Brain Injury can happen many ways. The most common is blunt force trauma, typically from a car accident, called Traumatic Brain Injury (TBI) or from a stroke . TBI and stroke is easy for most people to understand and be emphatic towards.  In general the half-life of TBI preventing employment is 2 years [reference]. The rate of recovery depends on many issues and the ability to be employed is often dependent on the ability of the person or their recovery therapist to be adaptive. I know because I have been thru the process three times!

In the case of Chronic Fatigue Syndrome, it is not the result of an one instance in time like TBI.  It is the ongoing consequence of the disease process and has some unique characteristics such as loss of brain mass. As readers may know, I have had CFS three times – each time with significant cognitive loss (1st time going from a triple 1st class honors student to barely passing my courses the following year). The last time with CFS, the SPECT scan was (mis)read as early Alzheimer’s – which “agreed” with general memory issues.  An evaluation by a subsequent neurologist who was familiar with CFS, dismissed that diagnosis because my memory issues did not match Alzheimer’s — in fact those issues have been decreasing year after year since recovery started.

In this first post, I will give the facts, what may scare some of you but should be accepted and you should move on to acting upon this. In the second post, I will give my view on recovery strategies for brain injury (with reference to literature).

Brain Injury in Chronic Fatigue Syndrome

First the bad news, the scary news — far worst than brain injury from someone that suffered an automobile accident or a fall.

• ” The results indicated abnormalities of the cerebral function in the prefrontal region, orbitofrontal region, and right temporal lobe in CFS patients  “[2017]
• ” 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)….  Importantly, replicated experimental findings suggest that the use of high-resolution SPECT imaging may have the capacity to differentiate patients afforded a diagnosis of CFS from those with a diagnosis of depression.  ” [2018]
• “most of the studies found gray matter (GM) volumes reduced in some brain regions in CFS”[2015]
• Patients with chronic fatigue syndrome have reduced absolute cortical blood flow [2006].
• “Most patients showed autonomic nervous system dysfunction and circadian rhythm disturbances, similar to those observed in jet lag. Radiological imaging studies (SPECT, Xe-CT, and MRS) revealed decreased blood flow in the frontal and thalamic areas, and accumulation of choline in the frontal lobe.” [2004]
• “Neuroinflammation is present in widespread brain areas in CFS/ME patients and was associated with the severity of neuropsychologic symptoms.” [2014]
• “Patients with AIDS dementia complex had the largest number of defects (9.15 per patient) and healthy patients had the fewest defects (1.66 per patient). Patients with chronic fatigue syndrome and depression had similar numbers of defects per patient (6.53 and 6.43, respectively). In all groups, defects were located predominantly in the frontal and temporal lobes.” [1994]
• “CFS subjects showed less perfusion in the anterior cingulate region, the change in CFS subjects’ activation of the left anterior cingulate region during the PASAT was greater than that observed for healthy subjects.” [2003]
• Patients with chronic fatigue syndrome have reduced absolute cortical blood flow.[2006]
• ” reports of WM [white Matter] volume losses and neuroinflammation in the midbrain, together with the upregulated prefrontal myelination suggested here, are consistent with the midbrain changes being associated with impaired nerve conduction which stimulates a plastic response on the cortical side of the thalamic relay in the same circuits.”[ Evidence in chronic fatigue syndrome for severity-dependent upregulation of prefrontal myelination that is independent of anxiety and depression.[2015]
• “Neuroimaging and EEG research has documented brain dysfunction in cases of CFS. Therefore, a quantitative EEG was done, comparing her to a normative data base. This revealed excessive left frontal theta brainwave activity in an area previously implicated in SPECTresearch.” [2001]
• “Bilateral white matter atrophy is present in CFS… Right hemispheric increased FA[piecewise fractional anisotropy] may reflect degeneration of crossing fibers or strengthening of short-range fibers. Right anterior arcuate FA may serve as a biomarker for CFS.” [2015]
• “Abnormal cerebral perfusion patterns in CFS subjects who are not depressed are similar but not identical to those in patients with depressive illness.” [2000]
• “symptoms of fatigue in CFS subjects were associated with reduced responsivity of the basal ganglia, possibly involving the disruption of projections from the globus pallidus to thalamic and cortical networks.” [2014]
• ” neurocognitive testing in CFS has demonstrated deficits in speed and efficiency of information processing, attention, concentration, and working memory.” [2013]
• “many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis–in both of which conditions chronic fatigue is characteristically present.” [1997]
• ” in chronic fatigue syndrome patients, there is discordance between SPET brain perfusion and 18F-FDG brain uptake.” [1998]
• “CFS patients showed a significant hypometabolism in right mediofrontal cortex (P = 0.010) and brainstem (P = 0.013) in comparison with the healthy controls. Moreover, comparing patients affected by CFS and depression, the latter group showed a significant and severe hypometabolism of the medial and upper frontal regions bilaterally (P = 0.037-0.001), whereas the metabolism of brain stem was normal. Brain 18FDG PET showed specific metabolism abnormalities in patients with CFS in comparison with both healthy controls and depressed patients.” [1998]
• ” In the midbrain, white matter volume was observed to decrease with increasing fatigue duration. For T(1) -weighted MR and white matter volume, group × hemodynamic score interactions were detected in the brainstem [strongest in midbrain grey matter (GM)], deep prefrontal white matter (WM), the caudal basal pons and hypothalamus. A strong correlation in CFS between brainstem GM volume and pulse pressure suggested impaired cerebrovascular autoregulation.” [2011]
• Sjögren syndrome presenting with encephalopathy mimicking Creutzfeldt-Jakob disease.[2013] Sjogren Syndrome is often co-morbid with CFS
• Brainstem perfusion is impaired in chronic fatigue syndrome. [1995]
• “The EEG abnormality is slow alpha wave contaminants on slow wave background, which is identical to EEG of CFS. The results clearly imply that CFS is not a hysterical or psychogenic disease, and that fibromyalgia may be a central fundamental of CFS. Fibromyalgia, however, has distinct features such as no antecedent inflammatory process and no endemics. Therefore, the syndrome has features distinct from, in addition to common features to CFS. It is also very difficult to distinguish CFS from depression. The above-mentioned features can be observed in depression. Now, study of brain blood flow or metabolism by PET or SPECT can be a possible tool for establishment of the CFS identity.” [1992]
• “The BP(ND) values of (11)C-(R)-PK11195 in the cingulate cortex, hippocampus, amygdala, thalamus, midbrain, and pons were 45%-199% higher in CFS/ME patients than in healthy controls.” [2014] via PET Scan

