[Alamo-Girl]

Thank you for your post!

But observeations of how external influences (like physical damage or certain chemical reactions) on our brains affect our minds point to this conclusion.

Conversely, there is no Medical Explanation for near death experiences or the power of prayer. Here are more articles on the subject:

Soul-searching doctors find life after death
Scientists find biological reality behind religious experience
Doctors increasingly find introducing prayer helps calm patients and speeds recovery
The healing power of prayer.
There is power in prayer

Lurkers might enjoy this thread with includes an interesting debate on miracles: The Unraveling of Scientific Materialism

[Dimensio]

Conversely, there is no Medical Explanation for near death experiences

I know that oxygen deprivation is a common explanation for NDEs, so I checked to see if the linked article made mention of that. It did: "It's always said that NDEs are just a phenomenon relating to the dying brain and the lack of oxygen to the brain cells. But that's not true. If there was a physiological cause, all the patients should have had an NDE."

That seems pretty flimsy for me. It's one person's opinion that everyone should react in the same fashion to the same physiological conditions, but it's well-documented that such isn't the case for other things.

[jennyp]

Conversely, there is no Medical Explanation for near death experiences or the power of prayer.

Ah, that's not true! There's good evidence that NDEs are induced by blocking of the PCP receptor in the brain: Taking ketamine will induce a near-death experience. This passage from the article hypothesizes about the precise mechanism & why it happens:

Most large neurones in the cerebral cortex use glutamate as their neurotransmitter. Glutamate, an excitatory amino acid, is central to the function of the hippocampus, temporal and frontal lobes and plays a vital role in all cognitive processes involving the cerebral cortex, including thinking, memory and perception.

The major neuronal binding site for ketamine is called the PCP receptor, which is itself attached to the NMDA receptor. As they are part of the same macromolecular complex, the two terms are sometimes used interchangeably. ...

There was initially some debate as to whether the hallucinogenic properties of ketamine were due to NMDA or sigma receptors. These effects are now largely attributed to NMDA receptor blockade. Sigma ligands with a high degree of specificity (e.g. (+)pentazocine) do not produce NDE's at doses where most of the binding is to sigma rather than NMDA and/or kappa opioid receptors (sigma receptor ligands frequently have affinity for NMDA and/or kappa opioid receptors at higher doses).

When glutamate is present in excess, neurones die via a process called excitotoxicity. Conditions which have been proven to lead to excessive release of glutamate include hypoxia/ischaemia, epilepsy and hypoglycaemia. Blockade of PCP receptors prevents cell death from excitotoxicity. The brain may thus have a protective mechanism against a glutamate flood: release of a counter-flood of substances which block PCP receptors, preventing neuronal death. Considering the sophistication of the brain's many known defences, and the vulnerability of neurones to hypoxia, a protective mechanism against excitotoxicity seems very likely. This is the only speculation in the process outlined above: the other statements are strongly supported by experimental evidence. A peptide called a-endopsychosin, which binds to the PCP receptor, has been found in the brain. Certain ions such as magnesium and zinc also act as endogenous PCP channel blockers, and it is possible that these ions are centrally involved in producing NDE's.