|Datum verdediging||21 februari 2019|
|(Co) promotoren||prof.dr. D.E. Grobbee, dr. C.S.P.M. Uiterwaal, dr. G.W. Dalmeijer|
|Titel proefschrift||Blood pressure: In the beginning|
Lees het proefschrift online
One of the major risk factors of cardiovascular disease is hypertension. The aim of this thesis was to clarify the impact of parental body size; genetic predisposition; hypertensive disorders of pregnancy and children’s body size on children’s blood pressure. Firstly, we investigated the association between parental body mass index and offspring’s blood pressure in 587 children by using data of the BReastfeeding Attitude and Volume Optimization (BRAVO) trial, which was performed in Jakarta, Indonesia. We demonstrated that mothers who were heavier before pregnancy led to higher blood pressure of their offspring. These higher blood pressure values by maternal body mass index were already seen from birth onwards and remained higher during the first year of life. Father’s body size had no influence on the offspring’s blood pressure. Secondly, we demonstrated that a part of the blood pressure variation in childhood was explained by adult derived genetic blood pressure scores – i.e. high blood pressure risk scores constructed from all combined single nucleotide polymorphisms known to be related to adult blood pressure. In 720 5-year-old children of the WHeezing-Illnesses-STudy-LEidsche-Rijn (WHISTLER) prospective birth cohort, Utrecht, The Netherlands, we calculated for each child a weighted genetic blood pressure risk score and measured the child’s blood pressure in both sitting and supine posture. Higher scores for adult derived diastolic and systolic blood pressure genes were related to higher supine systolic blood pressure at 5 years of age. Thirdly, we summarized the literature on intra-uterine exposure to hypertensive disorders of pregnancy in relation to offspring’s cardiovascular and –metabolic health. Children who had been exposed to pregnancy induced hypertension had higher blood pressure than children who were not exposed to pregnancy induced hypertension. We could not confirm an association with exposure to preeclampsia and blood pressure. Fourthly, the association between excess early postnatal weight gain of the infant (zero to three months after birth) and blood pressure in 853 5-year-old children of the WHISTLER cohort was studied. Children with excess weight gain, adjusted for length gain, particularly those with a relatively small birth size, had higher sitting systolic blood pressure. Part of this association was explained by children’s body mass index and visceral adipose tissue. Lastly, the association between abdominal fat and blood pressure in 862 5-year-old children of the WHISTLER study was determined. Children with a higher amount of visceral adipose tissue had higher blood pressure values. This association was independent of body mass index, waist circumference and early life growth. Subcutaneous adipose tissue was not associated with children’s blood pressure. We demonstrated that blood pressure variations already exist early in life and have multiple causes. Therefore, a healthy lifestyle of future parents and young families is important with the ultimate aim to start with healthy blood pressure levels of their offspring.