Undernutrition and Brain Development

Balázs, R.; Jordan, T. C.; Lewis, Paul D.; Patel, Ambrish J.

doi:10.1007/978-1-4615-7198-8_18

“…The foetus is not a perfect parasite, and has few strategies to deal with reduced nutrient supply due to dietary restriction. The major strategy for protection is a redistribution of blood flow to maintain placental, cardiac and cerebral blood flow (53)(54)(55). If this strategy is maintained over time it leads to somatic growth retardation with relative sparing of brain growth (53).…”

Section: Non-optimal Foetal Growthmentioning

confidence: 99%

“…The periods of inhibition increase towards the end of gestation and the foetus is in effect an obligatory anaerobe during delivery. This is safe provided there is a sufficient substrate for anaerobic metabolism via glycogen and subcutaneous fat stores (sometimes assessed by skinfold thickness) to provide ketones (54).…”

Section: Fast Foetal Growth -The Role Of Fatmentioning

confidence: 99%

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

Lf

¹

1999

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Saugstad LF. Optimality of the birth population reduces learning and behaviour disorders and sudden infant death after the first month. Acta Paediatr 1999; Suppl 429: 9-28. Stockholm. ISSN 0803-5326The 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 (b3500 g) 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. Minor environmental intervention almost eliminated excess mortality from this cause, supporting raised susceptibility with a depressed birthweight in postneonatal SIDS. This contrasts with classical neonatal low birthweight SIDS, which is stable despite numerous attempts at reduction, supporting a multifactorial aetiology: low maternal age, low education, low socioeconomic status, maternal smoking, infection, etc. The postneonatal SIDS epidemic associated with a deficit in heavy newborns is thought to be a result of changing behaviour in pregnancy: moderate iatrogenic dietary restriction and young women favouring a low-calorie, low-fat diet, especially in the third trimester when the foetus is most vulnerable, which delays myelination and somatic growth and renders the infant susceptible to minor morbidity and irregularity. The timing of death and neuropathological findings suggestive of repeated hypoxic episodes in more than 80% of cases of SIDS prior to death support this theory. The similar weight distribution patterns in SIDS and all births in Denmark, the UK and the USA suggest a substantial proportion of the neonates in these countries could be growthretarded and at risk of hypoxic episodes in infancy. A few cases, particularly males (sexratio = 1.7), suffer SIDS, the majority survive. Many, mostly males, present minor CNS signs and learning and behaviour problems. The male predominance accords with males more than 500 g higher optimal birthweight than females and susceptibility to a depressed weight at birth. In order to prevent postneonatal dying, SIDS and reduce learning/behaviour disorders it is necessary to raise the proportion of heavy newborns by promoting foetal growth rate equal to the maternal intrinsic rate by eating to one's appetite a balanced diet, favouring a diet high in marine fat, especially in third trimester, in order to ensure maturation of the CNS and prolong gestation, thereby increasing birthweight. Although the increased survival of some very low birthweight neonates confounds the issue, a division between SIDS in neonatal and postneonatal death is recommended in order to assess the proportion of "avoidable infant death" as opposed to persistent clas...

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“…The major strategy for protection is a redistribution of blood flow to maintain placental, cardiac and cerebral blood flow (53)(54)(55). The major strategy for protection is a redistribution of blood flow to maintain placental, cardiac and cerebral blood flow (53)(54)(55).…”

Section: Non-optimal Foetal Growthmentioning

confidence: 99%

“…The adversity of the high protein diet might be attributable to a lack of, or negligible amount of, unsaturated fatty acids. This is safe provided there is a sufficient substrate for anaerobic metabolism via glycogen and subcutaneous fat stores (sometimes assessed by skinfold thickness) to provide ketones (54). The supply depending on maternal nutrition also requires an adequately functioning utero-placental unit.…”

Section: Postnatal Retardation Of Somatic Growth In Sids Victimsmentioning

confidence: 99%

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

Saugstad¹

1999

View full text Add to dashboard Cite

Saugstad LF. Optimality of the birth population reduces learning and behaviour disorders and sudden infant death after the first month. Acta Paediatr 1999; Suppl 429: 9-28. Stockholm. ISSN 0803-5326The 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 (b3500 g) 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. Minor environmental intervention almost eliminated excess mortality from this cause, supporting raised susceptibility with a depressed birthweight in postneonatal SIDS. This contrasts with classical neonatal low birthweight SIDS, which is stable despite numerous attempts at reduction, supporting a multifactorial aetiology: low maternal age, low education, low socioeconomic status, maternal smoking, infection, etc. The postneonatal SIDS epidemic associated with a deficit in heavy newborns is thought to be a result of changing behaviour in pregnancy: moderate iatrogenic dietary restriction and young women favouring a low-calorie, low-fat diet, especially in the third trimester when the foetus is most vulnerable, which delays myelination and somatic growth and renders the infant susceptible to minor morbidity and irregularity. The timing of death and neuropathological findings suggestive of repeated hypoxic episodes in more than 80% of cases of SIDS prior to death support this theory. The similar weight distribution patterns in SIDS and all births in Denmark, the UK and the USA suggest a substantial proportion of the neonates in these countries could be growthretarded and at risk of hypoxic episodes in infancy. A few cases, particularly males (sexratio = 1.7), suffer SIDS, the majority survive. Many, mostly males, present minor CNS signs and learning and behaviour problems. The male predominance accords with males more than 500 g higher optimal birthweight than females and susceptibility to a depressed weight at birth. In order to prevent postneonatal dying, SIDS and reduce learning/behaviour disorders it is necessary to raise the proportion of heavy newborns by promoting foetal growth rate equal to the maternal intrinsic rate by eating to one's appetite a balanced diet, favouring a diet high in marine fat, especially in third trimester, in order to ensure maturation of the CNS and prolong gestation, thereby increasing birthweight. Although the increased survival of some very low birthweight neonates confounds the issue, a division between SIDS in neonatal and postneonatal death is recommended in order to assess the proportion of "avoidable infant death" as opposed to persistent clas...

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“…(Pediatr Res 35: 640-648,1994) Abbreviations BBB, blood-brain barrier IUGR, intrauterine growth retardation or retarded Early restriction of nutrients during perinatal life may have considerable influence on somatic development and may result in permanent alterations in mammalians (1, 2). Although the brain is protected by several homeostatic mechanisms against major fluctuations in the availability of essential nutrients (3), numerous studies have shown severe impairment of the CNS consecutive to undernutrition (4)(5)(6)(7). Perinatal life appears as a vulnerable period of development during which several organs, including brain with some late maturation structures, are sensitive to nutrient supply.…”

mentioning

confidence: 99%