Thankyou for this session and thankyou again for asking my questions. I regret that my phone signal was poor.
This is FASCINATING, especially given the fact that thiamine is co-released from neurons with acetylcholine. Thiamine appears to be essential for the production, release and action of acetylcholine at almost every level, and impaired cholinergic neurons seem to be a defining feature of thiamine deficiency. Enhancing cholinergic activity in the brain (via non-coenzyme effects) is maybe indeed be one of the primary mechanisms it works (on a 3D mechanistic level, at least)
Laura has discussed acetylcholine in the past, and the C's mentioned in a previous session that acetylcholine was involved in destruction of nanobots, through working on the level of information:
Well, we just published a paper on this exact topic (thiamine - acetylcholine relationship) last month, but it was focused on how this impacts the gut:
From another paper:
Something else that popped into my mind last week that might also be related, was a previous answer the C's provided about pork.
Lo and behold, pork has the highest thiamine (and thiamine triphosphate) content of all animals used for food, by a long-shot. Weight for weight, pork contains anywhere between 5 and 20 times higher concentrations of thiamine. It is the single best animal source of this vitamin.
So it had me thinking... if thiamine triphosphate is "essential for higher function transfer of information", is it a coincidence that pork is the highest source of ThTP?
Added later for clarity: As in, does the pig accumulate/retain higher thiamine level in its tissue partly as a means of interfacing/accessing "high function transfer of information", which humans then consume? Not sure.
As per Gilbert Ling's model, this would make a lot of sense and could help to explain real-life observations
There are a portion of people who have consistent, and frankly miraculous, responses to high dose thiamine. However, instead of being deficient in the traditional sense, many of these people are what we call "thiamine-dependent". They have debilitating and/or progressive degenerative diseases such as Alzheimer's, Parkinson's, or sometimes just chronic fatigue syndrome or fibromyalgia. They are reliant on continued high-doses for remission, although their symptoms relapse after discontinuation. The nutrient serves as a permanent drug needed in supraphysiological doses, rather than as a targeted, temporary intervention to resolve a nutritional deficiency. To complicate matters, the benefits have been shown to occur independent of thiamine's metabolic role as a coenzyme.
Furthermore, there are also non-responders, and not one has knows or has established the exact distribution or % of responders vs non-responders.
Ling's model is centered on ATP as the principle regulator of protein conformation and structure of the cell, and now based on the C's answer, "more complex" functions probably relating to information. If TTP could substitute ATP, as the C's say it can in "genetically viable individuals", this might explain two seperate observations:
1. Why some people respond, and why some people do not = based on "genetic viability"
2. Why some responders require extremely high doses on a continued basis = because of TTP playing a role as a substitute for ATP
This is FASCINATING, especially given the fact that thiamine is co-released from neurons with acetylcholine. Thiamine appears to be essential for the production, release and action of acetylcholine at almost every level, and impaired cholinergic neurons seem to be a defining feature of thiamine deficiency. Enhancing cholinergic activity in the brain (via non-coenzyme effects) is maybe indeed be one of the primary mechanisms it works (on a 3D mechanistic level, at least)
Laura has discussed acetylcholine in the past, and the C's mentioned in a previous session that acetylcholine was involved in destruction of nanobots, through working on the level of information:
Well, we just published a paper on this exact topic (thiamine - acetylcholine relationship) last month, but it was focused on how this impacts the gut:
Thiamine triphosphate is a non-coenzyme derivative of thiamine, probably involved in acetylcholine neurotransmission (141–143). An intimate relationship between thiamine and cholinergic neurotransmission relies on both the coenzyme and non-coenzyme actions of thiamine and its derivatives. In cholinergic cells, the ThDP-dependent pyruvate dehydrogenase complex synthesizes the ACh precursor acetyl-CoA (Figure 1) (219, 220). Distribution of this acetyl-CoA between the oxidation in the TCA cycle and participation in ACh synthesis is regulated through limitation of the TCA cycle rate by the ThDP-dependent OGDH, and the non-coenzyme action of thiamine and derivatives on the other enzymes involved (221). TD-perturbed function of ThDP-dependent dehydrogenases of TCA cycle (Figure 1) is a well-known contributor to impaired synthesis of ACh (219). The ensuing mitochondrial dysfunction of cholinergic cells increases their susceptibility to different insults (222–224).