Bottom Line:

Next time that someone says “CFS is your head”, do not disagree, instead haul out the above and say that they are correct, it is physical disruption of the brain!

Recently I suddenly started encountering problems with getting sleep at night. The usual suspect, change, stress, etc were not there. Last night after waking up for the 2nd time at 2:30 AM, I decided to “waterpik”(Water Flosser) my mouth followed by a hydrogen peroxide rinse. I went back to bed and slept hard until the alarms went off. Speculation: chemicals, were being produced by bacteria in the mouth, were keeping me awake.

My wife also discovered a different biological sleep aid this week, something that caused her to sleep unusually hard – bed time probiotics:

• One Mutaflor and two Prescript Assist capsules.

Again, speculation is that either the chemicals produced by bacteria that cause excessive wakefulness OR chemicals caused by killing off bacteria that cause deep sleep is the root.

We know that microbiome bacteria impacts cognitive function, so the speculation seems appropriate.

If neither of the above help with sleep, then try 2-3 “00” capsules of Neem, Haritaki or Tulsi at bedtime.

A reader sent me a link to a Danish article that talked about the use of charcoal for microbiome disruptions. On first consideration, it means that a variety of chemical produced by bacteria in the gut may be absorbed and thus “jack the chemical signalling” of the evil [jacked] bacteria. This is speculation, so I thought that I would see what PubMed knows about it.

