I am taking orally Life Extension brand Mega Benfotiamine (B1) 250mg 2x a day plus R Alpha Lipoic Acid 100mg 2x a day and B12 300 mcg .
With these Vitamins and my DBS, I feel "normal". I am trying to reverse or slow down the natural degeneration of PDby regenerating my nervous system. My family has noticed a remarkable improvement.
There is a product out there that combines all called nerve renew.

I can't help but notice the date on this article, and while it's great that this work was done, am frustrated at the lack of progress on pursuing it further. Makes me crazy

the profit engines keep turning.....meanwhile the rats of Nimh are quietly working.....

saying yes to thiamine
 

quick update - I got an immediate positive response to 1st dose allithiamine 50mg though lots of symptoms are fluctuating with a general overall feeling of improvement. I think dose is key. So nice to have the support! :) I will add B2 next to see if I can optimize and finesse this edge a little further.

Kind Regards
MD

Thiamine Deficiency and Neurodegeneration 2017
 

Are there others here that are using Thiamine and do they see any positive results?

This paper states that Thiamine doses of several grams were used in tests.



Thiamine Deficiency and Neurodegeneration: The Interplay among Oxidative Stress, Endoplasmic Reticulum Stress and Autophagy


PD is the second most common form of neurodegeneration in the elderly population, characterized by resting tremor, rigidity, slowness of movement, and postural imbalance [63]. It affects more than 1% of individuals older than 55 years of age and more than 3% of those older than 75 years of age [64]. The loss of dopaminergic neurons in the substantia nigra is a major pathophysiological feature of patients with PD [65]. Several lines of evidence have shown that thiamine or thiamine-dependent processes may be involved in the pathogenesis of PD. For example, lower free thiamine levels in the cerebrospinal fluid were found in PD patients in comparison to normal individuals, while levels of thiamine-derivatives, such as thiamine-diphosphate and thiamine-monophosphate, did not differ significantly [66]. Additionally, the immunoreactivity of KGDHC, one of the most important thiamine-dependent enzymes, was decreased in the substantia nigra of patients with PD, and the reduction seemed correlated with the severity of degeneration [67, 68]. In some studies, thiamine supplementation seemed to improve the outcomes for PD patients. For example, administration of parenteral high-dose thiamine was effective in reversing motor and non-motor symptoms in PD patients [28, 30]. These findings suggest that TD may be involved in the pathophysiology of PD.

Respect
 

I am nothing short of astonished at the depth and rapidity this venue of treatment holds agency.

Todays Facebook post to thiamine group: fyi......

"My initial exposure to learning about B1 led me to try allithiamine - partially because the recommended dose was lower and because it came with cofactors that I hypothesized would address absorption across the blood brain barrier. Also, it was an intuitive call. What I have learned since is that alliithiamine is fat soluble -does that mean it might stay in my system longer than its' water soluble cousin (B1HCL) -or would that be dependent on the individual GI ecosystem? My very first dose I felt my breath ease and drop deeper into my belly! It was wonderful and for the first couple of weeks I felt improvement - more energy, longer sleep, some very light indications of peristalsis awakening deep in my bowel. Another thing I noticed was my craving for sweet lessened. These were so very welcome as have been coping with parkinsons sx for over 25 years fortunately with slow progression (at times). The following weeks I noticed waking in the mornings feeling restless - that would later turn to anxiety and chest pain with a hint of depression-but I also found that my habit for eating sweets and thoughts of worry would make this worse. So, I backed off the allithiamine though I feel even though what started as a feeling of restlessness became an opportunity for me to experience how choices on my thinking and eating and activity habits could feed my problems directlly .I am coonsiidering going to small dose of B1hcl though hesittate because I'm thinking just going lower in dose of the allithiamine may ease the roller coaster ride a bit. Its a bit scary when the ease of breath becomes so easy that not inhaling automatically can cause issues. I respect this stuff. I think I am still feeling benefits of a dose I took over a week ago and what started as restlessness has backed off so as long as I still feel benefits I hesitate to repeat the dose! Am wondering if a barometer for when to repeat dose is tendency to fall......???"


Something this experience has made apparent to me-something I haven't seen discussed even in this forum is respiratory function is a Parkinsons sx!
Makes sense as common cause of death from PD is consumption in the lungs...Our autonomic nervous system must employ some very clever and subtle adaptive strategies that hide this from our general awareness.

Excerpt from a paper written by K.M. Torsney and D Forsyth called "Respiratory dysfunction in Parkinsons Disease" :

"shortness of breath in Pd can be very distressing for patients
and clinicians alike. extensive investigations are carried
out, often repeatedly during recurrent admissions, looking
for infection, pulmonary emboli, heart failure and anxiety.
although these are possible in Pd patients and should be
excluded, clinicians must remember that Pd itself and its
medications can lead to shortness of breath through various
mechanisms. effi cient ventilation depends on several factors
including adequate airways, suffi cient respiratory muscular
function and a chemoreceptor drive to breathing.
Pd can affect each of these to a varying degree. several
patterns of respiratory dysfunction have been described in Pd,
including: restrictive changes secondary to chest wall rigidity
and reduction in lung volume secondary to kyphoscoliosis,
upper airway obstruction, abnormal ventilatory control,
diaphragmatic dyskinesias and pleuropulmonary complications
of medications. in addition, although rare, shortness of breath
is an important non-motor wearing off symptom.
There is controversy as to whether levodopa improves or
worsens respiratory function. This review will not cover in
detail the respiratory complications of Pd but rather look at
the spectrum of respiratory dysfunction in Pd as well as the
effects of levodopa on pulmonary function tests."


Kind regards,
-MD

International attention
 

Much to learn from worldwide research.
Vitamin B1 and Parkinson : The final results of the research carried out by WeAreParky – WeAreParky

I was particularly interested in the part where there was caution for those with heart conditions. I'm curious if they found any correlation to arrhythmia. Also , of interest was the finding that combining oral dose of B1 with magnesium proved more effective than B1 alone.

and this: "Should one decide to start integration of Vitamin B1, we suggest to do so at a time when the symptoms are stable and by simply not altering the medication regime (levodopa), this would allows us to have a clearer picture should new symptoms arise" ...when things go south ....could it also be that treatment of those 20-25 years into pd symptoms may be susceptible to serious complications from this treatment? "To maintain the level B1 near the maximum levels for prolonged periods can cause an acceleration of the biorhythms"


Kind Regards,
MD