said, “You need to tell your doctor about all these things that are happening to you."
A new doctor outside the military network examined her skin, eyes, and scalp. He ran tests and told her, “I think we found the answer.” She was diagnosed with:
- Rheumatoid arthritis
- Sjögren’s
- Lupus
Managing her autoimmune diseases has her feeling better at age 59 than she did at 46.
Common signs include joint pain, rashes, extreme fatigue, dryness, anemia, and more.
If your symptoms linger without answers from your doctor, maybe it’s time to find another doctor. Always keep advocating for yourself.
Read more: msn.com/en-us/news/other/she…
There are currently no licensed treatments specifically for Sjögren’s disease. However, results from phase III clinical trials suggest this may soon change.
Ianalumab produced a meaningful reduction in systemic disease activity, reduced oral dryness, and improved salivary flow compared with placebo.
This monoclonal antibody is a dual-action biologic that:
1. Depletes antibody-producing B cells, and
2. Inhibits the activation and survival of those cells (via BAFF-receptor blockade).
In January, the FDA granted Novartis Breakthrough Therapy designation for ianalumab to expedite its review and potential licensing. If approved, the drug could become available around mid-2027.
Clinical trials are also evaluating ianalumab’s efficacy and safety in other autoimmune diseases, including lupus.
We at the Brain Inflammation Collaborative are particularly interested in both Sjögren’s disease and lupus because of the well-documented increased risk of neuropsychiatric complications, which stem from the effects of systemic inflammation on the brain.
Read more here: buff.ly/EWfRrpx
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Validated survey instruments provide a reliable way to measure symptoms and overall quality of life. But one of the biggest misconceptions about health tracking is that a single score can tell you specifically what's wrong.
It doesn't.
Instead, measuring scores over time can help catch setbacks and improvements to help you to adjust care. In this way, your trend reports help answer questions like:
• Am I improving over time?
• Have my symptoms been getting worse?
• What does "normal" look like for me?
• When did things begin to change?
A single score is a snapshot.
A series of scores over time tells a story.
That's why unhide® doesn't just show your latest survey result; it helps you see your health over time.
Your reports aren't designed to diagnose a condition. They're designed to help you recognize patterns that may otherwise be difficult to see.
Explore: unhidenow.org/validated-heal…
In 2017, Alina Sternberg, a psychiatrist, was hit with crushing fatigue and brain fog.
Neurologists told her the symptoms were caused by depression.
"No, I can enjoy my life, and I know what depression is... I’m a psychiatrist!”
It took 6 years to discover the culprit...🧵
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ME/CFS, Long COVID, PTSD, rheumatoid arthritis, and multiple sclerosis have one thing in common.
Prof Dmitry Pshezhetskiy explains, "patients frequently report remarkably similar symptoms," such as:
- brain fog
- disturbed sleep
- poor concentration
- overwhelming fatigue
- autonomic dysfunction
- dramatic reduction in everyday functioning
Researchers at the University of East Anglia and Oxford BioDynamics investigated the causes of many shared symptoms. Here is what they found.
Using 3D genome analysis rather than linear DNA sequences, the team discovered little overlap in individual genes. "But when we analyzed how those genes interact in complex biological networks, a completely different picture emerged. Suddenly, the diseases appeared deeply connected," noted lead researcher Prof Dmitry Pshezhetskiy.
The shared systems involve:
- stress responses
- immune signaling
- mitochondrial energy production
Different triggers, from viral infection to trauma, may converge on these circuits to drive the overlapping symptoms. "What we discovered is something approaching a biological unifying theory of fatigue," Pshezhetskiy said.
Read more: buff.ly/aUYyxOW
ALT ID: Close-up stylized DNA double helix in grayscale with the "Brain Inflammation Collaborative" logo, suggesting genetic research into brain inflammation.
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Progress in treating depression has largely stalled over the last 30 years.
Could this be because the field has largely ignored a key biological driver present in a substantial subset of patients: chronic low-grade inflammation?
Multiple meta-analyses of randomized trials show that anti-inflammatory agents (as add-ons or in patients with elevated inflammatory markers) can reduce depressive symptoms, with moderate effect sizes (1,2,3).
This is especially relevant for treatment-resistant depression, where standard antidepressants often fall short in 1/3 of treated patients.
At the Brain Inflammation Collaborative, we recognize the strong link between chronic inflammatory conditions and psychiatric disorders such as major depressive disorder, and we actively incorporate this relationship into our research.
Learn more at buff.ly/X9I08WE
Literature Cited:
1. Köhler O, et al. (2014). JAMA Psychiatry. PMID: 25322082
2. Bai S, et al. (2020). Journal of Neurology, Neurosurgery & Psychiatry. PMID: 31658959
3. Kappelmann N, et al. (2018). Molecular Psychiatry. PMID: 27752078
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