How to Take Sulbutiamine
Recommended dosage, active amounts, other details
Human studies using sulbutiamine supplementation have used 400mg daily. It is not clear if this is near the optimal dosage, and an ideal dosing regimen (with or without meals and how many divided doses a day) is not currently known.
Human Effect Matrix
The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects sulbutiamine has on your body, and how strong these effects are.
|Grade||Level of Evidence [show legend]|
|Robust research conducted with repeated double-blind clinical trials|
|Multiple studies where at least two are double-blind and placebo controlled|
|Single double-blind study or multiple cohort studies|
|Uncontrolled or observational studies only|
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
|Blood Glucose||-||- See study|
|HbA1c||-||- See study|
|Symptoms of Diabetic Neuropathy||-||- See study|
Scientific Research on Sulbutiamine
Click on any below to expand the corresponding section. Click on to collapse it.
Sulbutiamine is a molecule which is two Thiamine (B1) molecules bound together, similar to how Pyritinol is two Pyridoxine (B6) molecules bound together. Sulbutiamine is known as isobutyryl thiamine disulfide and sometimes referred to by its Brand Names of Ereon or Arcalion; it is most commonly used for Asthenia, or weakness (part neurological and part myopathic) as well as treatment of somatic and psychic inhibition. It is said to not possess psychostimulant properties, although it is designed to act centrally (in the brain).
Sulbutiamine is synthesized from Thiamine, where after opening of the thiazole ring of Thiamine and dimerisation to a disulfide compound it is then esterified.
Due to the lipophilicity (fat-solubility) of Sulbutiamine, transport into the brain from systemic circulation is greater relative to Thiamine. After an injection of Sulbutiamine (16mg/kg) and Thiamine (15.4mg/kg) were both able to acutely increase plasma thiamine levels without influencing serum Thiamine Diphosphate (demonstrating the efficacy of Sulbutiamine as a vitamin delivery form, able to biotransform into Thiamine in vivo). A chronic study of injecting sulbutiamine (52mg/kg) and thiamine (50mg/kg) daily for 2 weeks in rats noted that despite these similar doses that sulbutiamine was able to increase total circulating thiamine, Thiamine diphosphate, and Thiamine Monophosphate levels 2.41 times higher than that of Thiamin itself. In other measured organs (hippocampus, medulla, cerebellum, cortex, and kidney) levels of Thiamine Triphophate were only increased with sulbutiamine, and sulbutiamine increased total thiamine compounds higher than Thiamine in all organs except the hippocampus.
Sulbutiamine may protect neuronal cells (in the hippocampus) from oxygen/glucose deprivation according to one study. This study used a staining protocol to identify dead cells from glucose/oxygen deprivation, and the 6.1-fold increase seen in control was attenuated to a 4.1-fold increase when Sulbutiamine was incubated at 50uM. The disruption of synaptic transmission that occurs under these conditions of nutrient deprivation was preserved with sulbutiamine to a degree, measuring preservation at 25.1+/-2.21%, 47.3+/-3.11% and 66.3+/-11.0% for the concentrations of 1, 10, and 50uM when control was standardized to 100% and the group without Sulbutiamine recorded 12.8+/-9.8%.
A 6 week trial in humans with type II diabetes and diabetic neuropathy using Sulbutiamine at 400mg daily noted that on the signs and symptoms scores (constricting sensation, paraesthesia, pain and weakness for symptoms; etc.) there was an improvement when compared against baseline but no improvement against placebo (and thus it was deemed no overall improvement). Improvement was noted in electrophysical measures, including nerve conduction velocity and compound motor action potential.
Positive glutaminergic and dopaminergic transmission has been noted in anterior corticol regions, specifically the prefrontal and cingular cortices which organize decisions and strategies. Daily injections of 12.5mg/kg sulbutiamine for 2 weeks prior to sacrifice noted decreases in kainate receptors in tested areas as well as decreased dopamine levels, despite no changes in dopamine receptor content.
No variations in dopaminergic or glutaminergic receptors were noted in the nuclear accumbens, and in a model of glucose/oxygen deprivation, Sulbutiamine at 1, 5, and 50uM failed to modify excitability of neurons in the hippocampus.
In an animal model where Sulbutiamine was fed at 300mg/kg for 10 days, the rate of sodium-dependent choline uptake into the hippocampus appeared to be increased approximately 10.1% when compared to gum acacia control.
In a model of BALB/c mice 14-16 weeks of age, 10 days of 300mg/kg sulbutiamine by oral gavage with 5% gum acacia appeared to improve memory (assessed by operant task); this study noted that there were no differences between groups in acquisition but there were significant differences in retention which resulted in increased performance.
Injections of 12.5 and 25mg/kg Sulbutiamine daily for 9 weeks failed to modify performance in a DNMTS task (operant conditioning maze) and at times 12.5mg sulbutiamine was associated with a greater amount of encoding errors. When dizocilpine (NMDA antagonist that induces amnesia) was administered during the DNMTS task, sulbutiamine was able to negate the amnesiac effects of it on the mice and preserve performance.
Sulbutiamine has been implicated in increasing object-recognition memory in mice at both 12.5 and 25mg/kg injections over 9 weeks.
