#Endometriosis is now considered a systemic disease rather than a disease predominantly affecting the pelvis. Endometriosis affects metabolism in liver & adipose tissue, leads to systemic inflammation, & alters gene expression in the brain..."
#Endometriosis affects 5–10% of women of reproductive age...Despite this high prevalence, disease recognition is inadequate & diagnosis time ranges
from 4 to 11 years, with 65% of women being initially
misdiagnosed." 65%!! /2
"Women often report having difficulty articulating their symptoms or feeling that their symptoms are INAPPROPRIATELY NORMALISED." #Endometriosis /3
"Early identification and treatment of #endometriosis
is essential & facilitated by a shift towards clinical
diagnosis instead of relying on surgical diagnosis alone.
Clinical diagnosis of endometriosis & initiation of
therapy at an earlier stage of the disease is possible." /4
"antibodies to endometrial & ovarian antigens have also been detected...These results suggest #endometriosis has features similar to autoimmune diseases...with four studies showing a statistically significant association with at least one classic autoimmune disease." /5
"Lesion survival might also be enhanced by the decreased cytotoxicity of natural killer cells." #Endometriosis
Interesting because NK cell function has been shown to be decreased for many #MECFS patients. /6
"Careful attention to CYCLIC BOWEL & BLADDER PAIN helps distinguish #endometriosis from non-gynecological causes of abdominopelvic discomfort." /7
"Additionally, PROGRESSIVE DYSMENORRHEA (painful periods) should raise suspicion for #endometriosis since primary dysmenorrhoea does not increase in severity over time." /8
"Primary dysmenorrhea also responds consistently to NSAIDs since it is non-progressive. Chronic, cyclic pelvic pain, non-menstrual pelvic pain, deep dyspareunia, dyschezia, & dysuria are frequently reported in women with #endometriosis." /9
"...research has focused on identifying alternative markers, which take into account the systemic nature of #endometriosis. Circulating miRNAs have been considered promising biomarker candidates bc they are stable in circulation and have highly specific expression profiles." /10
"...research in murine models of #endometriosis has identified let-7b (which has anti-inflammatory effects) & miR-451 as potential therapeutic targets.
..administration of let-7b resulted in regression of lesions & decreased expression of ER-beta, aromatase, and IL-6." /11
"The implications of such an approach will ideally lead to an expansion of available medical therapies that incorporate novel, non-hormonal treatments.
Such therapies can include immunomodulating agents, miRNA modulators, & stem-cell-based therapies." /12
An important fact: #Endometriosis may be severe enough that uterus, tubes & /or ovaries are adherent to ureter, bladder, pelvic wall, bowel, rectum etc which cannot be picked up on exam, MRI, transvaginal US or CT & is only discovered during laparoscopy & treated surgically. /13
Nancy's Nook has an educational Facebook page on #Endometriosis which contains a list of vetted gynecologists around the world who are experienced at performing #excision surgery that the average gynecologist may not be able to perform. facebook.com/groups/4181369…
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“It’s really quite shocking. Your patients don’t have any energy in their lymphocytes.”
Unfortunately, they applied for a grant to do this work, & of course, because the grant was labeled “Studying mitochondria in chronic fatigue syndrome,” it was promptly denied by the NIH."
"Cellular Energy Deficit Disorder"; "Energy Deficit Disorder"; "Mitochondrial Energy Production Disorder"; this appears to be the basis for much of our symptomatology, w/multiple different causes;
There were so many more options than "Chronic Fatigue Syndrome". What a travesty.
Cheney's discussion about the significant drop in cardiac output for #MECFS w/standing:
"So when they stand up, they are not being perfused very well. And that’s one of the reasons that these patients have significant problems standing.... /1
@sfcem_mexico It may help for those experiencing co-morbidities of ME/CFS to find specialists who may be able to help some symptoms:
1) Cardiologist to test for POTS w/NASA Lean Test or Tilt Table; sometimes treatment for POTS helps (sometimes it doesn't); /1
@sfcem_mexico 2) Neurologist who can diagnose Small Fiber Neuropathy w/skin biopsy; ideal if they understand Autoimmune Autonomic Dysfunction;
3) Rheumatologist to investigate autoimmunity, particularly Sjogren's; sometimes treatment helps (sometimes it doesn't); /2
@sfcem_mexico 4) Low Dose Naltrexone (LDN) helps some w/fatigue--others it only helps w/pain. Any physician can order from a compounding pharmacy, but some patients instead request a regular script for Naltrexone & dilute it themselves. /3
Just found this on Google Scholar. Will look thru on better brain day:
OSF Preprints | Broken Connections: The Evidence for Neuroglial Failure in ME/CFS #MECFS#pwMEosf.io/ef3n4
"...identified the CNS neuroglia - microglia & astroglia - as the one functional unit in the human body which may best explain all & any of the clinical and pathological features, dysfunctions and observations described for ME/CFS...this points to neuroinflammation..." /2
"Of note, this is not a unifying theory about the etiology, the triggers or the inception process of ME/CFS. This approach is focused solely on finding the final pathogenetic pathway(s) which may underlie the clinical manifestations of ME/CFS." /3
Patterson found S1 spike protein in monocytes of both #LongCovid & post-vax symptomatic patients (plans to look for virus in tissue)
Viral sequences/envelope proteins are enough w/o a replicating virus to create cytokine storm->oxidative stress->mitochondrial dysfunction /1
Are there researchers looking for retroviral sequences in #MECFS monocytes?
Since exosomes can contain miRNA from viruses, is anyone looking at these sequences? Is this the "something in the blood" that is affecting our mitochondria? /2
Are we in a Metabolic Trap because there are viral proteins constantly being expressed from a non-replicating retrovirus or sequences of the virus or just envelope proteins like S1 causing inflammatory cytokine storm, perpetuating this trap? /3
At 20:00 of the podcast: "each virus or pathogen a person acquires can stifle the immune system in a way that makes it somewhat easier for each of the different hits to actually begin to cause more problems, a little like a snowball rolling down a hill..." /1
"...factor hits in that are not just direct infections [mold, mycotoxins, stressful event, injury]...anything else that is compromising the immune system & debilitating it can feed into that picture in which the pathogens begin to...express more protein, become more virulent" /2
"hypothesized that in some patients w/MECFS the vagus nerve could be directly infected...nervous system may be infected...often patients can have gut reservoirs of enterovirus & then vagus may be a conduit by which a neurotropic pathogen can reach the brain or CNS." /3