I touched upon noise sensitivity in my Hyperacusis, Phonophobia and DNA SNPs earlier this year. A reader forward a link to a 2017-11-18 article and it is definitely time to re-examine this condition often seen with CFS.
“According to our findings, noise sensitivity is associated with the grey matter volume in the selected structures. Among those, we propose and discuss particular areas, previously linked to auditory perceptual, emotional and interoceptive processing, in which larger grey matter volume seems to be related to higher noise sensitivity.” 
” A recent epidemiological study reports that up to 88% of individuals with high noise sensitivity self-declare at least one other environmental sensitivity ”
- “In our paediatric cohort, hyperacusis is more common in boys and in those children with Autistic Spectrum Disorder”  – i.e. some brain damage likely
- “Severe hyperacusis is characterized by low uncomfortable loudness levels(ULL) for specific frequencies and no or mild hearing loss. Given the high incidence of tinnitus, otological abnormalities, and mental health problems, the management of patients with severe hyperacusis should involve otologists and psychiatrists in addition to audiologists.” 
- Another study found that ULL were lowest (most sensitive) at 8000 hertz than at lower frequencies. 
- “Results indicated that the sport-related Concussed group scored higher on the Hyperacusis questionnaire and displayed greater sensitivity to sounds in psychoacoustic tasks compared to the Control group.”  – that is physical brain trauma
The CFS Brain
- “We found a significant decrease in white matter (WM) volumes in the left inferior fronto-occipital fasciculus (IFOF) in CFS while in NCs it was unchanged (family wise error adjusted cluster level P value, PFWE < 0.05). This longitudinal finding was consolidated by the group comparisons which detected significantly decreased regional WM volumes in adjacent regions (PFWE < 0.05) and decreased GM and blood volumes in contralateral regions (PFWE < 0.05). Moreover, the regional GM and WM volumes and T2w in those areas showed significant correlations with CFS symptom scores (PFWE < 0.05).” 
- “Accounting for total intracranial volume, patients had larger Gray Matter volume and lower White Matter volume. ” 
- “In the same mPFC location, both MT and T1w intensities were lower in CFS patients compared with NCs (uncorrected voxel P < 0.001). This study is the first to report that brain structural differences are associated with unrefreshing sleep in CFS. ” 
- “There is copious evidence of abnormalities in resting-state functional network connectivity states, grey and white matter pathology and impaired cerebral perfusion in patients afforded a diagnosis of multiple sclerosis, major depression or chronic fatigue syndrome (CFS) (myalgic encephalomyelitis). ” 
The Microbiome Data
There are no published studies, but fortunately due to readers contributing their ubiome/thryve/american gut microbiome AND adding their symptoms, we can do some explorations and speculations.
Again, the problem is that 50 of the 56 also report CFS. So is this a pattern for CFS and not noise sensitivity? On the other hand of those reporting general fatigue (99 at present) only 50 have noise issue.
The following seem significant
- Lipid metabolism: Arachidonic acid metabolism
- Amino acid metabolism: D-Arginine and D-ornithine metabolism
I need to do some analysis comparing CFS with Noise Issues with CFS without Noise Issue to be sure that these are actually significant and not picking up CFS.
End Product Patterns?
- High Acetate, Hydrogen Values
- High B vitamins levels (B1,B2,B3,B5,B9, B12)
Something feels slightly off with this page… I am using averages and I suspect that I should be using median values (50% above, 50% below).
Challenge to Data Scientists
All of the data is at http://lassesen.com/ubiome ready for download and import into R. Try comparing the General Fatigue without Noise Sensitivity TO General Fatigue with Noise Sensitivity and see what you can discover that is statistically significant.
During my readings, I came across this report of a patient that died with a prior diagnosis of CFS.
“Atypical neurons displaying aberrant sprouting processes in response to injury are observed throughout cortical gray and white matter. Abundant amyloid deposits identical to Alzheimer’s Disease plaques with accompanying intracellular granular structures are observed as well. ” 
This is very significant to me, my SPECT scan from 8 years ago (during a flare) was read by the radiologist as Early Onset Alzheimer’s. He may have been doing a very reasonable read of my SPECT scan. I was having severe memory issues — now fully recovered. This causes me to speculate that the amyloid deposits may be microbiome bacteria triggered.
It forces me to ask the question — is the amyloid deposit hypothesis for Alzheimer’s Disease a red herring?
Lights Went On
A reader after this was posted sent me a link to a Jul 30, 2018 article: More Evidence for Gut-Brain Link in Alzheimer’s Disease which states:
- “Nho said three key findings emerged.
- First, lower serum concentrations of primary bile acids synthesized in the liver from cholesterol were significantly associated with worse cognitive function, decreased hippocampal volume, and decreased brain glucose metabolism.
- Second, higher serum concentrations of secondary bile acids produced in the gut by bacteria were significantly associated with higher CSF phosphorylated tau and CSF total tau levels, as well as larger brain structural atrophy and decreased brain glucose metabolism.
- Third, higher serum concentrations of ratios of bacterially produced secondary bile acids to primary bile acids were significantly associated with lower CSF Aβ1-42 values, larger brain structural atrophy, and decreased brain glucose metabolism.”
“”In addition,” said Carrillo, “if it turns out these gut bacteria are effective and accurate markers of Alzheimer’s disease cause or progression, or both, they might be useful as a noninvasive screening tool — a simple blood test. They could then be used to help identify high-risk people for clinical trials or track the impact of a therapy. However, we are only at step one. We don’t know yet exactly what the changes we are seeing mean — especially in animal models — whether they are cause or effect.”