One study has been conducted on chronic postinfectious fatigue (CPIF) with sulbutiamine at either 400 or 600mg daily for 28 days noted that both groups had significantly less fatigue than placebo, but that for the most part there was no significant difference between groups with the 600mg group inconsistently performing better at times. A similar study using a large (uncontrolled, unblinded) sample of persons seeing their doctors about infection who reported at least one symptom of fatigue given 400mg Sulbutiamine at breakfast daily for 15 days alongside their anti-infective treatment noted complete resolution of self-reported asthenic symptoms in 51.7% of the study population.
Improvement has also been noted regarding fatigue in 91.37% of persons tested (n=60) with Multiple Sclerosis, with 74.13% of the sample reporting the improvement as 'substantial' (analysis was done via subjective improvement) with no reported exacerbation in fatigue state.
A case study currently exists where a patient with bipolar disorder became addicted to sulbutiamine. The subject was using high dose antipsychotics (olanzapine and haloperidol at 20mg, the benzodiazepines diazepam and temazepam at 40mg and 10mg, 10mg biperiden, unspecified doses of lithium and carbamazepine) and reported that his large doses (above 600mg but otherwise unspecified) made him feel stronger and warmer.
One study in primeapes using a large dose of sulbutiamine (300mg/kg daily for 10 days) noted that Sulbutiamine was able to influence the circadian rhythm (increasing wakefulness and reducing phase 2 sleep while increasing phase 1 and not affecting REM). These effects persisted after 2-5 days of cessasion of sulbutiamine treatment.
An intervention over 6 weeks in type II diabetics using 400mg sulbutiamine failed to find a decrease in blood glucose or HbA1c associated with treatment.
Due to the interactions of prooxidation and excitotoxicity in glaucoma as well as Thaimine being lower in glaucoma patients with a case study showing Thiamine injections increase visual acuity, Sulbutiamine has been investigated for its interactions with retinal cells. An in vitro study using RGC-5 (Ganglion-like) cells noted that Sulbutiamine was able to attenuate cell death when cells were deprived of serum, and 10uM Sulbutiamine was as effective as 10uM Trolox (anti-oxidant standard) while attenuation was seen significantly at 1uM; these protective effects were associated with a sequestering the increase in superoxide and peroxide radicals, with no influence on hydroxyl radicals, and a relative increase in glutathione.
At least one study has noted benefits to psychogenic erectile dysfunction that can be treated with Sulbutiamine, increasing performance as assessed by the International Index of Erectile Function (IIEF) from 17.5 to 24.8 on average.
- Trovero F, et al. Evidence for a modulatory effect of sulbutiamine on glutamatergic and dopaminergic cortical transmissions in the rat brain. Neurosci Lett. (2000)
- Determination of sulbutiamine and its disulfide derivatives in human plasma by HPLC using on-line post-column reactors and fluorimetric detection.
- Bettendorff L, et al. Injection of sulbutiamine induces an increase in thiamine triphosphate in rat tissues. Biochem Pharmacol. (1990)
- Kwag J, Majid AS, Kang KD. Evidence for neuroprotective effect of sulbutiamine against oxygen-glucose deprivation in rat hippocampal CA1 pyramidal neurons. Biol Pharm Bull. (2011)
- Tanabe M, Nitta A, Ono H. Neuroprotection via strychnine-sensitive glycine receptors during post-ischemic recovery of excitatory synaptic transmission in the hippocampus. J Pharmacol Sci. (2010)
- Kiew KK, et al. Effects of sulbutiamine on diabetic polyneuropathy: an open randomised controlled study in type 2 diabetics. Malays J Med Sci. (2002)
- Micheau J, et al. Chronic administration of sulbutiamine improves long term memory formation in mice: possible cholinergic mediation. Pharmacol Biochem Behav. (1985)
- Bizot JC, et al. Chronic treatment with sulbutiamine improves memory in an object recognition task and reduces some amnesic effects of dizocilpine in a spatial delayed-non-match-to-sample task. Prog Neuropsychopharmacol Biol Psychiatry. (2005)
- Tiev KP, Cabane J, Imbert JC. Treatment of chronic postinfectious fatigue: randomized double-blind study of two doses of sulbutiamine (400-600 mg/day) versus placebo. Rev Med Interne. (1999)
- Shah SN; Sulbutiamine Study Group. Adjuvant role of vitamin B analogue (sulbutiamine) with anti-infective treatment in infection associated asthenia. J Assoc Physicians India. (2003)
- Sulbutiamine in the treatment of chronic fatigue in multiple sclerosis.
- Douzenis A, Michopoulos I, Lykouras L. Sulbutiamine, an 'innocent' over the counter drug, interferes with therapeutic outcome of bipolar disorder. World J Biol Psychiatry. (2006)
- Balzamo E, Vuillon-Cacciuttolo G. Facilitation of a state of wakefulness by semi-chronic treatment with sulbutiamin (Arcalion) in Macaca mulatta. Rev Electroencephalogr Neurophysiol Clin. (1982)
- Asregadoo ER. Blood levels of thiamine and ascorbic acid in chronic open-angle glaucoma. Ann Ophthalmol. (1979)
- Sedel F, et al. Thiamine responsive pyruvate dehydrogenase deficiency in an adult with peripheral neuropathy and optic neuropathy. J Neurol Neurosurg Psychiatry. (2008)
- Kang KD, et al. Sulbutiamine counteracts trophic factor deprivation induced apoptotic cell death in transformed retinal ganglion cells. Neurochem Res. (2010)
- Dmitriev DG, Gamidov SI, Permiakova OV. Clinical efficacy of the drug enerion in the treatment of patients with psychogenic (functional) erectile dysfunction. Urologiia. (2005)