Talk:Infant growth and development: Difference between revisions

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"There are now many epidemiological studies (1-3) relating impaired fetal growth (deduced from birth weight or body proportions) to an increased incidence of cardiovascular disease or type 2 diabetes mellitus (T2D) or their precursors: dyslipidemia, impaired glucose tolerance, or vascular endothelial dysfunction. Disease risk is higher in those born smaller who become relatively obese as adolescents or adults (1). Interpretation of these studies has led to debate about the magnitude of the effect (4), although the only published estimate based upon a long-term Finnish cohort (3) suggests it to be substantial. Prospective clinical studies on children born small also provide support for the concept (6, 7)."...There have been several models proposed to explain the changing demography of "life-style" diseases such as T2D. The "thrifty genotype" concept (57) proposed that populations have been selected for alleles favoring insulin resistance. Such "thrifty genes" confer advantage in a poor food/high energy expenditure environment by reducing glucose uptake and limiting body growth. When individuals of this genotype encounter an environment of plentiful food/low energy expenditure, they are at risk of developing T2D and the metabolic syndrome (58). So although selection for these genes enabled our ancestors to survive as hunter-gatherers, they put modern humans at greater risk of disease, especially as our longevity increases. Because insulin is a fetal growth factor, selection for such genes might also induce lower birth weight (5). For example, mutation in the glucokinase gene produces reduced fetal growth and later insulin resistance independently (59).
"There are now many epidemiological studies (1-3) relating impaired fetal growth (deduced from birth weight or body proportions) to an increased incidence of cardiovascular disease or type 2 diabetes mellitus (T2D) or their precursors: dyslipidemia, impaired glucose tolerance, or vascular endothelial dysfunction. Disease risk is higher in those born smaller who become relatively obese as adolescents or adults (1). Interpretation of these studies has led to debate about the magnitude of the effect (4), although the only published estimate based upon a long-term Finnish cohort (3) suggests it to be substantial. Prospective clinical studies on children born small also provide support for the concept (6, 7)."...There have been several models proposed to explain the changing demography of "life-style" diseases such as T2D. The "thrifty genotype" concept (57) proposed that populations have been selected for alleles favoring insulin resistance. Such "thrifty genes" confer advantage in a poor food/high energy expenditure environment by reducing glucose uptake and limiting body growth. When individuals of this genotype encounter an environment of plentiful food/low energy expenditure, they are at risk of developing T2D and the metabolic syndrome (58). So although selection for these genes enabled our ancestors to survive as hunter-gatherers, they put modern humans at greater risk of disease, especially as our longevity increases. Because insulin is a fetal growth factor, selection for such genes might also induce lower birth weight (5). For example, mutation in the glucokinase gene produces reduced fetal growth and later insulin resistance independently (59).
===Brain development===
Kapellou O, Counsell SJ, Kennea N, Dyet L, Saeed N, et al.: Abnormal Cortical Development after Premature Birth Shown by Altered Allometric Scaling of Brain Growth
PLoS Medicine Vol. 3, No. 8, e265 doi:10.1371/journal.pmed.0030265

Revision as of 19:19, 17 April 2007


Article Checklist for "Infant growth and development"
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Checklist last edited by Versuri 13:49, 15 April 2007 (CDT)

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writing it rough, outline should be self-evident. This is aimed to be a guide for parents that is accurate enough for a pediatrician to use as a reference. Nancy Sculerati 15:31, 14 April 2007 (CDT)

Pelvic size

To address one of the concerns raised by Nancy on my talk page, (expressing the idea of the mother's narrow pelvic size when giving birth), I suggest the following change. In this sentence:

  • That means that big headed babies are born to mothers with pelvic structures adapted to walking upright, and if both mother and baby are to survive the birth process, that means the baby's brain is not fully developed in size — or complexity — at birth.

I suggest inserting "the relatively narrow" before "pelvic structures", to give:

  • That means that big-headed babies are born to mothers with the relatively narrow pelvic structures adapted for walking upright, and if both mother and baby are to survive the birth process, that means the baby's brain is not fully developed in size — or complexity — at birth.

