Thiamine Deficiency and Delirium. [Thiamine magnesium PD]
The absorption of thiamine occurs in the duodenum by an active process and is converted to its active form thiamine pyrophosphate.7,8 This conversion process of thiamine to its active form requires magnesium as a cofactor, and hence hypomagnesaemia can mimic thiamine deficiency.6,9,10
An actual relevant citation, but you missed the critical issues. Nevertheless, Good job.
The take away message is simple. Some PD patients need to realize their hallucinations and delirium episodes (which are common as PD advances) are very frequently related to deficiencies in thiamine and its co-factor magnesium. Most importantly, your body cannot make thiamine, nor can you store it for much more than 2 weeks, so you need to either eat foods that contain it or use a supplement almost daily.
"Neuronal death often occurs in certain neuronal populations that have high metabolic requirements and high thiamine turnover." Sounds familiar.
I have wondered before when a co-factor is required, the implication for dosing the co-factor. Specifically here, with high dose thiamine, the implications for magnesium.
If you or anyone has any thoughts on the matter...
Nothing specific exists about the ratio of B-1 to Magnesium in the recent literature. However a 2019 study on AWS dealt with the discrepancy between the two in terms of 1 year mortality.
"The prevalence of low circulating thiamine concentrations were rare and it was regularly prescribed in patients with AWS. In contrast, low serum magnesium concentrations were common and not prescribed. Low serum magnesium was associated with more severe AWS and increased 1-year mortality."
My personal take is that B-1 really isn't the critical issue (if you believe the theory that HDT is an adjuvent therapy of value in terms of L-Dopa ingestion). Magnesium is actually, in some respects, more important especially if one's thiamine level is normal and one's magnesium level is low, which would probably be the norm, or soon after going on the HDT protocol.
The wild cards here are 1) chronic alcohol use and 2) type 2 diabetes plus hypertension.
The other issue is that the potassium to magnesium to calcium ratio should hover around the ideal ratio of 5:2:1.
Something to think about...AWS...is this discrepancy with AWS possibly related to DAs with pwp types and their withdrawal symptoms/problems? Interesting but heresy to the anti DA types.
However, let us contemplate duodenum and/or jejunum:
"Thiamine is a water-soluble vitamin that is absorbed in the jejunum by 2 processes. When the thiamine level in the small intestines is low, an active transport portal is responsible for absorption. When the thiamine concentration is high, a passive mucosal process takes place. Up to 5 mg of thiamine is absorbed through the small intestines. The small intestine is where phosphorylation of thiamine takes place. [1]"
Beriberi (Thiamine Deficiency): Practice Essentials, Pathophysiology, Etiology.
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