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Borte, S., Winsvold, B. S., Stensland, S. O., Smastuen, M. C., & Zwart, J. - A. (2017). The effect of foetal growth restriction on the development of migraine and tension-type headache in adulthood. The HUNT Study. PLoS One, 12(4), e0175908.
Abstract: BACKGROUND: There is little knowledge about how factors early in life affect the development of migraine and tension-type headache. We aimed to examine whether growth restriction in utero is associated with development of migraine and frequent tension-type headache in adults. METHODS: The population-based Nord-Trondelag Health Study (HUNT 3) contained a validated headache questionnaire, which differentiated between migraine and tension-type headache. These data were linked to information on weight and gestational age at birth from the Norwegian Medical Birth Registry. In total 4557 females and 2789 males, aged 19-41 years, were included in this registry-based study. Participants were categorized as appropriate for gestational age (AGA, 10th-90th percentile), small for gestational age (SGA, 3rd-10th percentile) or very small for gestational age (VSGA, < 3rd percentile). Logistic regression was used to calculate odds ratios (OR) with 95% confidence intervals (CI) for migraine and tension-type headache, with exposure being growth restriction at birth. RESULTS: The effect of growth restriction on migraine was modified by sex, with a significant association in males (p<0.001), but not in females (p = 0.20). In particular, males born VSGA were at increased risk of developing migraine (OR 2.73, 95% CI 1.63-4.58, p<0.001), with an intermediate risk among those born SGA (OR 1.50, 95% CI 0.96-2.35, p = 0.08) compared to those born AGA. There was no significant association between growth restriction and frequent TTH (p = 0.051). CONCLUSION: Growth restriction was associated with increased risk of migraine in adulthood among males, but not among females. This suggests that migraine might, in part, be influenced by early life events, and that males seem to be particularly vulnerable.
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Myklestad, K., Vatten, L. J., Magnussen, E. B., Salvesen, K. A., & Romundstad, P. R. (2013). Do parental heights influence pregnancy length?: A population-based prospective study, HUNT 2. BMC Pregnancy Childbirth, 13, 33.
Abstract: BACKGROUND: The objective of this study was to examine the association of maternal and paternal height with pregnancy length, and with the risk of pre- and post-term birth. In addition we aimed to study whether cardiovascular risk factors could explain possible associations. METHODS: Parents who participated in the Nord-Trondelag Health Study (HUNT 2; 1995-1997) were linked to offspring data from the Medical Birth Registry of Norway (1997-2005). The main analyses included 3497 women who had delivered 5010 children, and 2005 men who had fathered 2798 pregnancies. All births took place after parental participation in HUNT 2. Linear regression was used to estimate crude and adjusted differences in pregnancy length according to parental heights. Logistic regression was used to estimate crude and adjusted associations of parental heights with the risk of pre- and post-term births. RESULTS: We found a gradual increase in pregnancy length by increasing maternal height, and the association was essentially unchanged after adjustment for maternal cardiovascular risk factors, parental age, offspring sex, parity, and socioeconomic measures. When estimated date of delivery was based on ultrasound, the difference between mothers in the lower height quintile (<163 cm cm) and mothers in the upper height quintile (>/= 173 cm) was 4.3 days, and when estimated date of delivery was based on last menstrual period (LMP), the difference was 2.8 days. Shorter women (< 163 cm) had lower risk of post-term births, and when estimated date of delivery was based on ultrasound they also had higher risk of pre-term births. Paternal height was not associated with pregnancy length, or with the risks of pre- and post-term births. CONCLUSIONS: Women with shorter stature had shorter pregnancy length and lower risk of post-term births than taller women, and when EDD was based on ultrasound, they also had higher risk of preterm births. The effect of maternal height was generally stronger when pregnancy length was based on second trimester ultrasound compared to last menstrual period. The association of maternal height with pregnancy length could not be explained by cardiovascular risk factors. Paternal height was neither associated with pregnancy length nor with the risk of pre- and post-term birth.
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Myklestad, K., Vatten, L. J., Magnussen, E. B., Salvesen, K. A., Smith, G. D., & Romundstad, P. R. (2012). Offspring birth weight and cardiovascular risk in parents: a population-based HUNT 2 study. Am J Epidemiol, 175(6), 546–555.
Abstract: Low birth weight is associated with increased risk of cardiovascular disease and type 2 diabetes in later life. The fetal insulin hypothesis suggests that shared genetic factors partly explain this association. If fetal genes predispose to both low birth weight and cardiovascular disease in adulthood, fathers of offspring with low birth weight should display an unfavorable profile of cardiovascular risk factors. To study this, the authors linked data on more than 14,000 parents, collected from the second Health Study of Nord Trondelag County, Norway (HUNT 2, 1995-1997), to offspring data from the Norwegian Medical Birth Registry (1967-2005). Linear regression was used to study associations of offspring birth weight for gestational age with the parents' body mass index, waist circumference, blood pressure, glucose, and serum lipids. All analyses were adjusted for shared environment by means of the socioeconomic measures, lifestyle, and cardiovascular risk factors of the partner. The authors found that low offspring birth weight for gestational age was associated with increased paternal blood pressure, body mass index, waist circumference, and unfavorable levels of glucose and lipids. For mothers, associations similar to those for fathers were found for blood pressure, whereas associations in the opposite direction were found for glucose, lipids, and body mass index. The paternal findings strengthen the genetic hypothesis.
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