Apparently Parkinson's disease patients have a sub-clinical thiamine deficiency which is not bad enough to
cause beri beri or the Wernicke/Korsakoff syndrome. The following article entitled "The Beneficial Role of Thiamine in Parkinson’s Disease: Preliminary Report" states a deficiency is associated with PD.
"Lower central nervous system (CSF)-free thiamine levels were noted in PD patients compared with the controls [1]. In parkinsonism-dementia patients, thiamine-pyrophosphatase (TPP) activity was found to be significantly reduced in the frontal cortex [2]. In addition, Gold et al [3] reported that 70% and 33% of their PD patients had low plasma and red blood cell (RBC) thiamine levels, respectively."
In multiple articles (including the following wikipedia article) about thiamine-related diseases, there are several words
missing from every article: Parkinson's and parkinsonism. If this nutrient deficiency, which happens to POWs and alcoholics, were responsible for PD, they would have many case studies showing examples of parkinsonism induced by the absence of thiamine - but there are none. So thiamine deficiency is a contributory factor but not the cause of PD.
Beriberi: en.wikipedia.org/wiki/Beriberi
The nutritional deficiency of nicacin/tryptophan can cause parkinsonism on a large scale is a disease called Pellegra:
Parkinsonian features in a case of pellagra: a historical report.
ncbi.nlm.nih.gov/pubmed/240...
This raises the question as to how to best replenish thiamine levels in the body? The worst way, as has been established in alcoholics, is the oral route. The best, injections. Here is why. In an article entitled:
MECHANISMS OF VITAMIN DEFICIENCY IN CHRONIC ALCOHOL MISUSERS AND THE DEVELOPMENT OF THE WERNICKE-KORSAKOFF SYNDROME
Alcohol & Alcoholism Vol. 35, Suppl. 1, pp. 2-7, 2000
"Thiamine transport across the blood-brain barrier is by an active rate-limited process, which occurs at a maximum rate of 0.3 ug/h/g of brain tissue. This is equivalent to the level of brain thiamine turnover, suggesting that thiamine transport is only just sufficient to meet cerebral needs under normal circumstances. At higher blood concentrations thiamine is transported by passive diffusion, and therefore a high plasma:CNS concentration gradient, which is achieved by parenteral therapy, will ensure rapid correction of brain thiamine levels."
oup.silverchair-cdn.com/oup...
Parenteral = injection. Without a doubt this is the best way to replenish brain thiamine levels.
The second route to replenishing brain thiamine levels is by using a supplement called sulbutiamine.
Sulbuthiamine is a synthetic form of thiamine developed by the Japanese navy to eliminate the threat of beri
beri. Here is a reference and audio interview:
smartdrugsmarts.com/dr-step...
Use of sulbutiamine in the treatment of Parkinson's disease, schizophrenia, alcoholism, and dysthymia
"In Parkinson's patients, treated with sulbutiamine, an improvement in the cognitive, executive and mnesic
functions was observed, with diminution of the sensation of fatigue."
Sulbutiamine should not be used if someone has bipolar disorder:
Sulbutiamine, an ‘innocent’ over the counter drug, interferes with therapeutic outcome of bipolar disorder
tandfonline.com/doi/abs/10....
In the article above about Wernicke/Korsakoff Syndrome they note:
"Early symptoms of thiamine depletion include fatigue, weakness and emotional disturbance, which occur before other physical symptoms."
Sound familiar?
Aggravation of thiamine deficiency by magnesium depletion. A case report.
"A patient with Crohn's disease and long-standing diarrhea resulting in a combined thiamine and magnesium deficiency is presented. Despite massive doses of thiamine i.v., the symptoms of thiamine deficiency could not be suppressed until the magnesium deficiency was corrected as well. This case report emphasizes the dependence of thiamine on magnesium for an adequate function in the body."
ncbi.nlm.nih.gov/pubmed/405...
Like sulbutiamine, there is a synthetic form of magnesium which penetrates the central nervous system faster than other forms and it is called magnesium l threonate. MgThr was developed for Alzheimer's and is currently being tested on dementia patients:
Magnesium L-Threonate for the Enhancement of Learning and Memory in People With Dementia
clinicaltrials.gov/ct2/show...
MgThr is also considered a nootropic like sulbutiamine and I use MgThr every day. I think MgThr is a safer supplement and can be used at higher levels. Sulbutiamine should be taken only at what the bottle recommends. In the dementia study, MgThr is being used at 1,800 mg/day and considering the recommended dose of magnesium for an adult male is 420 mg that is an amazing amount of magnesium.
The open question is how will (or will) a combination of 2 nootropics affect the non-motor symptoms of PD. Certainly, the memory and learning will be enhanced but will sulbutiamine affect motor scores like injected thiamine?
Why You May Need Magnesium To Get The Most Out Of Thiamine
Excess Iron In The Brain Of PwP And The Role Of Thiamine, Melatonin And Hesperidin In Alleviating This Issue
Anti-thiamine factors
Thiamine and Dr Costantini, what we know and don't know
