Fetal nutrition

Obesity is a condition that is influenced by genetic and environmental factors (such as energy intake and expenditure, fetal nutrition, culture). There are four major physiological causes of obesity endocrine disorders (growth hormone deficiency, Cushing syndrome), genetic syndromes (Prader-Willi syndrome or Alstrom syndrome), disorders of the central nervous system (tumor, trauma) or the most common cause, multifactorial or primary obesity (caused by an interaction of multiple genes). 

Barker DJ, Gluckman PD, Godfrey KM, Harding JE, Owens JA, Robinson JS. 1993. Fetal nutrition and cardiovascular disease in adult life. Lancet 341 938-941. 

Using labeled substances injected into the araniotic cavity, it has been demonstrated that the human fetus not only swallows amniotic fluid but also that the amount of amniotic fluid swallowed at term is as much as 220 to 750 ml per day (Gitlin et al., 1972 Plentl and Hutchinson, 1958 Plentl, 1958). This corresponds to 25 to 807o of the total amniotic fluid. Thus, fetal nutrition via the amniotic fluid should theoretically be possible. 

Nutritional Requirements. The nutrient requirements of mammalian cells are many, varied, and complex. In addition to typical metaboHc requirements such as sugars, amino acids (qv), vitamins (qv), and minerals, cells also need growth factors and other proteins. Some of the proteins are not consumed, but play a catalytic role in the cell growth process. Historically, fetal calf semm of 1—20 vol % of the medium has been used as a rich source of all these complex protein requirements. However, the composition of semm varies from lot to lot, introducing significant variabiUty in manufacture of products from the mammalian cells. 

While unnecessary medications clearly should be avoided during pregnancy or lactation, clinicians also should avoid undertreating conditions that can lead to adverse maternal, fetal, or infant outcomes. Additionally, clinicians should avoid unnecessarily discouraging breast-feeding because breast milk provides nutritional and immunologic benefit to the infant. 

Further research on the relationship between paternal lead exposure and fetal/infant development should be conducted. Additional information on relationships between nutritional deficits and vulnerability of the fetus and child to lead would be valuable. 

Wu G, Bazer FW, Cudd TA, Meininger CJ, Spencer TE Maternal nutrition and fetal development. J Nutr 2004 134 2169-2172. 

Although we have discussed briefly the implications of biochemical individuality for alcoholism, for gout, and for arthritis, these are merely examples. A host of other diseases need to be attacked with the same point of view and hold the same promise of success. These include multiple sclerosis, muscular dystrophy, myasthenia gravis, atherosclerosis, essential hypertension, ulcers, diabetes, epilepsy, rheumatic heart disease, nephrosis, liver cirrhosis, congenital heart disease (as well as a host of other malformations which probably involve nutritional deficiencies during fetal life) and even infective diseases such as tuberculosis or poliomyelitis. 

Valenzuela A. and Nieto M. S. (2001). Docosahexaenoic acid (DFIA) in fetal development and infant nutrition. Revista Med. Chile 129 1203-1211. 

Dr. Meskin s major areas of research interest include (1) hepatic drug metabolism and the effects of nutritional factors on drug metabolism and clearance (2) nutrient-drug interactions (3) the role of bioactive non-nutrients (phytochemicals, herbs, botanicals, and nutritional supplements) in disease prevention and health promotion (4) fetal pharmacology and fetal, maternal, and pediatric nutrition (5) nutrition education and (6) the development of educational programs for improving science literacy and combating health fraud. 

Vulnerability of developing brain Relative effects of growth restriction during the fetal and suckling periods on behavior and brain composition of adult rats, J. Nutrition, 103 (1973) 1327-1338. 

Bosley AR, Sibert JR, Newcombe RG (1981) Effects of maternal smoking on fetal growth and nutrition. Arch Dis Child, 56 727-729. 

There is thus ample evidence supporting the idea that GH regulates somatomedin C levels. In many respects it appears to be the major factor affecting these levels, but it should be stressed that other hormones (including thyroxine and insulin) and nutritional factors are also of considerable importance. The effects of GH on IGF-II levels are less important than those on somatomedin C placental lactogen may be more important here, in partial accordance with the idea that IGF-II is concerned particularly with the regulation of growth of fetal tissues. 

Kuna and Kapp (1981) found decreased fetal weight after exposure to 50 ppm and demonstrated that there was only 1 exencephalic rat in a group of 151 pups examined after in utero exposure to 500 ppm benzene. In the same study, of 98 pups examined for skeletal effects after in utero exposures of 500 ppm, only 1 pup had angulated ribs and 2 others had nonsequential ossification of the forefeet. These anomalies were not statistically significant and may have resulted from maternal nutritional stress. 

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