Sharing the intro and two excerpts here:
In folk lore there is a belief that many people who have an
acute psychotic breakdown exhibit signs of psychic ability. Research
into this folk lore is virtually non-existent, but some interesting
work by Neppe (1980) and Persinger (Persinger & Makarec, 1987)
psi suggests that there might be some foundation for it. My research
into the pineal gland is now exploring this same area from a neurochemical
perspective.
The pineal gland makes a neurohormone called melatonin which
is one of the key regulators of the circadian and seasonal biological
rhythms. It also makes a mono-amine oxidase (MAO) inhibitor called
pinoline (Methoxytetrahydrobetacarboline (MeOTHBC)) which acts
on the GABA receptors and whose chemical structure is virtually
identical with the harmala alkaloids, which are key ingredients
in the ayahausca drink used by Amazonian people specifically for
inducing a state of consciousness in which they state that they
go out-of-body, experience travelling clairvoyance, divination
and shamanic healing. The suggested neurochemistry for these effects
implicates serotonin. Serotonin (5 Hydroxytryptamine (5HT)) has
frequently been implicated in certain aspects of psychoses. Pinoline
is a neuromodulator which prevents, amongst other effects, the
breakdown of serotonin. This results in an accumulation of physiologically
active amines including dimethyltryptamine (DMT) within the neuronal
synapses which may lead to hallucinations, depression or mania
depending on the amines being affected (Strassman, 1990). DMT
is the other main ingredient in ayahuasca. There are also interesting
links with the serotonergic activation by psychedelics such as
LSD, psilocybin and MDMA which have all been implicated in triggering
psychotic episodes, and more specifically with inducing a state
of consciousness which has many similarities with both an acute
psychotic breakdown and with shamanism, which traditionally uses
psychedelic plants in order to achieve the desired state of consciousness.
A key link between all of these various experiences is the dream
state of consciousness. Psychologically, both the shamanic initiation
experience and that of an acute psychotic breakdown share many
similarities with the dream state. It appears that the normal
every night experience of all human beings is connected with the
more extreme experiences of psychosis and shamanism through the
same neurochemical pathways that underlie all these experiences.
And, as the research at Maimonides (Ullman et al, 1975) and since
has shown, the dream state is a psychic state of consciousness
par excellence. This suggests that the anthropological reports
of psychic abilities being exhibited by shamans may have some
foundation, and suggests that some people who have experienced
a psychotic breakdown could be seen in other cultures as people
with a particular and highly valued gift - the gift of walking
between the worlds.
Geomagnetic Fields, Depression and the Role of Melatonin
One of the key factors in
linking the pineal with psychosis is the work of Kay (1994). Admission
to mental hospital varies with season and time of the month, and mental
illness is more common the further north you go, i.e., into long light
summers, and long dark winters.
Seasonal variation in the incidence of depressive illness has been
recognised since Hippocrates (Lewis, 1934). Onset of depressive illness,
admission to hospital, prescriptions of antidepressant medication and
incidence of suicide have all been found to show a bimodal annual
distribution with peaks in spring and autumn.
Kay (1994) has found, in a 10 year study of admission rates to
Lothian psychiatric hospitals, that two weeks after a geomagnetic storm
there was a significant rise (36.2%) for male admissions for depression
phase of manic-depression and a smaller non-significant rise for women
with psychotic and non-psychotic depression. There was no correlation
between intensity of storm and admission rates, i.e. if any sort of
storm happens, mild or severe, you get increased admission rate, which
is consistent with a threshold event affecting predisposed individuals.
The effect of geomagnetic storms could range from mild irritability to
full-blown depression. Monthly total psychiatric admissions have been
positively correlated with solar radioflux levels and indices of
geomagnetic ionospheric disturbance.
Kay suggests that geomagnetic storms partly account for the bimodal
annual distribution of depression by acting either through
desynchronisation of pineal circadian rhythms, or via an effect on
5HT-ergic and adrenergic systems leading to depressed mood and secondary
disruption of pineal melatonin synthesis. Alteration in geomagnetic
field (GMF) activity is associated with decreased serotonin NAT activity
and decreased melatonin synthesis. Geomagnetic storms in spring enhance
the suppressing effect of increasing daylight on melatonin synthesis,
leading to a phase advance in the circadian rhythm, while the effect of
storms in autumn tend to be partially compensated by the pineal response
to decreasing light intensity. This is consistent with a Southern
Hemisphere peak for psychotic depression admissions in September and
October, and a peak in Sweden in April.
The main innervation of the pineal is via adrenergic systems so
magnetic fields may affect pineal functioning via this mechanism. Sandyk
(1990a) associates depression with decreased melatonin secretion and
suggests that melatonin regulates dopaminergic, cholinergic and
GABA-ergic functions.
