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…..
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)” 
- 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. ” 
- “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.” 
- “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” 
- “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.” 
- “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” 
- “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” 
- Benfotiamine counteracts smoking-induced vascular dysfunction in healthy smokers. 
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.” 
- “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.”