Further evidence that infantile autism is a chronic psychosis distinguished by a deficient delayed response function affecting the connections between hippocampus and singulum in its center, the SMA and the inhibitory Purkinje cells in cerebellum.

Older literature on infantile autism accompanied by mental retardation, focussed on epilepsy, cerebral palsy and microcephaly. Multiple adversity was needed to delay growth sufficiently to pruning of connection between Hippocampus and Singulum in its centre, SMA and inhibitory cells in Cerebellum in the synaptogenesis in infancy. Temporary macrocephaly was observed.

Infantile autism: a chronic psychosis since infancy due to synaptic pruning of the supplementary motor area.

The rise in infantile autism, learning problems, cognitive decline with age, Alzheimer's, Parkinson's diseases and the SIDS epidemic, has a common cause in the rising dietary deficit in Omega-3 brain-food. This paper suggests that aside from the wider concept of autism spectrum disorders (ASD) and pervasive developmental disorders (PDD), the rise in infantile autism (IA) in the last decade is the effect of deficient brain-food (Omega-3). The consequent delay of development, prolongs the 2nd regressive event in infancy to pruning of the centre in the Medial Frontal Lobe System that connects hippocampus and singulum.

Sexual behaviour does not reflect HIV-1 prevalence differences: a comparison study of Zimbabwe and Tanzania.

Background: Substantial heterogeneity in HIV prevalence has been observed within sub-Saharan Africa. It is not clear which factors can explain these differences. Our aim was to identify risk factors that could explain the large differences in HIV-1 prevalence among pregnant women in Harare, Zimbabwe, and Moshi, Tanzania.

What is a psychosis and where is it located?

Kraepelin's dichotomy, manic-depressive insanity and dementia praecox, are contrasting and true endogenous disease entities which affect excitability, the fundamental property of the CNS. Kraepelin wanted to establish a valid classification and hit the extremes in brain structure and function at a time when we had no knowledge of brain dysfunction in "functional" psychoses. The aetiology is now known: the psychoses are part of human growth and maturation and might be classified according to their brain dysfunction, which is exactly what Kraepelin wanted.

Infantile autism: a chronic psychosis since infancy due to synaptic pruning of the supplementary motor area.

The rise in Infantile Autism, learning problems, cognitive decline with age, Alzheimer's, Parkinson's Diseases and the SIDS epidemic, has a common cause in the rising dietary deficit in Omega-3 brain-food. This paper suggests that aside from the wider concept of Autism Spectrum Disorders (ASD) and Pervasive Developmental Disorders (PDD), the rise in Infantile Autism (IA) in the last decade is the effect of deficient brain-food (Omega-3). The consequent delay of development prolongs the 2nd regressive event in infancy to pruning of the centre in the Medial Frontal Lobe System that connects Hippocampus and Cingulum.

Kraepelin's dichotomy is true: contrasting brain dysfunction at the extremes of human growth and maturation. Excitability, the fundamental property of nervous tissue, is affected.

The distribution of Kraepelin's ubiquitous dichotomy varies with standard of living and pubertal age: when one rises, the other declines. The universal similar clinical picture--mortality risk, manic depressive psychosis, episodic dysfunction of brainstem control systems (sleep-wake cycle, food, mood control mechanism)--is caused by abridged pubertal pruning of excitatory synapses, which is treated with anti-epileptics, as opposed to convulsant neuroleptics in dementia praecox, where the clinical variation reflects varying degrees of excessive pruning and deficit in excitability. Localization of cortical breakdown of circuitry, silent spots and persistent dysfunction due to insufficient fill-in mechanisms, determine the clinical picture.

From genetics to epigenetics.

In the post human-genome area, the challenge is to derive details of heritable variation in relation to how human variation reflects adaptation to the different environments. Heterozygote advantage represents a superior genetic adaptation presumably explaining the presence of the allele at frequencies above those to be expected from a simple replacement of a homozygous lethal allele by mutation alone (Saugstad 1977a, 1975b, 1972). Mean birthweight of unaffected offspring of parents heterozygous for the phenylketonuria (PKU) allele averaged significantly above mean weight of all Norwegian births, rendering unaffected offspring more viable at birth and thus improving the chance for survival of the allele.

Are neurodegenerative disorder and psychotic manifestations avoidable brain dysfunctions with adequate dietary omega-3?

The present mismatch between what our brain needs, and the modern diet neglects our marine heritage. Last century, the priority in nutrition and food production was to achieve a high protein diet and somatic growth and function. The dietary content of omega-3 (N-3) required by the brain was neglected although evidence for the essentiality of certain fatty acids was published in 1929 and specifically re-affirmed for omega 3 in the brain in the 1970s.

Are neurodegenerative disorder and psychotic manifestations avoidable brain dysfunctions with adequate dietary omega-3?

The present mismatch between what our brain needs, and the modern diet neglects our marine heritage. Last century, the priority in nutrition and food production was to achieve a high protein diet and somatic growth and function. The dietary content of omega-3 (N-3) required by the brain was neglected although evidence for the essentiality of certain fatty acids was published in 1929 and specifically re-affirmed for omega 3 in the brain in the 1970s.

From superior adaptation and function to brain dysfunction--the neglect of epigenetic factors.

