Common Mechanism in Consciousness, Dreaming, Positive Symptoms of Schizophrenia, Hallucinations, Near- Death Experiences, etc
James Howard
Schizophrenia, Hallucinations, Near- Death Experiences, etc.
Copyright 2009, James Michael Howard, Fayetteville, Arkansas, U.S.A.
It is my hypothesis that sleep and consciousness are controlled by levels of
melatonin and DHEA (http://www.anthropogeny.com/Sleep%20and%20SIDS.htm ).
The effects of this mechanism control our circadian rhythms and our
relationship with the environment and the self. More specifically, these
control the activity of the forebrain. They turn it on and off. When we
sleep, activity of the forebrain declines and the ratio of lower brain
activity increases. The input of the midbrain increases and is interpreted
by a forebrain which is not fully active. This is dreaming, a time when
DHEA availability is reduced, overall. Activity of both systems is reduced.
As forebrain activity is reduced, momentarily, the availability of DHEA is
increased for the midbrain; this is the "dream." The ratio of use of DHEA
by these competing systems determines their activity. As DHEA begins to
increase at morning, the forebrain, again, becomes active.
When we are conscious, the forebrain and the middle / hind brain are all
activated. While this is occurring, the forebrain controls interpretation
of the input and output systems. While active, the forebrain sequesters
DHEA at the expense of the midbrain. The activity of the midbrain does not
penetrate our conscious activity without examination and analysis. When
active, the forebrain brings relevant association areas into decisions and
interpretation.
It is also my hypothesis that schizophrenia represents a situation whereby
activity of the forebrain is diminished
(http://www.anthropogeny.com/Schizophrenia.htm ). DHEA levels have been
found to be low and high in schizophrenia. Low levels probably are
connected with "negative" symptoms of schizophrenia, thus, producing reduced
brain activity concerned with self-awareness. High levels of DHEA may
indicate further use of DHEA by the forebrain, therefore, increasing
availability of DHEA for the midbrain. This allows midbrain activities to
penetrate the "consciousness" during inattention of the forebrain. I
suggest this is how "positive" symptoms of schizophrenia are produced, that
is, hallucinations. That is, hallucinations are the product of an over
stimulated midbrain without proper interpretation.
It is also my hypothesis that death occurs when DHEA declines to very low
levels. Specifically, I suggest death occurs when there is insufficient
DHEA to support activity in the brainstem. Prior to death, the declines of
DHEA reach a point when forebrain activity declines, just as it does in
sleep and in schizophrenia. At some point in this decline, the activities
of the midbrain, momentarily, become stronger as the ratio of forebrain to
midbrain activities change. Association areas come into action in relevant
and irrelevant connections to the dying person producing hallucinations,
just as in schizophrenia and dreaming.
Differences in the relative activity of the forebrain and the midbrain
produce differences that are interpreted as consciousness, dreaming, or
hallucinating. I suggest the same mechanism is responsible for all of
these.