Thiamine is needed for at least 3 enzymes that produce energy from carbohydrates. It usually becomes effective for proteins after it gets 2 phosphate groups added to it. Alcohol stops thiamine absorption from stomach and also slows its activation by slower addition of phosphate groups (that last reaction is slowed because it needs magnesium and ethanol also lowers magnesium levels). While all cells seem to need it, heart and neurons are most sensitive. Serious lack of B1 can cause coma leading to death or deadly heart failure. It is also needed to produce GABA, acetylcholine and building materials to proteins, myelin and DNA plus many other substances. Usually thiamine levels become low if there are problems with absorbing it from intestines due to alcohol and drugs or due to health problems like chronic diarrhea, vomiting, stomach surgery or excessive urination with diuretics. Thiamine requirements are about 0,33 mg for each 1000 kcal of nutrients eaten. Meat is one main source of thiamine like also whole grains and brown rice. White rice on other hand cause lack of thiamine which is often called beriberi. Wernicke-Korsakoff syndrome is common name for this deficiency if caused by chronic alcoholism.
Common symptoms of thiamine deficiency: weakness, apathy, faster heart rate, weaker reflexes, unwanted eye movements, trouble breathing, possibly fluid in lungs related to heart problems, edema of lower legs and droopy eyelids. In case of Korsakoff syndrome (more extreme deficiency) it can cause problems with remembering past, learning new memories and may lead to memories of events that didn't happen (confabulation). Alcoholic delirium and brain damage are likely to come from thiamine deficiency. These last memory problems are somewhat common if brain is very low on acetylcholine.
Un-cited personal part: i recently noticed that almost all the unwanted side effects my sedative (pregabalin) causes overlapped with thiamine deficiency. I've experienced almost all previously mentioned temporary symptoms with that except serious memory problems. Pregabalin blocks calcium channels and it has mostly weak effect on all neurotransmitters (each is released after calcium triggers release). During minor withdrawal phase ~12 after dosing i often notice weird weakness and changes in posture with very foggy thinking with runny nose. Maybe it was because GABA and acetylcholine were being released too fast after calcium channel normalized and ran low so thiamine was diverted to producing those neurotransmitters and after awhile also run low causing deficiency symptoms. While inside cells neurotransmitters should preserve well but after releasing they get broken up often in split second. For example acetylcholine activates muscles controlled by willpower and this effect on muscles disappears fast because it gets broken up fast outside cells by acetylcholinesterase (each enzyme molecule breaking about 25 000 acetylcholine molecules per second). Acetylcholine is involved in nose mucus gland activation so anything causing that could cause problems with thiamine reserves. After noticing that it could explain why these outwardly visible symptoms happened i almost quit pregabalin overnight after taking it ~300 mg daily for over 3 years and got rid of these symptoms (surprising lack of withdrawals after 24 hour pause). I suspect most antipsychotics and sedatives could cause this effect on small scale but ethanol is still the most obvious cause for thiamine deficiency with worst magnitude that i know about. One nonacademic source listed diuretics, nicotine (binding with nicotinic acetylcholine receptors) and barbiturates (GABA receptor blockers) as substances that can adversely affect thiamine levels.
No comments:
Post a Comment