The McCarrison Society - NL 40/1: Special Generating Healthy Brains Edition

NL 40/1: Special Generating Healthy Brains Edition

Article Index
NL 40/1: Special Generating Healthy Brains Edition
Chairman's comments
GHB Special Report On The McCarrison Society
GHB:Report by Conference Organiser Rev Simon House, MA
GHB: Preconception to late adolescence:
GHB: From past to present: evolution and epigenetics
GHB: CLEAVE LECTURE Nutrition, the brain and mental ill health
GHB: Our changing diet; deficits and disorders
GHB: Genomic imprinting for brain development and behaviour
GHB: 'Brainfoods': Modulating brain structure and function
GHB: The effects of maternal anxiety or stress during pregnancy
GHB: Cornerstones in the Psychobiological Development of Mankind:
GHB: A psycho-soma integration perspective
GHB: 'New Parenting', psychotherapy, prenatal
GHB: Attention deficit disorders
GHB: Priorities in Research Funding
GHB:Into the future; avoiding the cost of folly
GHB: References
News
Mind What You Eat
McCarrison meeting with Sustain
Future Events

Page 9 of 22

GHB: The significance of genomic imprinting for brain development and behaviour.

Professor Barry Keverne FRS, FMedSci – Behavioural Neuroscience, King's College, Cambridge, described how genetic imprinting provides for outstanding co-adaptation of mother and foetus, for maternal provision and foetal use of resources. On the other hand it is open to genetic transmission of clinical disorders, for instance Prada-Willli syndrome leading to obesity, and Angelman’s syndrome with unusual behaviour. Genetic imprinting only evolved in mammals and the placenta is deeply involved.

Imprinting also explains the much greater variety of species from such a small percentage difference in genes, and the small number of human genes that so surprised scientists of the Human Genome Project.

There are certain genes in mammals that are only expressed if inherited from one parent rather than from the other. More often the paternal gene – allele – is expressed which means that the maternal allele is silenced, usually by methylation, bonding of a CH3 group.

Genomic imprinting, distinct from epigenesis, occurs in germ-line cells, with transgenerational effect. Epigenesis, in somatic cells, genetically affects the individual only, though if it causes a change of behaviour – better mothering say – that can affect the next generation culturally. Imprinting is reversible and there is no change in the gene sequence, unlike mutation.

Genomic imprinting acts primarily through key regulatory genes that in turn have a cascade effect through other genes. Possible effects vary widely, for instance the mother’s food intake and weight gain; maternal fat and blood glucose; letdown of milk and post-natal pup growth. Other affects include her maternal behaviour, nest-building, and placental hormones, placental blood flow and nutrient transfer, foetal growth, and early weaning and puberty onset.

In these ways the placenta enables the foetus to regulate its own destiny, mainly by genomic co-adaptation affecting hormonal action on receptors in the maternal hypothalamus. The two genomes, infant and maternal, are co-
adaptive for infant well-being and reproductive success. Offspring that have extracted “good” maternal nurturing will be genetically predisposed towards good mothering.

Early foetal mortality helps selection for fitness. Through imprinting, a gene contributing to fitness is established in the population more quickly, especially when paternally expressed.

Although imprinting affects hormonal activity and nutrient metabolism, there is no evidence that hormones or nutrients affect genomic imprinting. Hormones and nutrients can, particularly in early life, epigenetically affect the individual’s future life for better or for worse, and seriously contribute to obesity.

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