It is also possible that the association between geomagnetic storms
and depression could be due to an indirect association with changes in
meteorological factors. Atmospheric ionisation and barometric pressure
have been shown to affect measures of 5HT activity. Prolonged exposure
to abnormal magnetic fields may also have an effect, acting through a
similar mechanism to geomagnetic storms. Depression admissions have been
associated with exposure to 50Hz e-m fields in the home.
Role of Circadian Rhythms, Melatonin and Manic-Depression
We have two circadian
clocks - one is a biological clock which includes the ventromedial
nucleus of the hypothalamus, the locus ceruleus and the dorsal raphe
nucleus - food is the zeitgeber for this clock; the second clock
includes the retina, hypothalamic suprachalasmic nuceus (SCN) and pineal
gland - light is the zeitgeber for this clock. The two clocks are
normally in synchrony but in view of the independence of the two clocks
asynchrony is possible, and the affective disorders may be caused by
such a dysfunction (Maurizi, 1984).
Disturbances of the noradrenergic activity of the central nervous
system (CNS) have been related to affective disorders, which are also
accompanied by depressed melatonin secretion and sleep disturbances.
Manic-depression is associated with a sleep disorder: in the manic phase
the person suffers from insomnia, in the depression state they sleep
too much.
Melatonin is mainly secreted at night through noradrenergic
stimulation of beta-receptors on the pinealocoytes. Melatonin secretion
can therefore be inhibited by beta-blocking drugs. Melatonin secretion
is depressed in mental disorders with sleep disturbances such as the
manic phase of certain affective disorders, alcoholic abuse and dts with
hallucinations.
There are mixed results regarding melatonin secretion in affective
disorders - some find decreased nocturnal melatonin secretion in
unipolar depressed adults, others do not. Lewy et al (1979) reports
increased melatonin levels in bipolar subjects through a 24 hour cycle.
Lam et al (1990) report decreased nocturnal melatonin production in
bipolar patients compared with unipolar depressed and control subjects.
Reiter (1982) suggests that manic-depressives have a low melatonin
concentration during suicidal episodes and a high melatonin
concentration during manic episodes.
Affective disorders involving circadian dysregulation may respond to
interventions that restore a normal sleep-wake cycle. Robertson &
Tanguay (1997) describe a boy with bipolar disorder. A trial of
melatonin led to rapid relief of insomnia and aborted manic episodes for
at least a two year period. Insomnia can be both a symptom and a
precursor of mania (Wehr et al, 1987; Leibenluft et al, 1995). On the
other hand, sleep deprivation therapy for depression is thought to exert
its effect by resynchronising circadian rhythms, while antidepressants
and lithium lengthen the pineal circadian cycle period re-synchronising a
phase advanced cycle.
In addition, melatonin administration to clinically depressed
patients gives negative effects (Carman et al, 1976). The treatment of
psychotic depression with daytime melatonin increases psychotic symptoms
and abolishes diurnal mood variation. The timing of this treatment
would tend to exacerbate a desynchronised rhythm. De-synchronising
circadian rhythms is therefore a possible mechanism for mood switching
in manic-depressive illness, and manic-depressive patients have been
found to be supersensitive to the suppressing effect of light on
night-time melatonin synthesis, suggesting that in these people the
pineal gland may be generally supersensitive to environmental factors
including geomagnetic storms.
Brismar (1987) studied people on beta blockers because of angina,
hypertension, etc. and found that those with depressed nightly urinary
melatonin excretion suffered from CNS symptoms such as nightmares and
hallucinations. Not many people suffer these effects. Another possible
site of action for melatonin is the dorsal raphe nucleus. (LSD also acts
on the dorsal raphe nucleus.) Melatonin could enhance 5HT levels by
acting as a MAO inhibitor in the synapses of the dorsal raphe nucleus.
Abnormalities in circadian rhythm organization are consistent
features in manic-depressive illness (Wehr & Goodwin, 1980).
Wetterberg et al (1981) suggest pineal involvement. Manic-depressives
have an earlier onset of melatonin secretion during depression, with
this secretory onset being even earlier in mania (Lewy & Kern,
1984). Manic depressives are also super-sensitive to light with 50%
reduction in melatonin production on exposure to 500 lux. Normally one
needs 2500 lux for this suppression whereas manic-depressives have
complete melatonin suppression at 1500 lux (Lewy & Kern, 1984). It
is possible that supersensitivity to light with alteration in retinal
perception of light could contribute to a phase advance of those rhythms
that are entrained to the light-dark cycle and thus lead to alterations
in those function that are influenced secondarily by such rhythms (for
review see Kripke & Risch 1986; Rosenthal, 1986; Thompson, 1987).
Thus melatonin, as an integral aspect of our circadian rhythm is implicated in manic- depression.
