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Terminal Lucidity
Explores the relationship between acetaldehyde toxicity and terminal lucidity
Date: 3/20/2013 3:26:05 PM ( 11 y ) ... viewed 11507 times Terminal lucidity is the unexpected return of mental clarity and memory shortly before death in patients suffering from severe psychiatric and neurologic disorders (brain abscesses, tumors, strokes, meningitis, dementia or Alzheimer's disease, schizophrenia, and affective disorders). Although this condition has been observed and reported for over 250 years in the medical literature, it is poorly understood. It has even been suggested that lucidity, memory and cognitive abilities may function by distinctly "different" processes during this time from "normal" brain activities impaired by the disease state [1].
Another possibility, however, is that the mechanisms contributing to the cognitive and neurological impairment are altered somehow by a shift in the biochemical status of the body shortly before death in such a way as to restore some normalcy to existing brain function. Anecdotal reports suggest that individuals suffering from Alzheimer's actually go into a transient remission of symptoms subsequent to fits of uncontrollable rage. The rage and potentially its biochemical consequences somehow reinstate lucidity for a time subsequent to the episodes. Does this behavior share a commonality with terminal lucidity?
Real or perceived threats associated with both fear and rage "fight or flight" reactions result in autonomic nervous system stimuli to the adrenals which release adrenaline (epinephrine), the "stress" hormone, to prepare the body for the impending crisis [2].
Biogenic amines are particularly vulnerable to reaction with yeast-released acetaldehyde via the spontaneous Pictet-Spengler condensation reaction which has already been studied in this series:
• See "Acetaldehyde + Serotonin" http://curezone.com/forums/fm.asp?i=1963129
• See "Acetaldehyde + Dopamine" http://curezone.com/forums/fm.asp?i=1956462
• See "Acetaldehyde + Histamine" http://curezone.com/forums/fm.asp?i=1963358
• See "Acetaldehyde + Monoamine Oxidase" http://curezone.com/forums/fm.asp?i=1972530
The catecholamine neurotransmitters, norepinephrine and epinephrine (adrenaline), are also susceptible to this type of chemical reaction [3] forming a tetrahydroisoquinoline.
The resulting product is stable because of the closed double-ring structure and the reaction irreversible with the implications that any acetaldehyde snared in this manner by epinephrine will no longer be available for interference with other body processes.
Epinephrine is already known to be depressed in individuals with dementia of the Alzheimer type [4] suggesting that it is the target of some aspect of the disease process. Furthermore, neurofibrillary tangles in alcoholics result when acetaldehyde binds to epsilon-amino groups of lysine and thiol groups of cysteine exposed on the surface of the tau proteins essential for the assembly and stabilization of cellular microtubule structures [5]. But these amyloid plaques are also found in patients with Alzheimer's disease. And, the cholinergic system responsible for mental clarity can be severely impaired by exposure to acetaldehyde [6]. Is acetaldehyde the link between these apparently unrelated manifestations of disease?
• See "Acetaldehyde + Acetylcholine" http://curezone.com/forums/fm.asp?i=1949530
Rage is often an indication that adequate supplies of magnesium aren't reaching the brain. Although aldehyde dehydrogenase isn't a magnesium-containing enzyme, per se, it does function better with magnesium in its proximity. This suggests that the body's innate aldehyde neutralization mechanisms may not only be overloaded but also commandeering magnesium near the blood-brain barrier and preventing it from reaching the required reactions.
The point here is that the sudden increase in epinephrine concentrations precipitated by the fear or rage stimulus to the adrenals provides additional, albeit transient, support to the innate aldehyde scavenging systems which may be saturated and overloaded by chronic exposure to yeast-released acetaldehyde. This reduction in acetaldehyde levels relieves the interference with other brain biochemistry mechanisms responsible for lucidity.
Yeast colonization near the nutrient-rich blood-brain barrier pathway could easily result in biochemical havoc in brain function. As a small lipid-soluble molecule, acetaldehyde is able to cross membranes by simple diffusion [7]. It is also capable of disrupting the tight junctions of the blood-brain barrier leading to degradation of this protective membrane [8]. Either or both of these techniques would eventually provide it with free access to react with whatever provides an attractive locus for its polarized aldehyde moiety.
• See "Acetaldehyde + Pseudo-Heavy Metal" http://curezone.com/forums/fm.asp?i=1953097
The inference gleaned here from terminal lucidity is that acetaldehyde scavenging and yeast abatement strategies aimed at reducing the concentrations of this substance below toxic levels, instituted early-on, may be effective in not only avoiding potentially fatal consequences, but also of providing relief to those suffering from these chronic psychiatric and neurologic maladies.
[1] Nahm, M et al., "Terminal lucidity: a review and a case collection.", Arch Gerontol Geriatr. 2012 Jul-Aug;55(1):138-42. doi: 10.1016/j.archger.2011.06.031. Epub 2011 Jul 20.
http://www.ncbi.nlm.nih.gov/pubmed/21764150
[2] Funkenstein DH,"The physiology of fear and anger" in "Psychopathology: A Source Book", Reed CF, ed., 1958.
http://books.google.ca/books?hl=en&lr=&id=6tCKBatwpyUC&oi=fnd&pg=PA223
[3] Bates HA, "Pictet-Spengler reactions of epinephrine with formaldehyde and acetaldehyde", J. Org. Chem., 1981, 46 (24), pp 4931–4935.
http://pubs.acs.org/doi/abs/10.1021/jo00337a022
[4] Umegaki H et al., "Low plasma epinephrine in elderly female subjects of dementia of Alzheimer type.", Brain Res. 2000 Mar 6;858(1):67-70.
http://www.ncbi.nlm.nih.gov/pubmed/10700598
[5] Luo J et al., "Effect of Acetaldehyde On Aggregation Of Neuronal Tau", Protein and Peptide Letters, Vol. 6 No. 2, pp. 105-110, 1999.
http://books.google.ca/books?hl=en&lr=&id=WJaE7cDq1HwC&oi=fnd&pg=PA105
[6] Jamal M et al., "Changes in cholinergic function in the frontal cortex and hippocampus of rat exposed to ethanol and acetaldehyde.", Neuroscience. 2007 Jan 5;144(1):232-8.
http://www.ncbi.nlm.nih.gov/pubmed/17045751
[7] Zorzano A et al., "Decreased in vivo rate of ethanol metabolism in the suckling rat.", Alcohol Clin Exp Res. 1989 Aug;13(4):527-32.
http://www.ncbi.nlm.nih.gov/pubmed/2679210
[8] Atkinson KJ, Rao RK, "Role of protein tyrosine phosphorylation in acetaldehyde-induced disruption of epithelial tight junctions", AJP - GI June 1, 2001 vol. 280 no. 6 G1280-G1288.
http://www.ncbi.nlm.nih.gov/pubmed/11352822
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