The theory on establishment of programmed in the fetal period and chronic diseases haven’t still given out anything clearly but in most of studies, they showed that there is a relation between fetal growing with cardiovascular diseases, hypertension and metabolic syndrome. Its establishment of programmed in fetal period doesn’t replace other risk factors but adding more the environmental factor to these diseases. Currently, the important of fetal nutrition and mother nutrition in pregnancy period are paid attention as well as other nutrition issue in the transition period.
Nutrition Therapy ; Cardiovascular Diseases ; Chronic Disease ; Fetal Nutrition Disorders

OBJECTIVE: To study the application of ponderal index (PI), body mass index (BMI), mid-arm circumference/head circumference (MAC/HC), and Clinical Assessment of Nutritional Status (CANS) score in assessing the nutritional status of neonates at birth, and to find a simple and reliable scheme for the assessment of fetal nutritional status. METHODS: PI, BMI, MAC/HC, and CANS were used to assess the nutritional status of full-term infants and preterm infants shortly after birth. The assessment results of these methods were analyzed. RESULTS: Among the 678 full-term infants, 61, 102, 47, and 131 were diagnosed with malnutrition by PI, BMI, MAC/HC, and CANS respectively. Among the 140 preterm infants, 30, 87, 9, and 112 were diagnosed with malnutrition by PI, BMI, MAC/HC, and CANS respectively. The combination of BMI and CANS had a detection rate of 99.3% in full-term infants and 100% in preterm infants. Compared with the single method, the combination significantly improved the detection rate of malnutrition ( CONCLUSIONS The combination of BMI+CANS can reduce the rate of missed diagnosis of fetal malnutrition. It is therefore a simple and reliable method for the assessment of fetal malnutrition.
Body Mass Index ; Fetal Nutrition Disorders/diagnosis* ; Humans ; Infant, Newborn ; Infant, Premature ; Nutrition Assessment ; Nutritional Status

The “Barker hypothesis” postulates that a number of organ structures and associated functions undergo programming during embryonic and fetal life, which determines the set point of physiological and metabolic responses that carry into adulthood. Hence, any stimulus or insult at a critical period of embryonic and fetal development can result in developmental adaptations that produce permanent structural, physiological and metabolic changes, thereby predisposing an individual to cardiovascular, metabolic and endocrine disease in adult life. This article will provide evidence linking these diseases to fetal undernutrition and an overview of previous studies in this area as well as current advances in understanding the mechanism and the role of the placenta in fetal programming.
Adult ; Chronic Disease ; Critical Period (Psychology) ; Embryonic and Fetal Development ; Endocrine System Diseases ; Fetal Development* ; Fetal Nutrition Disorders ; Humans ; Malnutrition ; Placenta

Persistent organic pollutants (POPs) are known to cause mitochondrial dysfunction and this in turn is linked to insulin resistance, a key biochemical abnormality underlying the metabolic syndrome. To establish the cause and effect relationship between exposure to POPs and the development of the metabolic syndrome, Koch's postulates were considered. Problems arising from this approach were discussed and possible solutions were suggested. In particular, the difficulty of establishing a cause and effect relationship due to the vagueness of the metabolic syndrome as a disease entity was discussed. Recently a bioassay, aryl-hydrocarbon receptor (AhR) trans-activation activity using a cell line expressing AhR-luciferase, showed that its activity is linearly related with the parameters of the metabolic syndrome in a population. This finding suggests the possible role of bioassays in the analysis of multiple pollutants of similar kinds in the pathogenesis of several closely related diseases, such as type 2 diabetes and the metabolic syndrome. Understanding the effects of POPs on mitochondrial function will be very useful in understanding the integration of various factors involved in this process, such as genes, fetal malnutrition and environmental toxins and their protectors, as mitochondria act as a unit according to the metabolic scaling law.
Biological Assay ; Cell Line ; Fetal Nutrition Disorders ; Insulin ; Insulin Resistance ; Jurisprudence ; Mitochondria

Metabolic syndrome comprises central obesity, dyslipidemia, hypertension, glucose intolerance, and insulin resistance. Children sometimes develop metabolic syndrome, and it is strongly associated with the same syndrome in adulthood. Recently, there is evidence that obesity and metabolic syndrome originate from fetal life. Possible explanations of fetal and developmental origin of metabolic syndrome are the thrifty genotype and thrifty phenotype hypothesis, which together confer insulin resistance on developing fetus. Poor nutrition in utero as well as extrauterine growth restriction of preterm infants are important triggers of this hypothesis. Like metabolic syndrome in adulthood, the high levels of inflammatory cytokines and adipokines are certainly characteristic in pediatric patients. Increased fat mass was also observed in these patients, although their birth weight was lower than average. The mitochondrial genome is responsible for the inheritance of obesity from the maternal line. This can be a key as to why the phenotypes of obesity and metabolic syndrome start in fetal life with an association with poor maternal nutrition. In such circumstances, catch-up growth with an over-nutrition strategy can aggravate those features, suggesting that rapid catch-up growth in early infancy should not be encouraged.
Adipokines ; Birth Weight ; Child ; Cytokines ; Dyslipidemias ; Fetal Nutrition Disorders ; Fetus ; Genome, Mitochondrial ; Genotype ; Glucose Intolerance ; Humans ; Hypertension ; Infant, Newborn ; Infant, Premature ; Insulin Resistance ; Obesity* ; Obesity, Abdominal ; Pediatric Obesity ; Phenotype ; Wills