From: gts (gts@optexinc.com)
Date: Fri Oct 11 2002 - 11:24:22 MDT
Rafal and Robert...
Here are some additional research abstracts that should be of interest
here and which support my case.
The first abstract supports my point to Rafal that non-DNA neural
parameters change in response to the environment, implying that a record
of today's non-genetic neuronal structures is insufficient for
preserving the personality into the future.
The first abstract shows us that in seasonal affective disorder (SAD),
BMax for the serotonin receptor ligands paroxetine (Paxil) and LSD (Yes,
Lucy in the Sky with Diamonds) decreased in response to light therapy,
indicating a structural change in the serotonergic system in response to
increased light. The serotonergic system is comprised of serotonin and
its receptors and transporters, the synthesis of each of which is under
control of the DNA in the nucleus of serotonergic neurons. In SAD, the
genes that code for these structural elements express differently
according to the season. It is for this reason that a person with SAD
must encode and upload those genetic instructions if he wishes to
preserve the manner in which his personality responds to changes of the
seasons (of course may chose not to do so, but doing so would defeat our
purpose here of preserving the personality).
The second article also refers to evidence of seasonal changes in the
serotonergic system in SAD.
ABSTRACT:
Platelet [3H]paroxetine and [3H]lysergic acid diethylamide binding in
seasonal affective disorder and the effect of bright light therapy.
Biol Psychiatry 1999 Feb 15;45(4):464-70 (ISSN: 0006-3223)
Smedh K; Spigset O; Allard P; Mjorndal T; Adolfsson R
Department of Psychiatry, Umea Universitet, Sweden. \/
BACKGROUND: Seasonal affective disorder (SAD) has been regarded as a
melatonin disorder, but the pathophysiological mechanisms of SAD are to
a large extent unclarified. Serotonergic mechanisms have also been
studied, but they have shown inconsistent results. METHODS: We have
compared [3H]paroxetine and [3H]lysergic acid diethylamide (LSD) binding
in platelets from 23 SAD patients and 23 controls. Then SAD patients had
4 weeks of light therapy. On the last treatment day new blood samples
were drawn. Symptoms before and after light treatment were measured by
SIGH-SAD. RESULTS: Bmax for paroxetine binding before light treatment
was higher in SAD patients compared to controls and also higher in
responders than in nonresponders. Bmax decreased significantly during
light treatment. We also found a negative correlation between the two
Bmax values before but not after light treatment. There was a negative
correlation between Bmax for paroxetine binding before treatment and
clinical status after treatment. Patients with reduced Bmax for LSD
binding after treatment had a better clinical treatment response.
CONCLUSIONS: The present study indicates that serotonin receptor
parameters might be suitable in the prediction of clinical response to
light treatment.
ABSTRACT:
Monoaminergic function in the pathogenesis of seasonal affective
disorder.
Int J Neuropsychopharmacol 2001 Dec;4(4):409-20 (ISSN: 1461-1457)
Neumeister A; Konstantinidis A; Praschak-Rieder N; Willeit M; Hilger E;
Stastny J; Kasper S
National Institutes of Health, NIMH/Mood and Anxiety Disorders Program,
Bethesda, MD 20892-2670, USA. neumeisa@intra.nimh.nih.gov.
Seasonal affective disorder/winter type (SAD) is characterized by
recurrent depressive episodes during autumn and winter alternating with
non-depressive episodes during spring and summer. Light therapy with
full-spectrum, bright white light has been shown to be effective for
this condition. Several hypotheses have been discussed in the literature
about the pathogenesis of SAD. The most prominent includes disturbances
in central monoaminergic transmission. Evidence can be inferred from
studies showing a seasonal rhythm of central and peripheral serotonergic
functioning which may be a predisposing factor for SAD. Some of the
symptoms of SAD are believed to represent an attempt to overcome a
putative deficit in brain serotonergic transmission. Moreover, 5-HT
receptor challenge studies suggest altered activity at or downstream to
central 5-HT receptors. Monoamine depletion studies support hypotheses
about serotonergic and catecholaminergic dysfunctions in SAD and suggest
that light therapy may well compensate for this underlying deficit.
Further, albeit indirect, support for the importance of monoaminergic
mechanisms in SAD and its involvement in the mechanism of the action of
light therapy comes from studies showing antidepressant efficacy of
serotonergic and noradrenergic antidepressants in the treatment of SAD.
Altogether, disturbances in brain monoaminergic transmission seem to
play a key role in the pathogenesis of SAD; monoaminergic systems may
also play an important role in the mechanisms of the action of light
therapy.
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