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Letten F Saugstad

Publications and source records attributed to Letten F Saugstad.

10 recordsLinked to original sources
PubMed2006

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. Cognitive decline with age and neurodegenerative disorder with dementia are now rising. This review describes signs of N-3 deficit in Alzheimer and Parkinson Disease, where maximum change involves the primary sites: olfactory cortex and the hippocampus. The olfactory agnosia observed in schizophrenia supports an N-3 deficit as does a reduction of key ologodendrocyte- and myelin-related genes in this disorder and affective disorder, where a rise in dementia accords with a deficit of N-3 also in this disorder. N-3 normalizes cerebral excitability at all levels. That the two disorders are localized at the extremes of excitability, is supported by their opposing treatments: convulsant neuroleptics and anti-epileptic anti-depressants. An adequate N-3 diet will probably prevent most psychotic episodes and prove that neurodegenerative disorder with dementia is also to a large extent not only preventable but avoidable.

Aged↗
PubMed2006

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. Cognitive decline with age and neurodegenerative disorder with dementia are now rising. This review describes signs of N-3 deficit in Alzheimer and Parkinson Disease, where maximum change involves the primary sites: olfactory cortex and the hippocampus. The olfactory agnosia observed in schizophrenia supports an N-3 deficit as does a reduction of key ologodendrocyte- and myelin-related genes in this disorder and affective disorder, where a rise in dementia accords with a deficit of N-3 also in this disorder. N-3 normalizes cerebral excitability at all levels. That the two disorders are localized at the extremes of excitability, is supported by their opposing treatments: convulsant neuroleptics and anti-epileptic antidepressants. An adequate N-3 diet will probably prevent most psychotic episodes and prove that neurodegenerative disorder with dementia is also to a large extent not only preventable but avoidable.

Journal Article↗
PubMed2006

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. A successful adaptation requires natural selection acting on that part of the body that makes a difference in survival. Skin colour variation is such a successful adaptation, for the North as opposed to the dark skins of the equator. Human Evolution in Africa and subsequent adaptations have enabled human survival all over the world with highly different light intensity (Jablonski & Chaplin 2000). That continuous variables, height, pubertal age and brain development, are multifactorially inherited and affected by epigenetic factors, was nicely demonstrated in the increase in height in Norway 1860-1960 with at the same time a reduction in pubertal age by 4yrs which may have affected the final stage in brain development. This created an increased need for brain food, N-3, to secure optimal brain function. Body growth is not brain growth. Given that the consumption of brain food (N-3) has declined to 20% only of the level 100yrs ago, what disorders are to be expected with an N-3 dietary deficit: in pregnancy, infancy and later in life? In this paper I discuss the significance of prepubertal selective pruning of excitatory synapses compared to delayed pruning and suggest relationships with brain disorders.

Adaptation, Physiological↗
PubMed2005

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. 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.

Adolescent↗
PubMed2004

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. Sudden Infant Death Syndrome victims have depressed birth weight, lower levels of marine fat in brainstem than controls, and >80 suffer multiple hypoxic episodes prior to death. Depressed birth weight (more than 10% below mean) is seen in learning and behaviour disorders, and a trend towards weights of less than 3kg is increasing, which supports a rise in antenatal sub optimality. Given marine fat deficiency in pregnancy and infancy, neurons starved for fuel could delay myelination and maturation in the latest developed Frontal Lobes. The phylogenetic oldest Lateral Frontal Lobe System (feed-back mechanism etc.) derived from olfactory bulb-amygdala, which crosses in Anterior Commisure is probably spared, while the Medial Frontal Lobe System derived from Hippocampus-Cingulum and crosses in Corpus Callosum (delayed response task) is most likely affected. The rise in infantile autism (intact vision and hearing) with deficit in delayed response task only, could suggest a deficit in the Medial Frontal Lobe System. The human species is unique; 70% of total energy to the foetus goes to development of the brain, which mainly consists of marine fat. It undergoes pervasive regressive events, before birth, in infancy and at puberty. Minimal retraction of neuronal arborisation is advantageous. Attributable to adverse pregnancy childrearing practice, excessive retraction is likely prenatally and in infancy. Pubertal age affects the fundamental property of nervous tissue, excitability: excessive excitatory drive is seen in early, and a deficiency in late puberty. It is postulated that with adequate marine fat, there is probably no risk of psychopathology at the extremes, whereas a deficiency could lead to paroxysmal (subcortical) dysfunction in early puberty, and breakdown of cortical circuitry and cognitive dysfunctions in late puberty. The post-pubertal psychoses, schizophrenia and manic-depressive psychosis at the extremes of the pubertal age continuum, with contrasting excitability and biological treatment, are probably the result of continuous dietary deficiency, which has inactivated the expression of genes for myelin development and oligodendrocyte-related genes in their production of myelin. The beneficial effect of marine fat in both disorders, in other CNS disorders as well as in developmental dyslexia (DD) and ADHD among others, supports our usual diet is persistently deficient. We have neglected the similarity of our great brain to other mammals, and our marine heritage. Given the amount of marine fat needed to secure normal brain development and function is not known, nor the present dietary level, it seems unduly conjectural to postulate that a dietary deficiency in marine fat is causing brain dysfunction and death. However, all observations point in the same direction: our diet focusing on protein mainly, is deficient, the deficiency is most pronounced in maternal nutrition and in infancy.

Adolescent↗
PubMed2003

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. Another environmental factor which has to be provided by diet is marine fat which our brain consists of. It normalizes brain function at all levels of excitability and possibly prevents psychotic episodes if adequately supplied. As part of Human Variation in Growth and Maturation, Schizophrenia and Manic-depressive psychosis are multifactorially inherited and share susceptibility loci. They are localized at the extremes of variation. Excitability, body-built, clinical picture and CNS finding accord with this, their phenotypic characteristics might prove valuable in a hunt for genes not common to both disorders.

Brain↗
PubMed2002

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. I argue against the commonly held view that this is mainly attributable to the four hundred years of traffic in men. According to the late K.O. Dike, middle men along the African coast barred foreign merchants from the hinterland, and because of this the social, political structure and sovereignty of the African states remained fundamentally unchanged during the period 1400-1807, whereas a few decades after colonisation the socio-political system collapsed and was replaced by a small rich elite and many poor, while resources were taken out of Africa. Present poverty and underdevelopment represent as great a challenge as the trade in slaves. As did the African Middle-Men of that time, African leaders now must unite in an ambitious and confident Pan-African Union demonstrating strength. Western countries should focus on reducing poverty and improving nutrition. This also makes terrorism and legal and illegal migration less likely. Education is important, but the West should not limit its effort to fighting illiteracy but should also support the establishment of institutions for higher education. Africa possessed optimal conditions and an enriched environment for human evolution. African Infant Precocity is a persistent example. The human brain, like other brains, consists 60% of poly-unsaturated fatty acids (Marine-Fat), the rest being water. A sufficient amount is required to secure optimal brain growth. It normalizes brain function, and prevents sudden cardiac and infant death, which have been increasing in Western societies. Humans are unique in having a mismatch between the need for brain food--marine fat--and our common high protein diet. Nowhere is the neglect of the brain greater than in pregnancy when protein is the only major nutrient considered. Declining levels of polyunsaturated fatty acids have been observed in human milk. Deficient intake could, if not corrected, gradually impair brain function as has been seen in animal experiments.

Africa↗