Abstract
Cerebral excitability is normally distributed, and pubertal age is a distinguishing factor. The final developmental event in CNS comprising selective pruning of excitatory synapses coincides with puberty. With early puberty, excess excitation and synaptic density, we have photic susceptibility, paroxysmal EEGs, disturbed circadian rhythms, paroxysmal disorders treated with drugs lowering excitation. Manic-depressive psychosis accords with this. Migraine with paroxysmal EEG, photophobia, hemianopsia, scintillating scotomas, excess excitation in the visual system, benefits from lowering excitation. With late puberty, attenuated CNS, we have disorders in need of raising excitation to avoid breakdown of circuitry, insufficient fill-in mechanism, silent spots, subjectively experienced only – objectively verifiable psychosis: i.e., schizophrenia treated with convulsant neuroleptics. By affecting pubertal age, we affect the distribution of excitation and of post-pubertal brain disorders in accordance with their level of excitation. Excitation is equally important in chronic disorders: l'dopa adversity in Parkinsonism could be due to further lowering of excitation in patients with a deficiency, a schizophrenia-like psychosis develops. Given unavoidable adversity of anti-psychotics, and a marked rise in suicide in schizophrenic and manic-depressive since their introduction, we want to prevent the occurrence of disorders at the extremes, whether very early or late puberty. DHA normalises excitability at all levels of excitation. An adequate daily intake of DHA, before puberty as well as after, might probably reduce or eliminate a development of psychopathology. Lithium is a robust neurotropic agent, and lithiation of the drinking water could be a way of reducing suicide, homicide, violent behaviour, and drug abuse.
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