• “Commonly employed doses of activated charcoal do not appreciably influence the liberation of fecal gases.” [1999]
• “a herbal treatment with myrrh, dry extract of chamomile flowers, and coffee charcoal for ulcerative colitis…demonstrates a distinctly different pattern during treatment with myrrh, chamomile extract, and coffee charcoal than during treatment with mesalazine.” [2014] Does something – unclear what 😦
• “Oral Activated Charcoal Prevents Experimental Cerebral Malaria in Mice …” [2010]
• “The most effective material in the prevention of endotoxemia provided to be bentonite[Bentonite is an absorbent aluminium phyllosilicate, impure clay consisting mostly of montmorillonite} followed by Kaopectate and charcoal particles.” [1983]
• • “Lipopolysaccharides (LPS), also known as lipoglycans and endotoxin, are large molecules consisting of a lipid and a polysaccharide composed of O-antigen, outer core and inner core joined by a covalent bond; they are found in the outer membrane of Gram-negative bacteria, and elicit strong immune responses in animals.” Wikipedia
• It is cited as being used for Crohn’s Disease [2010] but I could not locate any published studies.

In short, not much published — it has been investigated for removing foul smells from fecal material without success. An old article hints that it may moderate immune responses.

There appear to be a clinical trial attempted in 2006 by Dr. Kenneth Kenigsberg (who appears to have a patent on this approach,  WO 2007/015102 A1: ‘The use of charcoal for the treatment of inflammatory conditions’. Inventors: BMJF, PS, PMK, KJT, Kenneth Kenigsberg and LU.) The patent describes the use of charcoal in association with other drugs/supplements and thus is an adjunct (something that helps but may be ineffectual by itself). There are no results about the clinical trial that I could locate.

Bottom Line

• It’s cheap, i”Activated charcoal is “generally felt to be a very benign” unless it absorbs medications that a person is taking, she said…. “The dosing recommendations for activated charcoal are not well-established,”” [source]
• There is discussion about it on Crohn’s Groups
  • It can absorb medications/supplements – so timing is important.
• There is a “hint” that it may be effective
  • the results of the clinical trial was not published BUT a patent was filed.
  • for a condition with inflammation, it appears to work
• I am a strong advocate of the “three wise men coming from the east”, i.e. using myrrh and frankincense (aka Boswellia) gums and would suggest using those with the charcoal because they also reduce inflammation.

A reader sent me their observations on benfotiamine, which according to wikipedia  ” is marketed as a medicine and/or dietary supplement, depending on the respective Regulatory Authority”

“I have noticed extra energy and less affects from when I eat starches/sugars (I don’t eat white sugar, but I eat honey, coconut sugar, agave, etc). I used to get pretty severe joint pain and stiffness from eating any sort of starches/sugars. Benfotiamine has helped alleviate that on days when I am not 100% Wahls Paleo compliant. My brain fog has been mild or rare since going on a Wahls diet, but even that is improved notably.”

which corresponded to a anecdotal responses to benfotiamine

“…Benfotiamine, at 900 mg a day, tripled my energy in about four days, reduced my sugar cravings, made me able to sense my muscles again for the first time in years, improved my brain fog, and rendered my insomnia total…..

http://www.adnuther.com/2012/02/intravenous-thiamine/

So it looks interesting because it appears to cause a change to the better. The question is whether there is good evidence for it and the mechanism

Material on PubMed is relatively sparse — just 170+ articles.

