Monday, May 6, 2013

Walking Between the Worlds: Links between Psi, Psychedelics, Shamanism and Psychosis An Overview of the Literature

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.

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