What links conditions comorbid with ME/CFS?

 

Comorbidity… describes the existence of more than one disease or condition within your body at the same time. Comorbidities are usually long-term, or chronic. They may or may not interact with each other.  WebMD

 

German researchers have been looking at the many conditions that are experienced by people in addition to ME/CFS to see if there is a common thread running through them. They concluded that the problem might be in the blood vessels. Vascular dysfunction appears to be a strong common denominator. The main comorbid conditions investigated were:

  • mast cell activation (MCA)
  • dysmenorrhea (severe menstrual cramps) and endometriosis
  • postural tachycardia (POTS) and orthostatic intolerance
  • small fiber neuropathy (SFN)
  • decreased cerebral blood flow
  • brain fog

 

 

ME/CFS and comorbidities: linked by vascular pathomechanisms and vasoactive mediators? by  Klaus J Wirth and Matthias Löhn in
Medicina 2023, 59(5), 978; [doi.org/10.3390/medicina59050978] 18 May 2023 (This article belongs to the Special Issue Advances in ME/CFS Research and Clinical Care)

Hypothesis abstract:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is often associated with various other syndromes or conditions including mast cell activation (MCA), dysmenorrhea and endometriosis, postural tachycardia (POTS) and small fiber neuropathy (SFN). The causes of these syndromes and the reason for their frequent association are not yet fully understood.

We previously published a comprehensive hypothesis of the ME/CFS pathophysiology that explains the majority of symptoms, findings and chronicity of the disease. We wondered whether some of the identified key pathomechanisms in ME/CFS are also operative in MCA, endometriosis and dysmenorrhea, POTS, decreased cerebral blood flow and SFN, and possibly may provide clues on their causes and frequent co-occurrence.

Our analysis indeed provides strong arguments in favor of this assumption, and we conclude that the main pathomechanisms responsible for this association are excessive generation and spillover into the systemic circulation of inflammatory and vasoactive tissue mediators, dysfunctional β2AdR, and the mutual triggering of symptomatology and disease initiation.

Overall, vascular dysfunction appears to be a strong common denominator in these linkages.

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