With optimal pregnancy conditions (natural, enriched diet which includes fish) African (Digo) infants are 3-4 weeks ahead of European/American infants in sensorimotor terms at birth, and during the first year. Infants of semi-aquatic sea-gypsies swim before they walk, and have superior visual acuity compared with us. With adverse pregnancy behaviour (fear of fat, a trend to dieting), neglecting the need for brain fat to secure normal brain development and function, we run a risk of dysfunction--death.

A "new-old" way of thinking about brain disorder, cerebral excitability--the fundamental property of nervous tissue.

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.

Our neglect of the normal variation is linked to a reluctance to accept multifactorial inheritance and the role of environment.

One of the most surprising evolutionary discoveries is that wild species similar to human contain a vast reservoir of variability. Why are we persistently reluctant to discuss normal variation in brain structure and function and label any deviation pathological? Despite the failure of Mendelian Genetics to solve the genetic puzzle in psychiatry, we refuse to discuss multifactorial inheritance and the role of environmental factors. Rising living conditions (high protein diet) accelerate maturation, lower pubertal age, shift body-built toward more weight for height and cerebral excitability toward higher levels.

Third World adversity: African infant precocity and the role of environment.

The war against illiteracy has not been won. The number of illiterates approaches a billion. Most reside in Third World countries--former colonies--where they are caught in a poverty trap of disease, low agricultural production and environmental adversity requiring technology beyond their means.

Manic depressive psychosis and schizophrenia are neurological disorders at the extremes of CNS maturation and nutritional disorders associated with a deficit in marine fat.

The maturational theory of brain development comprises manic depressive psychosis and schizophrenia. It holds that the disorders are part of human diversity in growth and maturation, which explains their ubiquity, shared susceptibility genes and multifactorial inheritance. Rate of maturation and age at puberty are the genotype; the disorders are localized at the extremes with normality in between.

A lack of cerebral lateralization in schizophrenia is within the normal variation in brain maturation but indicates late, slow maturation.

The planum temporale (PT) bias, PT leftward, PT symmetry, and PT rightward reversal and sidedness preference, consistent right-handedness, ambilaterality, and consistent left-handedness are placed on a continuum mirroring the normal variation in rate of brain maturation. Maturational rate declines as we pass from PT leftward bias and consistent right-handedness to PT reversal and consistent left-handedness. Concomitantly, we expect an increased prevalence of males due to their pubertal age being about 2 years later than that of females, and a shift in cognitive profile from higher verbal scores than performance scores on the WAIS to higher performance than verbal scores.

Optimality of the birth population reduces learning and behaviour disorders and sudden infant death after the first month.

The weight distribution pattern of all births can be divided into a "skewing to the left" to lower weights and high neonatal mortality, a "skewing to the right" to higher weights (>3500g) and minimum neonatal and postneonatal mortality, and a "symmetrical distribution" with mortality in between. This study was initiated with the hypothesis that a deficit in newborns of more than 3500 g would adversely affect postneonatal death. Higher and rising postneonatal mortality solely attributable to sudden infant death of unknown cause (sudden infant death syndrome; SIDS) was observed in the Nordic countries with a lower proportion of heavy newborns.

Cerebral lateralisation and rate of maturation.

Multifactorial inheritance applied to brain development implies a large continuum of normal variation with deviation from the norm at the extremes of maturational rate. The greater population of neurons, greater arborization of neural networks and excessive synaptic density in early maturation imply that adaptability (plasticity) is a main advantage, as opposed to a deficit in adaptability associated with the reduced number of neurons, reduced connectivity and reduced synaptic density in late slow maturation. It is hypothesised that Planum Temporale (PT) asymmetry and hand-preference predict the rate of CNS maturation as does the cognitive profile on the Wechsler Adult Intelligence Scale (WAIS): PT leftward asymmetry, right-handedness and a left-hemisphere cognitive advantage signifies early fast maturation: PT rightward asymmetry, left-handedness and a right-hemisphere cognitive advantage signify late maturation, while PT symmetry and ambilaterality represent rates of maturation in between.

Optimal foetal growth in the reduction of learning and behaviour disorder and prevention of sudden infant death (SIDS) after the first month.

A theory is presented that a diet low in polyunsaturated fatty acids (PUFA) in the third trimester of pregnancy may delay myelination and brain maturation. This may underpin learning and behaviour disorders and sudden infant death (SIDS) after the first month, conditions that are associated with lower than average birthweight. Epidemiological evidence is reviewed showing an inverse relation between the proportion of heavy newborns (> 3500 g) and infant mortality rate.

Deviation in cerebral excitability: possible clinical implications.

Schizophrenia, a chemical signaling disorder in the brain, is also a deteriorating neurological disorder. The deficit in cerebral excitability, and associated reduced synaptic density, imply a risk of cortical breakdown of circuitry accompanied by an insufficient fill-in mechanism, and persistent silent spots, but no total loss of function, only dysfunction. This is subjectively experienced as deficiencies of cognition, perception and sensorimotor phenomena depending upon localization and connections of the disconnected circuitry.

The maturational theory of brain development and cerebral excitability in the multifactorially inherited manic-depressive psychosis and schizophrenia.

An association has been established between the multifactorially inherited rate of physical maturation and the final step in brain development, when some 40% of synapses are eliminated. This may imply that similarly to endocrine disease entities, we have cerebral disease entities at the extremes of the maturational rate continuum. The restriction of prepubertal pruning to excitatory synapses leaving the number of inhibitory ones fairly constant, implies changes in cerebral excitability as a function of rate of maturation (age at puberty).