I'm sorry
BJ, but I'm not quite sure where you would like to me to attempt to comment. I have no memory stores relating to Levi-Strauss or Eliade. To date they have been outside of my fields of thinking. It may be to my loss, but no one has heretofore ever related any of their thinking to me.
You have mentioned
" ... the psychological effect and the neuropsychological happenings in an empirical sense - ie what the brain chemistry can correlate to; if anything?"I have feeling that you are alluding to something different from the well-known effects of psychedelic chemicals on the interpretations of sensory inputs, and of the effects of legitimate pharma-psychotropic-drugs on mood states such as depression and anxiety.
There's a massive amount of literature on these subjects. The effects are all biochemical.
Maybe you are looking along the lines of things like Kimberly Horse Disease, wherein an apparently 'normal' horse eats a particular plant (This is off the top of my head and not researched for the post), and then abnormally begins to walk like a zombie in a straight line and is found dead at the foot of a tree. The tree has obviously obstructed its progression and it has kept pressing into it till has dropped dead.
In line with the above, I once tried a new 'pre-medication' for a horse. I was always looking for such in the literature. For decades I'd been trying new 'tranquillisers', but all turned out to be unpredictable in their effects. I had to castrate two young horses. An article appeared in the Australian Veterinary Journal suggesting that thiambutane ("Themalon") before Thiopentobarbitone was useful. I was familiar with this drug because I'd used it extensively in dogs with success. After I'd injected the first colt, it began to ambulate like a horse with Kimberley horse disease. It was compulsive and incessant. The best we could do was to keep the animal walking in a circle while controlling it by its halter. We were hoping it would pause so that we could inject it with the pentothal: it was very fatiguing. In the finish I injected the pentothal into the jugular vein while it was still pressing on, and did the castration while it was down. I regarded this response as an idiosynchrasy and tried it on the second colt with exactly the same result. I went back home, reviewed the article, only to find small print stating that some horses could develop hyperkinesis from the Themalon.
So an alkaloid in a plant and a pharma-product could biochemically alter the mind set and locomotory behaviour of an animal.
I'm sure that the literature could provide dozens of examples of this sort of chemical modification of behaviour.
Take vitamin B1 deficiency. Acute deficiency results in ataxia, loss of consciousness, and convulsions in sheep and cattle and even humans. At the stage of a biochemical lesion, the condition can be miraculously reversed in sheep with 4 mL of 10% thiamine solution into the jugular vein. I published a case history in 1967. Left to die, such animals show polioencephalomalacia or cerebrocortical necrosis lesions.
I'm still not sure whether this is the sort of biochemical interactions you are seeking.
But on the question of vitamin K and brain function --
"Vitamin K doesn't seem to have much direct impact upon the brain right? I guess you'll point out where my thought is wrong..", there is some indirect and direct literature available.
Firstly, I have to emphasise that vitamin K has been amply shown to be a REGULATOR of blood clotting processes (It is a cofactor in the manufacture of two anticlotting agents - proteins C & S). It has also been amply shown to be a REGULATOR of whether calcium is deposited in bones or soft tissue. What is not well known is that it also appears to be an essential co-factor in vascular tissue endothelial integrity. There is a protein called THROMBOMODULIN, produced by vascular endothelial cells, that combines with free thrombin in the blood stream to form a complex that is taken into endothelial cells where the thrombin is metabolised and the thrombomodulin recycled. This process fails if Proteins C and S are not present. Proteins C and S are not available if vitamin K is not available for their manufacture. So thrombomodulin cannot maintain the integrity of vascular endothelium unless there is adequate vitamin K.
I have not found any literature yet associating this with the 'fatty streaks' that represent the initial stages of atherosclerosis, but I am willing to bet that vitamin K has something to do with the prevention of monocytes from migrating between endometrial cells into the intima layer to produce atheromas. I do know that vitamin K reversed my arterial stenosis in all arteries with a 50% closure.
I now believe that primary atherosclerosis due to vitamin K deficiency is the cause of osteoarthritis, nephrosis, myocardial ischaemia, strokes, dementia and who knows whatever other organs that become deficient in blood supply
.
Literature associated with dementia from atherosclerosis and direct effects of vitamin K on brain health:
http://www.sciencedirect.com/science/ar ... 3696093282 --
Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study by Bots et al
Interpretation"These findings suggest that dementia and its two major subtypes Alzheimer's disease and vascular dementia are associated with atherosclerosis and that there is an interaction between apolipoprotein E and atherosclerosis in the aetiology of Alzheimer's disease."https://academic.oup.com/brain/article/ ... 49/284432/ --
Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementias by Mark Yarchoan et al
" These results provide further confirmation and specificity that vascular disease and Alzheimer’s disease are interrelated and suggest that common aetiologic or reciprocally synergistic pathophysiological mechanisms promote both vascular pathology and plaque and tangle pathology"http://advances.nutrition.org/content/3/2/204.full --
Vitamin K and the Nervous System: An Overview of its Actions by Guylaine Ferland
Abstract"The role of vitamin K in the nervous system has been somewhat neglected compared with other physiological systems despite the fact that this nutrient was identified some 40 y ago as essential for the synthesis of sphingolipids. Present in high concentrations in brain cell membranes, sphingolipids are now known to possess important cell signaling functions in addition to their structural role. In the past 20 y, additional support for vitamin K functions in the nervous system has come from the discovery and characterization of vitamin K–dependent proteins that are now known to play key roles in the central and peripheral nervous systems. Notably, protein Gas6 has been shown to be actively involved in cell survival, chemotaxis, mitogenesis, and cell growth of neurons and glial cells. Although limited in number, studies focusing on the relationship between vitamin K nutritional status and behavior and cognition have also become available, pointing to diet and certain drug treatments (i.e., warfarin derivatives) as potential modulators of the action of vitamin K in the nervous system. This review presents an overview of the research that first identified vitamin K as an important nutrient for the nervous system and summarizes recent findings that support this notion."The full article is available free. It is an excellent review and leaves no doubt that vitamin K is essential for a healthy functioning brain.
http://www.ncbi.nlm.nih.gov/pubmed/1902 ... t=Abstract --
Low vitamin K intakes in community-dwelling elders at an early stage of Alzheimer's disease. by N Presse et al.
The authors concluded
" Despite their limitations, results are in line with the most recent research in both vitamin K and Alzheimer's disease and suggest a need to consider vitamin K in future investigations on the role of diet in Alzheimer's disease."As a personal comment, I absolutely do not understand why everybody, let alone geriatrics with dementia have never been subjected to controlled supplementation with vitamin K and other fat-soluble vitamins. The literature has been available for more than forty years.
The Alzheimers research appears to be focussed on esoteric pursuits -- tau proteins, beta amyloids and a myriad of other irrelevant biochemical anomalies without addressing the obvious. There is an obvious reason, isn't there?