A Possible Explanation of Schizophrenia and How Cannabis
Affects Schizophrenia
Copyright 2011, James Michael Howard, Fayetteville, Arkansas, U.S.A.
It is my hypothesis that schizophrenia is caused by low DHEA
in utero. This results in poor brain development. Later in life, cortisol and
testosterone act to reduce the effects of already low DHEA and adversely affect
brain function as well as maintenance of anatomy. DHEA naturally begins to
decline in the early twenties. This is why schizophrenia often occurs in the
late teens / early twenties (puberty and loss of DHEA) and is often triggered
by a stressful event (cortisol). Therefore, at this time, brain function and
maintenance is inhibited and, in the case of cortisol, may be reduced. I
suggest this reduces prefrontal function and increases lower brain function,
the seat of hallucinations. It is known that DHEA is low in schizophrenia and
that DHEA acts positively in neuron growth and function. (DHEA has also been
found to be high in schizophrenia. I suggest low DHEA may account for
"negative" symptoms and high DHEA may account for
"positive" symptoms of schizophrenia.)
Derived from the foregoing, I have developed
an explanation of how cannabis exerts its effects. I suggest that cannabis may
affect binding of DHEA to androgen receptors. I think
cannabis attaches to the androgen receptor and this has been supported
(Endocrinology. 1980 Sep;107(3):848-50). Since DHEA uses the androgen receptor,
cannabis will adversely affect the effects of DHEA. Part of my work includes an
explanation that production of DHEA at morning triggers consciousness, so
cannabis will reduce consciousness. By displacing DHEA from frontal receptors, DHEA
availability increases for other parts of the brain. (I think all tissues,
including various tissues of the brain, compete for available DHEA.) This
produces the effects of cannabis. Consciousness is reduced with concomitant
increase in midbrain function. This explains increased appetite, hearing, etc
caused by cannabis.
I explain the positive symptoms of
schizophrenia in the same way cannabis increases midbrain structures. As DHEA
declines in frontal areas which stimulate consciousness in schizophrenia,
midbrain structures are subsequently increased. Even in reduced DHEA
conditions, the available DHEA is sequestered by the midbrain. Hence, positive
symptoms are increased as the frontal areas are reduced in function. That is
midbrain activity (metabolism) is increased. It is known that cannabis
increases positive symptoms in psychosis. Cannabis, in psychosis, further
reduces the function of DHEA in the frontal areas and increase available DHEA
for the midbrain. (DHEA stimulates metabolism and frontal metabolism is reduced
in schizophrenia.)
As I suggested in my explanation of schizophrenia in the first paragraph,
above, cortisol increases at the expense of DHEA and reduces the effects of
DHEA. It is known that cortisol, in excess quantities over prolonged exposure,
is a neurotoxin. I suggest this occurs because the effects of DHEA are reduced.
DHEA is known to positively affect growth and maintenance of neurons.
I think the brains of schizophrenics are not as developed as normals in
utero and, perhaps, early on in neonates. This is why they are vulnerable to
the effects of cortisol and testosterone. Reducing DHEA by these hormones
reduces maintenance of the frontal areas and they experience declines in
function and anatomy. To finally respond to your findings, I suggest in these
individuals whose brains did not form robustly in utero, the effects of
cannabis on DHEA cause further decline and exacerbate the onset of psychosis.
Some research has indicated that cannabis use may improve negative symptoms
of schizophrenia. The increase in available DHEA, as a result of cannabis
use, which I described above that increases positive symptoms should improve
negative symptoms. (See my explanation of schizophrenia in the first
paragraph of this post.)