The dissertation is devoted to the reduction of the frequency of obstetric and perinatal complications in women with pathological gestational weight gain (GWG) by studying new aspects of pathogenesis based on the relationship between social-demographic, medical-biological and genetic factors, psycho-emotional state, genetic determinism, eating behavior, physical activity level, changes in carbohydrate, lipid and adipokine metabolism with the dynamics of the body composition components, and improvement of diagnostic algorithm, risk factors, introduction of a complex of preventive measures. There were determined the main risk factors and structure of pathological gestational weight gain. It is shown that pathological weight gain is associated with high psycho-emotional stress, which causes the behavior dysadaptive forms during pregnancy and leads to complicated pregnancy. The concept of genetic predisposition to the development of excessive gestational weight gain based on the study of the clinical and prognostic role of polymorphisms of PPAR Pro12Ala, LEPR Q223R, еNOS Glu298Asp genes in the genesis of metabolic disorders and endothelial dysfunction was offered. It was demonstrated an association between polymorphic variants of Pro/Ala and Ala/Ala PPAR- , GG of the LEPR gene and preeclampsia, macrosomia, postpartum delayed weight reduction. Carriers of TT - Glu298Asp (G894T) gene polymorphism eNOS have a tendency to develop gestational hypertension, preeclampsia, fetal growth retardation and postpartum delayed weight reduction. The results of the analysis of the quality of women's counseling about weight gain as a routine component of antenatal care have revealed an insufficient level of knowledge of both patients and professionals about the gestational weight gain and postpartum weight retention preventive measures. The association between the concentrations of carbohydrate, lipid and adipokine metabolism, inadequate growth of body fat mass and shifts in the water sectors of the body with pathological weight gain and gestational pathology has been proved. The body composition was calculated on the basis of bioelectrical impedance analysis and it was shown that the recommended gestational weight gain is characterized by an increase in body fat mass in the first and second trimesters with subsequent stabilization, a progressive increase in total body water at 28.3 % with normal percentage of extracellular water. Insufficient weight gain is characterized by the absence of body fat mass increase during pregnancy, reduced total body water accumulation 1.7-fold with its normal percentage and normal extracellular and intracellular water balance. In a group of women with excessive gestational weight gain body fat mass and its percentage in the first trimester are 1.2-fold higher than in pregnant women with the recommended weight gain and this trend remains until delivery at 40.0 % (р<0.05). In women with pre-pregnancy excessive body mass index (BMI), body fat mass is 1.8-fold higher in early pregnancy and the elevation of its percentage starts from the second trimester and continues to grow until delivery only in excessive gestational weight gain women at 13.9 % (р<0.05). An increase in total body water volume at 32.0 % and its percentage at 13.1 % by the end of pregnancy, significant water-sector shifts in the form of abnormal fluid retention, mainly due to extracellular fluid from the first to the second trimester and mainly to the third trimester lead to excessive GWG. Patients with normal and excessive pre-pregnancy BMI are in a group of the most attention. The imbalance of the water components in these groups is a risk factor for edema and preeclampsia development. It is proved that changes in carbohydrate and fat metabolisms during pregnancy are determined by the level of GWG. Excessive GWG is associated with the development of pathological insulin resistance and dyslipidemia, regardless of baseline weight. In a group of women with normal pre-pregnancy BMI and excessive GWG hypertriglyceridemia and hyperlipoproteinemia due to the progression of insulin resistance during pregnancy occur at the same level as overweight and obese pregnant. Pathological GWG, diagnosed in the second and third trimesters, is a clinical manifestation of impaired carbohydrate and fat metabolism at earlier terms with deepening to the end of pregnancy. Adipocyte dysfunction, manifested by hyperleptinemia and hyperresistinemia, as an inducer of insulin resistance, contributes to the deepening of metabolic changes in pregnant and is associated with an increase in body fat mass and initiates excessive GWG. From a practical point of view, gestational complications are one of the most important aspects of GWG. Insufficient weight gain patients have high chances of early gestosis and fetal growth retardation, excessive weight gain - placental dysfunction, preeclampsia, gestational hypertension, gestational diabetes compared to recommended GWG patients. In the excessive GWG group there is higher frequency of induced delivery, abnormal uterine action, shoulder dystocia, maternal injuries, operative delivery compared to recommended GWG group. Excessive GWG increases the chances of delayed weight reduction 1 year after delivery, reduces the chances of exclusive breastfeeding for up to 3 months and increases the chances of premature termination of lactation and macrosomia. Low GWG increases the chances of fetal growth retardation, which correlates with biochemical and hormonal indicators beginning from the second trimester. Evaluation of the effectiveness of the offered prevention program have showed reducing the proportion of women with insufficient GWG 1.9-fold and excessive GWG 2.0-fold, reducing the chances of excess GWG in women of all weight categories, leading to reduction in the development of preeclampsia 1.8-fold, abnormal uterine action 2.2-fold, maternal injuries 1.5-fold, operative delivery 1.9-fold, macrosomia 2.2-fold, delayed weight reduction 1 year after delivery 2.7-fold (p<0.05), which indicates the importance of its supplement to the routine antenatal care.
