Nutritions taken during pregnancy can have significant and lasting effects on maternal and newborn health. If associated with pathophysiological changes that occur during pregnancy, this may result in epigenetic changes with insufficient or excessive nutritional intake, short- and long-term adverse effects on the fetus. Optimum energy and nutrient intake during pregnancy and lactation is essential for initiating and maintaining a healthy life during childhood. It may also protect against several adult diseases.
Zinc is essential for normal fetal growth and development and is a component of more than 200 enzymes involved in the formation and release of various proteins, hormones, and neuropeptides. component. The element is involved in the transcription process where the DNA sequence of a gene is copied to make an RNA molecule. Zinc is essential for proper cell division, growth and differentiation. Severe zinc deficiency is embryotoxic and teratogenic and can cause fatal fetal developmental and structural anomalies. It has been shown that maternal zinc deficiency can affect embryonic protein and DNA synthesis and cause chromosomal damage characterized by terminal deletion.
If maternal zinc deficiency is short-lived, cell cycle may not be adversely affected. Zinc deficiency results in increased oxidative stress and teratogenicity, while the formation of free radicals increases in these membranes, the intracellular regions of redox-active metals such as copper and iron, nonbinding. Zinc can inhibit the oxidation of numerous proteins, including zinc finger transcription factors of redox-sensitive cysteine and sulfhydryl groups. It is a metal binding protein. Metallothionein releases zinc, which plays a central role in the antioxidant defense system during oxidative stress. As shown in both animals and humans, insufficient maternal zinc intake leads to a decrease in circulating zinc levels, which can adversely affect fetal neural tube development. In humans, it has been found that the risk of neural tube defects is increased in women with acrodermatitis enteropathica, a rare genetic disorder of zinc metabolism.
It is stated that the prevalence of neural tube defects is higher in Africa and the Middle East where zinc intake is chronically low for ecological reasons.It also has a protective effect against heart diseases. This reduces the risk of delivery in infants with neural tube disorders (Spina bifida), obstructive urinary tract anomalies, leg deficiencies, orofacial clefts, and congenital hypertrophic pyloric stenosis. After absorption of folic acid, it is transported as monoglutamate in the blood and converted into various compounds, the most important of which is the reductase enzyme tetrahydrofolate (THF). sees. Research on the effect of folic acid on NTD began in the 1980s, when studies showed that FA was effective in preventing both primary NTD and its recurrence. In a multicenter randomized controlled study including 1200 women with a history of NTD in previous pregnancies, starting 0.4 mg/day FA intake at least 1 month before conception and continuing in the first 3 months of pregnancy reduced the risk of pregnancy. In a cohort study involving approximately 250,000 women in China, maternal intake of 0.4 mg of folic acid was shown to reduce the risk of NTD in the fetus by 85% in high-prevalence regions and 40% in low-prevalence regions.The use of folic acid antagonist drugs, which cause inhibition of the dihydrofolate reductase enzyme, increases the frequency of CHD.
The discovery of insulin in 1922, developments in obstetrics and neonatal intensive care, complications complicated with diabetes mellitus reduced perinatal mortality in pregnancies approximately 30 times. By maintaining maternal euglycemia, such pregnancies were able to continue into term and resulted in a reduction in complications related to prematurity, including respiratory distress syndrome. Nevertheless, perinatal mortality in diabetic women remains approximately twice that of non-diabetic women. In addition, spontaneous abortion rates are higher in diabetic women, especially if glycemic control is sub-optimal during the periconceptional period. Increased ROS concentrations cause organ malformation and birth defects through membrane changes, mitochondrial dysfunction, and initiation of aberrantly programmed cell death (apoptosis).
If appropriate glycemic control is achieved during the third and sixth weeks of pregnancy, that is, when the embryo is most sensitive to teratogens, the rates of congenital anomalies will be the same as in the general population. The antioxidant vitamins E and C have been shown to reduce abnormalities associated with hyperglycemia in animal models, and some prostaglandins may have the same effects. The incidence of congenital anomalies, which is 1-2% in the general population, is 4-8 times higher in babies of mothers with pregestational diabetes.
Congenital anomalies are the most important cause of perinatal death in pregnancies complicated by diabetes mellitus. Although anomalies can be seen in all organ systems in newborns of diabetic mothers, the most important ones are anomalies in the heart and central nervous system. Caudal regression syndrome is a rare congenital anomaly caused by maternal diabetes. The absence of an increase in the rate of congenital anomalies in normoglycemic mothers or those with gestational diabetes after the first trimester reiterates that glycemic control during embryogenesis plays an important role in the pathogenesis of fetal anomalies. It has been found that congenital anomalies are more common in pregnant women with high HbA1c levels in the first trimester, and this is directly related to its level and anomaly rate.
Maternal Phenylketonuria (PKU)
Increased phenylalanine levels are toxic and teratogenic to the developing fetus. Spontaneous abortions occur in 24% of pregnancies with phenylketonuria, and in survivors, microcephaly offsprings in 40%, mental retardation in 73%, 92%, congenital heart diseases in 12%, and intrauterine growth retardation. If maternal phenylalanine levels are well controlled before and during pregnancy, the incidence of microcephaly and abnormal physical and neurological fetal development is significantly reduced. the risk does not increase. Babies of mothers whose phenylalanine levels exceed 360 µmol/L during pregnancy are at higher risk of disease. Serious congenital heart diseases have been reported in babies born to untreated pregnant women with high blood phenylalanine levels, especially if dietary restriction was not initiated until the 7th and 18th weeks of pregnancy. However, there is no increased risk in pregnant women with a phenylalanine level of 120-360 mol/L in the first 8 weeks of pregnancy.
In pregnant women with phenylketonuria, (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin is an orally active synthetic form. Sapropterin dihydrochloride has been used at doses up to 20 mg/kg/day.Large neutral amino acid (LNAA) therapy, which is one of the other dietary alternatives used in patients with phenylketonuria, is contraindicated in pregnancy because it does not reduce blood phenylalanine levels to safe levels.
Infectious pathogens, especially Congenital anomalies caused by intrauterine exposure to certain viruses, vaccines (effective against rubella, varicella-zoster and hepatitis B viruses), drugs (herpes, toxoplasma and HIV), are specific and sensitive immunological diagnostic tests for most. With the aid of highly sensitive diagnostic procedures, the incidence of intrauterine infection during pregnancy is estimated to be approximately 12-20%. These infections cause a wide variety of major anomalies and dysfunctions, including deafness, blindness, neurodevelopmental abnormalities, growth retardation, and congenital heart defects. These diseases have traditionally been covered under the heading of the TORCH complex, which represents toxoplasmosis.The fetus does not synthesize IgG and cannot adequately synthesize IgM and IgA until the second half of pregnancy. It has a very weak cellular immunity and insufficient production of necessary cytokines. While some pathogens can infect the mother and placenta without showing clinical signs in the mother, they may result in miscarriage, congenital anomalies, preterm birth, fetal hydrops and premature rupture of membranes.
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