South African Medical Journal = Suid-Afrikaanse Tydskrif Vir Geneeskunde
Of all the theories purporting to uncover the roots of childhood behaviour and its extension into adult behaviour, the most cogent relates to the physical and psychological bonds of attachment between infant and mother. It is helpful to divide the human lifespan into three periods, each of which has alternating phases of attachment and detachment.
Current nutrition theory holds that maximization of human growth and stature is a desired anthropometric outcome. However, some evidence demonstrates that lower energy intakes may actually confer a degree of future protection against degenerative processes, particularly atherosclerosis and cancer.
Biological Reviews of the Cambridge Philosophical Society
Fetal growth and development is dependent upon the nutritional, hormonal and metabolic environment provided by the mother. Any disturbance in this environment can modify early fetal development with possible long-term outcomes as demonstrated by extensive work on 'programming'. Growth restriction resulting from a deficit in tissue/organ cell number (as measured by tissue DNA content) is irrecoverable. However, when the cell size (or cell protein content) is reduced, the effects on growth may not be permanent.
Inborn errors of the pyruvate dehydrogenase complex (PDC) are associated with lactic acidosis, neuroanatomic defects, developmental delay, and early death. PDC deficiency is a clinically heterogeneous disorder, with most mutations located in the coding region of the X-linked alpha subunit of the first catalytic component, pyruvate dehydrogenase (E1). Treatment of E1 deficiency hs included cofactor replacement, activation of PDC with dichloroacetate, and ketogenic diets. In this report, we describe the outcome of ketogenic diet treatment in seven boys with E1 deficiency.
BACKGROUND: Latino children are at increased risk for mirconutrient deficiencies and problems of overweight and obesity. Exposures in pregnancy and early postpartum may impact future growth trajectories. OBJECTIVES: To evaluate the relationship between prenatal and postnatal maternal depressive symptoms experienced in pregnancy and infant growth from birth to 2 years of age in a cohort of Latino infants. METHODS: We recruited pregnant Latina mothers at two San Francisco hospitals and followed their healthy infants to 24 months of age.
This article, based more on speculation than on clinical work, aims at clarifying the nature of child autistic syndromes using two elements: epigenetic findings concerning the construction of human brain and the idea that there is a self-organizing development and functioning of the living. First initiated by H. Atlan (1979) and A. Bourguignon (1981), this approach could lead to a fruitful understanding of autistic disturbances, both consistent with developmental neurobiology and psychodynamics.
The diversity of theories regarding children's development is commensurate with the enormity of the task of seeking ordering designs for explaining behavioral and psychic ontogeny in infants, children, and adults. The purpose of this paper is to look at these developmental theories as epigenetic stages themselves. I shall suggest that the next stage in the epigenesis of theories of development is to see variability and disorder on a continuum with order and stability, as a constant dialectic that moves development along, whether at the level of the cell or at the level of fantasy.
This mini-review describes recent discoveries demonstrating that experience can drive the production of epigenetic marks in the adult nervous system and that the experience-dependent regulation of epigenetic molecular mechanisms in the mature central nervous system participates in the control of gene transcription underlying the formation of long-term memories. In the mammalian experimental systems investigated thus far, epigenetic mechanisms have been linked to associative fear conditioning, extinction of learned fear, and hippocampus-dependent spatial memory formation.
Epidemiological evidence links exposure to stress hormones during fetal or early postnatal development with lifetime prevalence of cardiac, metabolic, auto-immune, neurological and psychiatric disorders. This has led to the concept of 'developmental programming through stress'. Importantly, these effects (specifically, hypertension, hyperglycaemia and neurodevelopmental and behavioural abnormalities) can be reproduced by exposure to high glucocorticoid levels, indicating a crucial role of glucocorticoids in their causation.
Research in the last decade has advanced our knowledge about biological factors underlying neurodevelopmental processes in childhood. Genetic research has gone beyond mapping the human genome to identifying epigenetic factors and explicating gene-environment interactions. Biological markers of vulnerability to specific disorders have been identified.