Any kind of chronic inflammation will make you fatigued all of the time, so it may be hard to differentiate.
However, the first thing I look for is Th2 dominance, which is the immune profile in CFS. Discover our favorite biohacks in our ebook, SelfHacked Secrets. You can download the first chapter absolutely free here.
What Causes CFS?
It seems like CFS is a result of a viral infection and the body’s inability to control it. The result is oxidative stress.
This means that the mechanisms to control viruses are low and other kinds of inflammation might be high.
Your Doc Won’t Order These Tests
The problem is no doctor or will order these tests. As I understand it, doctors are under pressure from insurance companies and insurance companies are out for profit.
They don’t want to shell out thousands of dollars on tests if they don’t see a clear way to benefit from these tests.
People with CFS show elevated:
One must keep in mind that one test will not tell you if you have CFS. You need to take many of these tests to put a picture together.
- CRP (R)
- Oxidative stress (isoprostanes) (R)
- Omega6 PUFAs, i.e. linoleic acid and arachidonic acid (AA), and mono-unsaturated fatty acids (MUFAs), i.e. oleic acid. Also omega9 fatty acids and one of the saturated fatty acids, i.e. palmitic acid (R)
- IL-17 (R)
- IL-10 (R)
- IFN-γ/Th1 (R)
- TNF-α (R)
- TGF-beta (R)
- IL-1 beta…LPS-stimulated (R)
- IL-6 …LPS and PHA-stimulated (R)
- TNF…LPS-stimulated (R)
- Tregs/CD4+CD25+ T cells (R)
- CD8+ cytotoxic T lymphocytes (R)
- Oxidized LDL (R)
- FoxP3 and VPACR2 expression (R)
- EBV IgM – in a subset (R)
- Perforin (R)
- CD38 and HLA-DR activation (R)
- CD28+ (R)
- CD20 (R) – rituximab had good effects in some CFS people
- Lactate in ventricular cerebrospinal fluid (CSF) (R) (A marker of reduced energy metabolism)
- Adenosine (R)
- NPY (R)
- Serotonin increase to tryptophan. (R)
- Eosinophil Protein X (R)
People with CFS show decreased:
- EPA (R)
- Zinc (R, R2)
- DHEAS (R) -contradictory (R)
- Glutathione/GSH (cortical) (R)
- Natural Killer Cell Activity/Cytotoxic activity of NK and CD8+T cells (R)
- LPS-stimulated TGF-b (R)
- HDL (R)
- CD56bright NK cells (R) – CD56 Bright NK Cells are also lower in Coronary Heart Disease, Asthma, Rhinitis (R)
- Granzyme A and granzyme K (R)
- CD11b (R)
- CD69 activation marker on T cells (CD3+, CD3+CD4+, and CD3+CD8+) and on NK cells (CD45+CD56+) – Since induction of CD69 surface expression is dependent on the activation of the protein kinase C (PKC) activation pathway, it is suggested that in CFS there is a disorder in the early activation of the immune system involving PKC. (R)
- DPPIV/C26 expressed on T cells and NK cells (R)
- Neutrophil respiratory burst (R)
- White matter in midbrain (R)
- PM Cortisol and 24hr urine free cortisol (R)
- Folinic acid/Folate/Methylation (R, R2)
- Bilateral white matter volumes (R)
Lesions in frontal white matter (R).
Corticotropin-releasing hormone (CRH) and neurotensin (NT), secreted under stress, activate mast cells (MC) necessary for allergic reactions to release inflammatory mediators that could contribute to CFS symptoms. (R)
“Almost every adolescent with CFS had orthostatic tachycardia (Stewart et al.,1999), but this was not the case with adults (Natelson et al., 2007) where rates appear to be lower ranging from 10% (Naschitz et al., 2006) to 27% (Hoad et al., 2008) with the higher rate found in UK patients who reported having the diagnosis of CFS rather than being directly diagnosed. In our own study of adult patients (Natelson et al., 2007), orthostatic tachycardia was not common, occurring in only 11% of patients, not significantly different from rates in healthy controls.” (R)
“Finding subgroups of CFS suggests different underlying pathophysiological processes responsible for the symptoms seen.”(R)
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