(Also inserting a hyphen in "big-headed" and changing "adapted to" to "adapted for".) I was going to also suggest moving the paragraph beginning "Even with the relatively small head diameter of the newborn," to before the previous paragraph, to move it closer to the mention of pelvic opening size, but I see that it flows very nicely into the paragraph after it, so that would probably not be a good idea. --Catherine Woodgold 15:18, 15 April 2007 (CDT)

Catherine, I think your change may be excellent, but perhaps we can hold off till more of the article gets written, and then -depending on overall length, I'd appreciate your input (and others) from start to finish-did put "relatively" in there. Nancy Sculerati 20:53, 16 April 2007 (CDT)

References - with notes

Birth size-weight-composition

1)Bernstein I. Fetal body composition. Current Opinion in Clinical Nutrition & Metabolic Care. 8(6):613-7, 2005 Nov. UI: 16205461

"Under conditions of fetal undergrowth, identified as fetal growth restriction (most commonly defined when estimated fetal weights or birth weights are below some preset percentile (third, fifth or 10th) of standardized population specific norms), the perinatal mortality rate is 6–10 times greater than that for a normally grown population, 120 per 1000 for all cases of growth restriction and 60–80 per 1000 if anomalous infants are excluded [2]. As many as 40% of all stillborns are growth restricted, including 53% of preterm stillbirths and 26% of term stillbirths [3]. Additional risks of poor fetal growth include the neonatal complications of respiratory distress syndrome, hypoglycemia, hypocalcemia, hyperphosphatemia, polycythemia, hyponatremia and hypothermia [4–7]."..."Fetal overgrowth is variably characterized as either fetal macrosomia (estimated fetal weight or birth weight greater than 4 or 4.5 kg) or large for gestational age where weight exceeds the 90th percentile for population-based norms. The primary perinatal risks of fetal overgrowth include difficult deliveries, with an increased risk for both shoulder dystocia and Cesarean sections and the traumatic injuries that can result form these dystocias [8]. There is also an increased risk of metabolic abnormalities in macrosomic neonates. The neonatal metabolic risks include neonatal hypoglycemia, polycythemia, hyperbilirubinemia and disorders of calcium metabolism [9]."..."Despite these risks the majority of individual fetuses whose weight is either under or over the defined limits of normal have uncomplicated antenatal, intrapartum and neonatal courses. This association of the significant health consequences for abnormal growth and the poor predictive value of fetal weight for these complications has led to a search for alternative markers of fetal growth abnormality beyond estimates of fetal weight to try and improve the prediction of perinatal risk."..."Suggestions that estimates of fetal body composition might improve the prediction of specific perinatal risks arise from both the fetal undergrowth and overgrowth literature. The ponderal index was first described by Rohrer in 1921 as an index of corpulence [10]. This index of neonatal size (weight/length3) appears to accurately describe the nutritional state of the neonate."...Galan et al. [29], employing measures of the proximal extremities, has shown that the fetal growth restriction observed at altitude results from disproportionate reductions in fat mass and Padoan et al. [30•] have demonstrated that the fat mass compartment is disproportionately reduced in growth-restricted fetuses defined by weight.

2) Gluckman PD. Hanson MA. Living with the past: evolution, development, and patterns of disease. Science. 305(5691):1733-6, 2004 Sep 17. UI: 15375258

"In evaluating the relative role of genetic and environmental factors, it is useful to note that birth size has only a small genetic component and primarily reflects the quality of the intrauterine environment."

"There are now many epidemiological studies (1-3) relating impaired fetal growth (deduced from birth weight or body proportions) to an increased incidence of cardiovascular disease or type 2 diabetes mellitus (T2D) or their precursors: dyslipidemia, impaired glucose tolerance, or vascular endothelial dysfunction. Disease risk is higher in those born smaller who become relatively obese as adolescents or adults (1). Interpretation of these studies has led to debate about the magnitude of the effect (4), although the only published estimate based upon a long-term Finnish cohort (3) suggests it to be substantial. Prospective clinical studies on children born small also provide support for the concept (6, 7)."...There have been several models proposed to explain the changing demography of "life-style" diseases such as T2D. The "thrifty genotype" concept (57) proposed that populations have been selected for alleles favoring insulin resistance. Such "thrifty genes" confer advantage in a poor food/high energy expenditure environment by reducing glucose uptake and limiting body growth. When individuals of this genotype encounter an environment of plentiful food/low energy expenditure, they are at risk of developing T2D and the metabolic syndrome (58). So although selection for these genes enabled our ancestors to survive as hunter-gatherers, they put modern humans at greater risk of disease, especially as our longevity increases. Because insulin is a fetal growth factor, selection for such genes might also induce lower birth weight (5). For example, mutation in the glucokinase gene produces reduced fetal growth and later insulin resistance independently (59).

Brain development

Kapellou O, Counsell SJ, Kennea N, Dyet L, Saeed N, et al.: Abnormal Cortical Development after Premature Birth Shown by Altered Allometric Scaling of Brain Growth PLoS Medicine Vol. 3, No. 8, e265 doi:10.1371/journal.pmed.0030265