Thanks for the vids. But i struggle to see how the microclots can be the cause of mecfs when ppl with diabetes type 2 have more severe clots. Sounds like a downstream effect given this info.
The occurrence of hyperactivated platelets and fibrinaloid microclots in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
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SWAlexander
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I think so too that microclots happen at a later stage in a process. First there is thrombosis most people don´t know they have it. "Blood Clots (DVT & PE) Q&A - with Dr. Weinberg"
Genetic Factors in Antiphospholipid Syndrome:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7765384/
Abstract
As in many autoimmune diseases, the pathogenesis of the antiphospholipid syndrome (APS) is the result of a complex interplay between predisposing genes and triggering environmental factors, leading to a loss of self-tolerance and immune-mediated tissue damage. While the first genetic studies in APS focused primarily on the human leukocytes antigen system (HLA) region, more recent data highlighted the role of other genes in APS susceptibility, including those involved in the immune response and in the hemostatic process. In order to join this intriguing debate, we analyzed the single-nucleotide polymorphisms (SNPs) derived from the whole exome sequencing (WES) of two siblings affected by APS and compared our findings with the available literature. We identified genes encoding proteins involved in the hemostatic process, the immune response, and the phospholipid metabolism (PLA2G6, HSPG2, BCL3, ZFAT, ATP2B2, CRTC3, and ADCY3) of potential interest when debating the pathogenesis of the syndrome. The study of the selected SNPs in a larger cohort of APS patients and the integration of WES results with the network-based approaches will help decipher the genetic risk factors involved in the diverse clinical features of APS.