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Originally posted by kingofmd
Pretty good website, apparently this doctor has been studying accounts around the world for some time
All in all this subject is worthy of great amounts of study, though I feel the answer to the question will only come to us after we have a much greater grasp of reality and how it is directly connected to consciousness.
Originally posted by miriam0566
it amazes me that people dont see the general flaw with these "accounts"...
the people who gave them are still alive. their acoount cant really prove anything because they werent really dead. if they were dead then they would be able to tell us about it.
Originally posted by Korg TrinityThough the term describes those that have had experience after they were pronounced clinically dead, i.e. no detectable brain function.
Neurologist and University of Toledo Neuroscience Researcher, Dr. John Greenfield considers the EEG data from patients with near death experience (NDE). eeg-book21For near death experience skeptics, medical evidence of a flat EEG during an out of body experience has always been a stumbling block. After all, a brain dead patient can’t hallucinate. But, does a flat EEG really mean no brain activity? NDE doubters have claimed activity deep inside the brain, beyond the reach of EEG instruments, must account for the complex “realer than real” experiences reported by those who briefly pass into the afterlife. Now, University of Toledo Neuroscience researcher, and EEG expert, Dr. John Greenfield explains why this claim doesn’t hold up. “It’s very unlikely that a hypoperfused brain [someone with no blood flow to the brain], with no evidence of electrical activity could generate NDEs. Human studies as well as animal studies have typically shown very little brain perfusion [blood flow] or glucose utilization when the EEG is flat. There are deep brain areas involved in generating memories that might still operate at some very reduced level during cardiac arrest, but of course any subcortically generated activity can’t be brought to consciousness without at least one functioning cerebral hemisphere. So even if there were some way that NDEs were generated during the hypoxic state [while the brain is shut off from oxygen], you would not experience them until reperfusion [blood flow] allowed you to dream them or wake up and talk about them”, Greenfield stated. NDE Researcher, Dr. Penny Sartori, examines memories of resuscitation by patients suffering cardiac arrest. With near death experience cases making there way into the, New England Journal of Medicine, Journal of Psychiatry, and other major medical journals, NDE doubters have looked to the timing of patient memories as a way of explaining this unexplainable phenomena. If memories of out of body travel, and all embracing love occur after ones brush with death, NDEs may still fit within our medical science worldview. The timing of NDE memories is the research question Dr. Penny Sartori sought to answer, “I worked in the intensive care unit and because of the nature of my job, of course, I’d come across a lot of death. And of course makes you wonder what happens when we die. For five years I gathered data, where I spoke to patients in the intensive care unit and particularly patients who’d had a cardiac arrest. When these patients revived, as soon as they were medically fit, I approached them and asked the simple question, ‘Did you have any memory of the time that you were unconscious?’” “For the people who had a near-death experience and out of body experience [their recollection of resuscitation] was really quite accurate and I decided then to ask the control group, the people who’d had a cardiac arrest but had no recollection of anything at all. I asked them if they would reenact their resuscitation scenario and tell me what they thought that we had done to resuscitate them. And what I found is that many of the patients couldn’t even guess as to what we’d done. They had no idea at all. And then some of them did make guesses, but these were based on TV hospital dramas that they’d seen. I found that what they reported was widely inaccurate. So there was a stark contrast really in the very accurate out of body experiences reported and then the guesses that the control group had made.”, Dr. Sartori reported. While research like this may never be enough to convince dogmatic skeptics, the medical evidence for near death experience continues to challenge us to reexamine our beliefs about what lies beyond death.
Unfortunately, sheep herders in Australian desired strains of low alkaloid phalaris plants. So now most commercially available phalaris are probably weak. Phalaris can be obtained through mail order herb companies, some of who advertise high alkaloid plants. Because I do not wish to associate these fine suppliers names' with an article on how to prepare a drug, I will not provide names or addresses. Just ask around on the net. SHEEP DEATH I put this as a separate section to highlight it's significance. Remember, if you try these drugs, you are using something that kills sheep. The toxic syndrome is called "phalaris staggers." It is manifested by apparent dizziness, staggering, and tremors, sometimes resulting in death. The syndrome affects sheep that have eaten high alkaloid phalaris. On autopsy, after naturally and experimentally induced phalaris staggers in sheep, portions of the lower brain are seen to be damaged and, oddly enough, tinted blue. The responsible agents are the alkaloids contained in the various phalaris species. There are whispered rumors that phalaris also contain beta carbolines, a type of MAOI. If so,it may be that sheep, in eating large quantities of phalaris, also obtain a dose of MAOI, making the already large dose (pounds of phalaris could easily be eaten by a sheep or cow in a day), of '___' active. However, MAOIs are not required for sheep death. Studies show that controlled injections of pure '___', at human recreational doses, kill sheep. Why sheep and humans respond differently to '___' is still an open question here. It may be that it is not an important question, but the possibility of human death on phalaris still looms.
Alkaloid Levels in Reed Canarygrass Grown on Wet Meadows in British Columbia, by W. Majak, R. E. McDiarmid, A. L. Van Ryswyk, K. Broersma and S. G. Bonin © 1979 Allen Press. Abstract Hordenine, gramine, and 5-methoxy-N-methyltryptamine (5MMT) were identified as the major basic alkaloids in reed canarygrass grown on wet meadows in Interior British Columbia. The concentrations of these anti-quality constituents, determined sequentially at four field locations, were exceptionally low compared with levels found for reed canarygrass grown under growth room conditions. Under field conditions, for example, 5MMT levels did not exceed 250 μg/g (dry wt), whereas a peak level of 4,250 μg/g 5MMT was recorded from the growth room. Depressed alkaloid levels under wet meadow field conditions were observed in all varieties tested including two experimental varieties, one registered variety, and a commercial type. Low alkaloid levels on wet meadows appeared to coincide with fewer types of alkaloids: 5-methoxy-N, N-dimethyltryptamine (5'___') was not detected under field conditions but it was present in all reed canarygrass samples analyzed from the growth room. Field applications of fertilizer (NPK) appeared to have marginal effects on alkaloid levels. On wet meadows the trends indicated that gramine and 5MMT concentrations increased toward the end of the growing season, but low total alkaloid levels were still maintained. The factor of soil moisture stress is reviewed in relation to alkaloid levels in reed canarygrass. Recently developed thin layer chromatography (TLC) scanning procedures were used to determine concentrations of gramine and 5MMT. New TLC fluorescence methods were devised for the quantitative determination of hordenine and 5'___' in reed canarygrass.