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