I am transitioning off a waitlist and gearing up for big news! Stay tuned and please direct virtual and in office consultation requests to drmichaelscoma@gmail.com and they will be answered in the order in which they are received. #MECFS #LongCovid #MCAS #LymeDisease

Crash dynamics reflect temporal dysregulation, not simply "overexertion.” As autonomic tone, immune mediators, and mitochondrial down-ramping fall out of synchrony, even low-level stressors generate disproportionate physiologic collapse. Temporal profiles > activity volume.

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The strongest predictor of an impending crash is post-exertional metabolic inflexibility, not task intensity. Patients unable to promptly re-establish oxidative metabolism following minimal exertion are the ones who enter a sustained crash trajectory.

Three under-recognized features of crash cycles (Long COVID, ME/CFS) Crash onset precedes symptoms. The initial failure is a disrupted transition from sympathetic activation to restorative parasympathetic physiology. By symptom onset, the cascade is already operational.

Many of my most severe ME/CFS patients can recall the exact moment of sickness, ie., when "a switch was flipped" in their brain. If there's an ON switch, there needs to be an OFF switch.

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Livedo reticularis in the setting of Bartonella reactivation amidst Long COVID - how many others are walking around like this?

The vast majority of the medical community is in the dark with respect to neuroinflammation and autonomic dysfunction. When a previously healthy patient comes to you seeing this ⬇️ how can this be written off as anxiety or functional neurologic disorder?

As a mild HDAC inhibitor, NaPB supports mitochondrial function, reduces oxidative stress, and even helps regulate neurotransmitters. In carefully monitored cases, I have observed remarkably strong physiologic responses in patients with complex post-viral patterns.

NaPB also delivers powerful anti-inflammatory effects, regulating NF-κB and modulating immune activity ▶️rebalancing lingering immune dysregulation seen in post-viral conditions such as Long COVID, EBV, HHV-6 and Enteroviruses.

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NaPB acts as a chemical chaperone, easing endoplasmic reticulum (ER) stress and helping cells fold proteins correctly - an issue often disrupted after viral infections. Less ER stress▶️calmer cells, reduced symptoms, and improved resilience.

🧬The Best Long COVID Mechanistic Candidate No One Is Talking About Sodium phenylbutyrate (NaPB) intersects directly with the cellular stress architecture seen in Long COVID: ER stress, protein misfolding, mitochondrial overload, and neuroimmune activation. 🧵

For patients with severe intolerance or GI issues, I often utilize non-oral neuromodulatory routes - such as intranasal delivery - to influence pathways governing sensory gating (GABAnergic, cholinergic, serotonergic, and NMDA-related). The goal is processing without crashing.

Management requires deliberate neuromodulation: restoring inhibitory-excitatory balance, stabilizing autonomic tone, and reducing neural load. NMDA receptor overactivation amplifies sensory input; modulating this pathway can help rebuild tolerance without forcing activity.

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Neurological crashes arise from disrupted autonomic balance, weakened inhibitory control, and unstable sensory gating. When inhibitory-excitatory signaling collapses, even normal stimuli become overwhelming.

Sensory overload in ME/CFS and Long COVID reflects a neurological energy failure. When sensory input exceeds the brain's processing capacity, it triggers defensive down-regulation and crashes. This is a systems-level impairment - not psychological sensitivity.

No wonder patients with Ehlers–Danlos syndrome are more prone to autonomic dysfunction, MCAS, long COVID, and ME/CFS. When collagen architecture is compromised, every system that relies on structural integrity breaks down.

MCAS is never isolated and each flare represents a pathologic interplay between mast cells, the vascular endothelium, the microglia, and autonomic circuits. Targeting histamine or mast cell stabilization treats echoes and fails to decode the system-level signals driving illness.

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In high-complexity MCAS, the problem is the network: endothelial leak, neuroinflammation, autonomic dysfunction and mitochondrial distress. Exosomal cross-talk amplifies these loops. When patients have disabling symptoms with "normal labs," this deeper layer is always missed.

MCAS is not an isolated "mast cell issue" - it's a communication disorder. Mast cells ➡️exosomes ➡️activation of endothelium, microglia, fibroblasts, and the autonomic nervous system. H1 and H2 blockade may help symptoms but fails to solve the architecture of the illness.