Independent of metabolic action as the coenzyme ThDP, thiamine is essential for axonal membrane excitability, playing a significant role in development of the action potential (231). This non-coenzyme action of thiamine in neuronal signaling is further supported by the identified molecular targets of thiamine and its non-coenzyme derivative ThTP. ThTP-dependent phosphorylation of rapsyn regulates ACh neurotransmission, as rapsyn is a scaffolding protein of the post-synaptic membrane of neuromuscular junctions, specifically associated with nicotinic ACh receptors (232). Hydrolysis of ThTP by synaptic membrane-bound protein(s) different from the well-characterized soluble ThTPase of cytosol, is supposed to be involved with synaptic function (233, 234). Thiamine binds to a bitter taste receptor, which modifies ileum contraction (235) and provokes ACh-induced contraction of jejunum (236). At a high concentration (0.05 mM), thiamine also binds to an isolated nicotinic ACh receptor (237). The non-coenzyme action of thiamine in neurotransmission is further supported by the action of the thiamine analog oxythiamine, whose diphosphorylated derivative (oxyThDP), formed by TPK in vivo, is an antagonist of the coenzyme action of thiamine. As a result, oxyThDP inhibits ThDP-dependent dehydrogenases, whose function is required for ACh synthesis, particularly pyruvate dehydrogenase complex generating ACh precursor acetyl-CoA (Figure 1). However, in superfused rat brain slices, oxythiamin enhances the release of synaptic acetylcholine, thus mimicking the non-coenzyme action of thiamine in facilitating ACh neurotransmission (238).
Frontiers | Thiamine, gastrointestinal beriberi and acetylcholine signaling
Research has highlighted numerous detrimental consequences of thiamine deficiency on digestive function. These range from impaired gastric and intestinal mot...www.frontiersin.org
From another paper:
Something else that popped into my mind last week that might also be related, was a previous answer the C's provided about pork.
Lo and behold, pork has the highest thiamine (and thiamine triphosphate) content of all animals used for food, by a long-shot. Weight for weight, pork contains anywhere between 5 and 20 times higher concentrations of thiamine. It is the single best animal source of this vitamin.
So it had me thinking... if thiamine triphosphate is "essential for higher function transfer of information", is it a coincidence that pork is the highest source of ThTP?
Added later for clarity: As in, does the pig accumulate/retain higher thiamine level in its tissue partly as a means of interfacing/accessing "high function transfer of information", which humans then consume? Not sure.
As per Gilbert Ling's model, this would make a lot of sense and could help to explain real-life observations
There are a portion of people who have consistent, and frankly miraculous, responses to high dose thiamine. However, instead of being deficient in the traditional sense, many of these people are what we call "thiamine-dependent". They have debilitating and/or progressive degenerative diseases such as Alzheimer's, Parkinson's, or sometimes just chronic fatigue syndrome or fibromyalgia. They are reliant on continued high-doses for remission, although their symptoms relapse after discontinuation. The nutrient serves as a permanent drug needed in supraphysiological doses, rather than as a targeted, temporary intervention to resolve a nutritional deficiency. To complicate matters, the benefits have been shown to occur independent of thiamine's metabolic role as a coenzyme.
Furthermore, there are also non-responders, and not one has knows or has established the exact distribution or % of responders vs non-responders.
Ling's model is centered on ATP as the principle regulator of protein conformation and structure of the cell, and now based on the C's answer, "more complex" functions probably relating to information. If TTP could substitute ATP, as the C's say it can in "genetically viable individuals", this might explain two seperate observations:
1. Why some people respond, and why some people do not = based on "genetic viability"
2. Why some responders require extremely high doses on a continued basis = because of TTP playing a role as a substitute for ATP
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and will order Mind+ soon. Ready to make our brains 4D!
