| dc.description.abstract | Background
During the last three to four decades, the prevalence of adiposity has increased in all age groups and in all layers of society. The World Health Organization has estimated that by 2015 approximately 2.3 billion adults will be overweight and more than 700 million will be obese3. The prevalence of adiposity among children is also increasing. Globally, more than one in ten children are overweight, and at least a quarter of these are obese4. Because of this increase in prevalence, we may for the first time in modern history observe a fall in life expectancy5.
The knowledge about adipose tissue has exploded with increasing occurrence of adiposity. While adipose tissue previously was considered as an inert storage compartment for metabolic energy, it is now appreciated as a dynamic endocrine organ producing a multitude of hormones involved in glucose and energy homeostasis. Despite this newfound knowledge, no effective pharmacologic intervention currently exists to treat adiposity, and the most effective method to attain lasting weight loss is still bariatric surgery, an unattractive alternative for many6.
Adiposity in childhood has several adverse consequences, both in the short- and in the long term. In the short term, childhood adiposity is associated with several other diseases such as psychological problems, insulin resistance and overt diabetes, hypertension, dyslipidaaemia and orthopaedic problems. In the long term, childhood adiposity is associated with a much higher risk of adiposity in adulthood, with all its comorbidities. Consequently, severe adiposity in adolescence is associated with a near doubling of the all-cause mortality in adulthood7.
Studies on the determinants of adiposity have implicated environmental factors acting from foetal life, throughout infancy and childhood as risk factors8-10. During foetal life, environmental exposure to conditions such as maternal undernutrition, maternal smoking, maternal stress and obstetric complications have been reported to be associated with increased occurrence of childhood adiposity. In infancy, factors such as rapid growth in the first years, type of feeding and duration of sleep have been implicated as risk factors. Later in childhood and adolescence, dietary habits and low physical activity have been reported to be associated with adiposity. Finally, several studies have examined the influence of parental habits, often manifested in parental adiposity, but also smoking habits, physical activity and dietary habits, and found that these have a profound effect on the risk of their child developing adiposity.
However, much of the evidence on risk factors for adiposity in childhood is unclear and debated, and the aim of this thesis was to further clarify some of the pre- and postnatal risk factors associated with different aspects of childhood adiposity.
Materials and methods
This thesis is based on data from three different sources. Paper I utilized data from the Prevention of Allergy among Children in Trondheim (PACT) study linked with data from the four-year check-up at public health stations in the Trondheim region. Paper II used data from prenatal questionnaires and the three-year check-up in Project Viva, a pre-birth cohort study carried out in Eastern Massachusetts, USA. Papers III and IV were based on data from the HUNT-study, a series of large, population based cohort studies carried out in Nord-Trøndelag, a county in Mid-Norway. In paper III, we used data from Young-HUNT (1995.97), the youth part of HUNT. In paper IV, we also included data from HUNT-1 (1984-86) and HUNT-2 (1995-97), in which some of the parents of the adolescents in Young-HUNT had participated.
Papers I and II studied the association of prenatal influences on the development of adiposity in early childhood. In paper I, we related maternal smoking in pregnancy and maternal smoking cessation to the occurrence of adiposity at four years. In paper II, we studied the association of maternal CRH measured in mid-pregnancy, a proxy for foetal glucocorticoids exposure, with blood levels of adiponectin and leptin in the three year old children of these mothers.
Papers III and IV studied the association of postnatal influences and the occurrence of adiposity in adolescence. In paper III, we related different adolescent life-style habits, such as dietary habits, smoking and physical activity, with the occurrence of adiposity.
In paper IV, we studied how parental life-style and life-style change, measured as parental weight, smoking habits and levels of physical activity, were associated with adolescent adiposity.
Results
In paper I, we found a clear positive association between maternal smoking in pregnancy and offspring adiposity at age four, but no increased risk of adiposity among children of mothers who managed to quit smoking in early pregnancy.
In paper II, we found a weak positive association between maternal levels of CRH, a proxy of foetal glucocorticoid exposure, and offspring levels of adiponectin at three years, but no association with offspring leptin. We did not find associations between maternal levels of CRH in pregnancy and adiposity in the three-year old offspring.
In paper III, we found that low levels of adolescent physical activity were associated with higher occurrence of adolescent adiposity. We also found several unexpected associations between various dietary habits and the occurrence of adiposity in adolescence, for example that lower consumption of sweets was associated with higher occurrence of adiposity. However, these associations were attenuated after adjusting for weight losing behaviour.
In paper IV, we found that parental adiposity was strongly associated with adiposity in their children. Additionally, children of parents who managed to maintain a normal weight, or who lost weight, had lower occurrence of adiposity than children of parents who stayed adipose. Maternal-, but not paternal smoking was associated with increased occurrence of adiposity in their adolescent offspring. Children of mothers who managed to stop smoking had lower occurrence of adiposity than the children of mothers who persisted in smoking.
Conclusions
This thesis has contributed with some pieces to the epidemiological puzzle of why and how children and adolescents become adipose. We confirmed previous findings that maternal smoking in pregnancy is associated with increased occurrence of adiposity, and expanded on these by showing that smoking cessation in early pregnancy negates the increased occurrence. Furthermore, we have shown that excess foetal glucocorticoid exposure lead to subtle alterations in adipose tissue endocrine function. The mechanism behind this finding is unclear, however. We have also demonstrated that the parentally created environment is important in determining if the child develops adiposity or not. Encouragingly, healthy changes in this environment, manifested as maternal smoking cessation or weight loss, is associated with lower occurrence of adiposity in the adolescents.
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