Impact of excessive gestational weight gain in non-smoking mothers on body fatness in infancy and early childhood. Prospective prebirth cohort study in Cracow.

Gestational weight gain (GWG) is important for health policy as it may be associated with overweight epidemics in childhood and adolescence. The purpose of the study was to perform the risk assessment of joint effects of the excessive GWG and the pregravid maternal BMI on overweight in infancy and childhood. The observations were collected in the ongoing prospective birth cohort study of 482 non-smoking mothers and their newborns in Cracow inner city area. At 5 years of age the subsample of 312 infants were reexamined in order to assess their nutritional status. Body fatness was assessed by means of the weight/length ratio (WLR) in neonates and weight/height ratio (WHR) in 5-year-olds since they showed the strongest correlation with subcutaneous fat mass of young children. In the statistical analysis the binary regression models were applied to identify predictors of overweight. The excessive GWG (>18 kg) increased more than twofold the adjusted relative risk (RR) of neonatal fatness (R=2.7; 95% CI 2.0-3.7) and was also a significant independent risk factor for postnatal body fatness at 5 years of age (RR=2.0; 95% CI: 1.3-3.3). The results confirmed earlier findings that pregravid overweight increased not only the relative risk of neonatal fatness (RR=2.9; 95% CI: 2.2-3.9) but also overweight in early childhood (RR=2.7; 95% CI: 1.7-4.4). The conclusion is that excessive GWG may be a risk factor for overweight in early childhood and should be a focus of public health policy.

Cardiac aldosterone production and ventricular remodeling.

An intracardiac production of aldosterone has been recently reported in rat. This production is increased both acutely and chronically by angiotensin II, observations suggesting that the heart contains a steroidogenic system that is regulated similarly to the adrenal one. Cardiac production of aldosterone is small compared with that of the adrenal, raising the question of its function in normal conditions. Moreover, the regulation of this synthesis in pathophysiologic states remains unknown. In an analysis of the effects of a one-month myocardial infarction (MI) on the cardiac steroidogenic system, it was observed that aldosterone-synthase mRNA and the aldosterone concentration were increased by 2- and 3.5-fold, respectively, in the noninfarcted part of the rat left ventricle. MI also induced a 1. 9-fold increase in the cardiac angiotensin II level. Losartan prevented these changes, and the MI-induced collagen deposition in noninfarcted area of the left ventricle was reduced by 1.6- and 2. 5-fold by both spironolactone and losartan treatments, respectively. Thus, these observations indicate that MI is associated with tissue-specific activation of myocardial aldosterone synthesis. This activation is mediated by cardiac angiotensin II via the angiotensin II type 1 (AT1) receptor, and the resultant increase of intracardiac aldosterone level may be involved in post-MI ventricular remodeling.