• “benfotiamine (prevents vascular damage in diabetes)” [2015]
  • this implies that it may improve oxygen delivery in the brain
• “Benfotiamine is a synthetic vitamin B1 (thiamine) derivate exerting potentially anti-inflammatory effects.Despite the encouraging results regarding benfotiamine potential to alleviate diabetic microangiopathy, neuropathy and other oxidative stress-induced pathological conditions, its activities and cellular mechanisms during microglial activation have yet to be elucidated… benfotiamine significantly decreased production of pro-inflammatory mediators such as inducible form of nitric oxide synthase (iNOS) and NO; cyclooxygenase-2 (COX-2), heat-shock protein 70 (Hsp70), tumor necrosis factor alpha α (TNF-α), interleukin-6 (IL-6), whereas it increased anti-inflammatory interleukin-10 (IL-10) production in LPS stimulated BV-2 microglia. Moreover, benfotiamine suppressed the phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and protein kinase B Akt/PKB… benfotiamine may have therapeutic potential for neurodegenerative diseases by inhibiting inflammatory mediators and enhancing anti-inflammatory factor production in activated microglia. ” [2015]
• “Benfotiamine, a derivative of thiamine, and pyridoxamine, a vitamer of vitamin B6, both have anti-AGE [ advanced glycation end-products] properties, making them valuable therapeutic adjuvants in the treatment of diabetic complications.” [2015]
  • “In erythrocytes, thiamine levels were 4- and 25-fold higher in the groups treated with thiamine and benfotiamine,.. we verified the high bioavailability especially of benfotiamine” [2013]
• “high potency thiamine[B1] analog benfotiamine..  [600mg/day] appears to reduce psychiatric distress and may facilitate recovery in severely affected males with a lifetime alcohol use disorder and should be considered for adjuvant therapy in alcohol rehabilitation.” [2015]
  • “benfotiamine (300 mg/day) supplementation over 24 months has no significant effects upon peripheral nerve function or soluble markers of inflammation in patients with type 1 diabetes” [2012]
• “With a simultaneous increase in energy expenditure, TD[Benfotiamine] caused an overall body weight loss. The results suggest that the status of thiamine levels in the body may affect food intake and body weight.”
• “The efficacy of traditional treatment combined with milgamma[benfotiamine] therapy in the patients with acute sensorineural impairment of hearing of allegedly viral etiology proved to be higher than that of conventional therapy alone” [2012]
• Benfotiamine counteracts smoking-induced vascular dysfunction in healthy smokers. [2012]
• Benfotiamine prevents increased β-amyloid production in HEK cells induced by high glucose [2012]
  • Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are crucially involved in Alzheimer’s disease as the main component of the amyloid plaques found in the brains of Alzheimer patients.

There are no studies specific on benfotiamine for Chronic Fatigue Syndrome. However there are two studies for thiamine.

• “These data provide preliminary evidence of reduced functional B vitamin status, particularly of pyridoxine, in CFS patients.” [1999]
• “The absence of blood thiamine deficiency and the efficacy of high-dose thiamine in our [CFS] patients suggest that fatigue is the manifestation of a thiamine deficiency, likely due to a dysfunction of the active transport of thiamine inside the cells, or due to structural enzymatic abnormalities. The administration of large quantities of thiamine increases the concentration in the blood to levels in which the passive transport restores the normal glucose metabolism in all cells and leads to a complete regression of fatigue.” [2013]

Bottom Line

• A supplementation of 600 mg/day of  benfotiamine is a recommended experiment for CFS patients, and other autoimmune diseases that are prone to mal-nutrition/
• A 30 day experiment has a cost of $10.00,  Swanson’s Benfotiamine (Fat-Soluble Vitamin B-1) 300 mg 60 Veg Caps

Readers of my last post expressed angst over trying to figure out what is safe to eat. First some more potential bad news:

• Studies indicate that Glyphosate is expelled from the body If it is applied in nature we find “The half-life for glyphosate at 25 °C in low-light was 47 days, extending to 267 days in the dark at 25 °C and 315 days in the dark at 31 °C, which is the longest persistence reported for this herbicide.” [2014] This means on a site where it was used, after 5 years (usually required for organic certification) it would be reduced to   0.01% to 3% of prior levels.
• “GlySH intoxication has a case fatality rate 3.2–29.3%.” [2014]
• The herbicide glyphosate causes behavioral changes and alterations in dopaminergic markers in male Sprague-Dawley rat. [2015]
• ” We present evidence from the biomedical research literature of a plausible link among glyphosate, nitrogen dysbiosis and ADHD.” [2015]
• “Among the suspected toxins surveyed, polybrominated diphenyl ethers, aluminum adjuvants, and the herbicide glyphosate have increasing trends that correlate positively to the rise in autism.” [2014]

In terms of good news,

• “The apparent elimination half life of glyphosate was 3.1 hours (95% CI 2.7 to 3.6 hours)..” [2010], so given low ingestion of more, your levels will drop. Note the key word “apparent”, this is in reference to circulating levels and if it has been stored in fat or other tissue, we do not know the clearance time.
  • If you look at the prior post on pigs and glyphosate, you would expect it to be zero (if they have not been sprayed with glyphosate immediately before slaughter) — that is not the case, hence we should assume storage in the body which can cause disruption.

The Good Food List for glyphosate reduction

Criteria: food must be 0.2 ppm or less according to EPA list. Here is the list.

The Dirty Ones

Over 1 ppm. This is based on EPA tolerance of over 1ppm. Some items that have been explicited tested (like Rye) has been omitted.