Chronic alcohol abuse may result in a wide spectrum of secondary disturbances of the absorption and utilisation of many nutrients, including glucose, amino acids, fat, sodium, and some vitamins (especially thia-min, vitamin B12, and folate). The inhibition of folate absorption by alcohol is of particular concern because of the risk of neural tube defects associated with an inadequate supply of this vitamin to the fetus before conception and during the first trimester of pregnancy. Alcohol may also directly impair the pla-cental transfer of nutrients essential for growth
Table 2 Foods to avoid during pregnancy to minimize the risk of food-borne infections
Undercooked meats, poultry, eggs, fish (e.g., smoked salmon or trout, sushi), and shellfish (e.g., oysters) Cook-chill meals and ready-to-eat poultry, unless they have been reheated until very hot Raw egg or uncooked eggs or foods made from them, such as homemade mayonnaise, soft-whip ice cream, cake mix, mousses, and hollandaise sauce (eggs should be cooked until both the white and yolk are solid) Unwashed fruit and vegetables All types of pate (including vegetable) Soft, mould-ripened, or blue-veined varieties of cheese (e.g., Brie, Camembert, and Stilton) (foods containing these cheeses that have been properly cooked will be safe to eat)
Table 3 Symptoms of fetal alcohol syndrome (FAS)a
Prenatal and postnatal growth retardation
Intrauterine growth retardation, including smaller than normal head circumference, continued growth below the 10th centile, and failure to thrive
Central nervous system involvement
Neurological abnormalities, developmental delay, intellectual impairment, brain malformation, and hearing and visual disabilities Physical anomalies
Characteristic facial deformity, including short upturned nose, receding forehead, and chin, smaller than normal eye appertures, absent philtrum, and asymmetrical ears aThe diagnosis of FAS requires signs in all three of the categories.
(e.g., amino acids), which at critical phases of fetal organogenesis could compound any direct fetotoxic effects of ethanol or acetaldehyde.
Both alcohol and its primary metabolite, acetaldehyde, are teratogenic. Excessive alcohol consumption (>80 g of ethanol or 10 units per day) during pregnancy can result in a child being born with a specific combination of physical and mental disabilities known as fetal alcohol syndrome (FAS). Such fetuses usually survive until birth but are growth retarded and display a characteristic range of clinical features, principally craniofa-cial abnormalities and neurological damage (Table 3).
It is estimated that 1 in 1000 infants worldwide are affected with the full syndrome, whereas 3 in 1000 may exhibit only some features. The damage varies depending on the stage of development at which high doses of alcohol are encountered. The fetus is most vulnerable to organ damage from the time the umbilical cord begins to function (5 weeks) to the completion of organ development (11 weeks). Inhibition of growth and neurobehavioral development occurs in the second and third trimester. Although the facial features of FAS become more subtle with age, growth deficits and central nervous system impairment may be permanent.
FAS is only seen in infants born to women who are excessive drinkers, but it is not an inevitable result of heavy drinking in pregnancy, and even children born to mothers who are active alcoholics may not show it. This differing susceptibility of fetuses to the syndrome is thought to reflect the interplay of genetic factors, social deprivation, nutritional deficiencies, and tobacco and other drug abuse, along with alcohol consumption.
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