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The selective pruning of excitatory synapses – the final stage in brain development coincides with puberty. This makes pubertal age a determinant of excitability, the fundamental property of nervous tissue: the earlier puberty, the earlier is pruning arrested, the greater excitability. Age at puberty is only partly genetically determined. The 4 years lowering of mean pubertal age, a phenotypic response to improved living conditions (high protein diet) has been accompanied by a rise in manic-depressive psychosis and a decline in schizophrenia, mainly the nonparanoid more malignant forms. The maturational theory holds that early puberty is the necessary factor for developing manic-depressive psychosis; schizophrenia requires extremely late puberty. Their characteristic body-build supports this, as does the biological treatment, convulsant neuroleptics and mood-stabilizing anti-epileptics. Kraepelin’s endogenous psychoses, localized at the extremes of the maturational continuum, are part of normal variation in brain development. None of the CNS findings is outside normal variation. More pronounced findings are associated with exogenous factors (genetic and other disease, infection, pre-/perinatal morbidity). Given manic-depressive illness and schizophrenia are part of human variation, concordance for multigenetic inheritance, shared loci and shared susceptibility but no single locus raising risk >3 are expected and observed. Findings of unique susceptibility loci for each disorder for regions of the genome where no linkage is reported for the other disorder accord with expectation. The adversity of neuroleptics: attenuation of a CNS distinguished by reduced density of synapses, creates a need for alternatives. The decline in schizophrenia with lowering age at puberty offers a possibility of prevention. But pubertal age is declining further, excessive excitation renders the brain more unstable, further rise in manicdepressive illness, eating disorders and other disorders in early maturers, anxiety, panic attack, etc. Our brain, probably because of its great size, is especially susceptible to dietary deficit in marine fat (DHA, Omega-3), its main component, which has to be provided by diet. Adding minor amounts markedly affect behaviour, and are used as adjunctive or sole anti-psychotic in disorders distinguished by excess/deficit in excitability, and other neurological disorders underlining the mismatch between the usual diet and our need for “brain-food”. Lithium is neuroprotective, population studies have demonstrated statistically significant reduced admission for psychosis, reduced violence, homicide etc. with higher levels of lithium in drinking water than with low levels (Dawson, 1991; Dawson et al, 1970, 1972). Substance abuse, a confounding factor in mental illness, might be reduced with lithium. With these important environmental factors – lithium and marine fat, we have the means to reduce psychopathology – improve well-being. We better start implementation.

Changing panorama of mental illness, the role of environment – a key to prevention?