As noted above, the type of carbohydrate intake directly influences birth weight and maternal weight gain, by influencing maternal blood glucose levels and insulin sensitivity. Clapp (2006) sets this out very clearly and his definition of low-glycaemic sources vs high glycaemic sources are reproduced in Table 1. This is not entirely straightforward as the accompanying notes suggest.
Eating primarily high-glycaemic carbohydrate results in feto-placental overgrowth and excessive maternal weight gain, while intake of low-glycaemic carbohydrate produces infants with birth weights between the 25th and the 50th percentile and normal maternal weight gain. Clapp’s study showed that women who reported eating carbohydrates mainly of low-glycaemic index gained less
weight and had smaller babies than women who ate primarily high glycaemic types of carbohyd-rates. When he randomised women to a high or low glycaemic diet, the women who were randomised to the high glycaemic diet had increased 1, 2 and 3 hour postprandial glucose
levels and insulin levels throughout pregnancy. They experienced larger weight gain and symmetrically larger infants and placentas. Interestingly, total calorie intake was 14% more on the LOW glycaemic index diet. The data indicate that a large part of the normal variance in
birth weight is related to differences in type of maternal dietary carbohydrate intake. Low-glycaemic food sources in the diet decrease growth rate and size at birth while high-glycaemic food sources increase it. Thus, extrapolating the findings to current care in pregnancy, in
the absence of severe malnutrition, it may be possible to decrease the need for CS in both healthy, low-risk women and a variety of high-risk populaces by simply modifying maternal physical activity and the type of carbohydrate eaten during pregnancy.
Despite the above scientific evidence, none of the eight papers associating 4000g babies with failed TOL, proposed low glycaemic diets as a possible means to prevent VBAC failure. One possible explanation is that both practitioners and researchers consider pregnant women unable to discipline themselves as far as diet and exercise, or perhaps even more worryingly, that such an essential aspect as diet and nutrition is not actually considered part of medical enquiry into well-being and preventive health measures. At the same time as dismissing women as unable to diet, or advising them against it, women are warned that dieting will produce a birth weight <2500g, which will increase the risk of stillbirth. This builds on the myth that bigger is always better/healthier, perhaps also confusing a smaller size as indicating poor growth and less healthy (small for gestational age (SGA)) without examining the cause. Such approaches do not reflect the current scientific evidence nor do they reflect the potential role for inquiry into the make up of the woman’s pre-pregnancy nutrition or diet during pregnancy.
SGA babies are known to have a higher stillbirth rate and higher morbidity and mortality rate after birth (Vashevnik et al 2007). The diverse causes of SGA in babies range from heart malformations, blood disorders, viral infections, maternal smoking, drug abuse, anaemia and malnutrition (Frøen et al 2004, Kalanda et al 2006). Neither stillbirth nor IUGR have been associated with balanced, low glycaemic diets in singleton pregnancies not complicated by smoking, drug abuse or pre-pregnancy
malnutrition (Kramer & Kakuma 2003). When prepregnancy malnutrition is present, high energy intake is associated with a reduced risk of preterm birth (Smith 2004). A seminal study of pregnant women affected by near starvation diets during the third trimester as a result of the German military regime at the latter part of the Second World War found a clear reduction in fetal growth,
but no effect on gestational duration (Stein et al 1995, Smith 2004). Cedegren (2004), in a careful summary of the sparse knowledge in the Western literature regarding fetal growth impairment, identified the following:
1. Small crown-rump length (CRL) measurements on first trimester ultrasounds appear to have some ability to predict low birth weight babies (<2500g). (No connection made to diet).
2. A suboptimal environment in the first trimester may permanently affect the fetus to restrict its growth potential. However, it is unknown whether a suboptimal environment is connected to
diet and/or genetics of the mother and/or fetus and/or environmental influences and
if so which?
The only evidence directly relating diet and poor outcomes is a single study in sheep who were either fed ad lib or undernourished to reduce the sheep’s weight by 15% from 60 days before until
30 days after conception (term = 145 days), comparable to a woman losing 20 pounds during the two months before conception (Bloomfield et al 2003). Periconceptual under-nutrition in sheep was associated with an increased risk of noninfectious preterm birth possibly related to premature
activation of the fetal hypothalamic-pituitary-adrenal axis. In layman’s terms this translates into long term starvation diets causing long term adrenaline/cortisol release by the fetus, causing preterm labour. This can hardly refer to obese women eating brown rice instead of white bread, or
eating a peach instead of half a cake with chocolate icing.
Тема: Роды после кс и питание (Прочитано 24410 раз)