Browsing by Subject "FINAL HEIGHT"

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  • Jelenkovic, Aline; Yokoyama, Yoshie; Sund, Reijo; Hur, Yoon-Mi; Harris, Jennifer R.; Brandt, Ingunn; Nilsen, Thomas Sevenius; Ooki, Syuichi; Ullemar, Vilhelmina; Almqvist, Catarina; Magnusson, Patrik K.E.; Saudino, Kimberly J.; Stazi, Maria A.; Fagnani, Corrado; Brescianini, Sonia; Nelson, Tracy L.; Whitfield, Keith E.; Knafo-Noam, Ariel; Mankuta, David; Abramson, Lior; Cutler, Tessa L.; Hopper, John L.; Llewellyn, Clare H.; Fisher, Abigail; Corley, Robin P.; Huibregtse, Brooke M.; Derom, Catherine A.; Vlietinck, Robert F.; Bjerregaard-Andersen, Morten; Beck-Nielsen, Henning; Sodemann, Morten; Krueger, Robert F.; McGue, Matt; Pahlen, Shandell; Alexandra Burt, S.; Klump, Kelly L.; Dubois, Lise; Boivin, Michel; Brendgen, Mara; Dionne, Ginette; Vitaro, Frank; Willemsen, Gonneke; Bartels, Meike; van Beijsterveld, Catharina E.M.; Craig, Jeffrey M.; Heikkilä, Kauko; Pietiläinen, Kirsi H.; Ning, Feng; Kaprio, Jaakko; Silventoinen, Karri (2018)
    Background: There is evidence that birth size is positively associated with height in later life, but it remains unclear whether this is explained by genetic factors or the intrauterine environment. Aim: To analyze the associations of birth weight, length and ponderal index with height from infancy through adulthood within mono- and dizygotic twin pairs, which provides insights into the role of genetic and environmental individual-specific factors. Methods: This study is based on the data from 28 twin cohorts in 17 countries. The pooled data included 41,852 complete twin pairs (55% monozygotic and 45% same-sex dizygotic) with information on birth weight and a total of 112,409 paired height measurements at ages ranging from 1 to 69 years. Birth length was available for 19,881 complete twin pairs, with a total of 72,692 paired height measurements. The association between birth size and later height was analyzed at both the individual and within-pair level by linear regression analyses. Results: Within twin pairs, regression coefficients showed that a 1-kg increase in birth weight and a 1-cm increase in birth length were associated with 1.14-4.25 cm and 0.18-0.90 cm taller height, respectively. The magnitude of the associations was generally greater within dizygotic than within monozygotic twin pairs, and this difference between zygosities was more pronounced for birth length. Conclusion: Both genetic and individual-specific environmental factors play a role in the association between birth size and later height from infancy to adulthood, with a larger role for genetics in the association with birth length than with birth weight.
  • Suikkanen, Julia; Nurhonen, Markku; Cole, Tim J.; Paalanne, Marika; Matinolli, Hanna-Maria; Tikanmaki, Marjaana; Vääräsmäki, Marja; Järvelin, Marjo-Riitta; Hovi, Petteri; Kajantie, Eero (2022)
    Background We evaluated pubertal growth and pubertal timing of participants born preterm compared to those born at term. Methods In the ESTER Preterm Birth Study, we collected growth data and measured final height of men/women born very or moderately preterm (= 37 weeks, 131/151), resulting in median 9 measurements at >= 6 years. Timing of menarche or voice break was self-reported. Peak height velocity (PHV, cm/year) and age at PHV (years) were compared with SuperImposition by Translation And Rotation (SITAR) model (sexes separately). Results Age at PHV (years) and PHV (cm/year) were similar in all gestational age groups. Compared to term controls, insignificant differences in age at PHV were 0.1 (95% CI: -0.2 to 0.4) years/0.2 (-0.1 to 0.4) for very or moderately/late preterm born men and -0.0 (-0.3 to 0.3)/-0.0 (-0.3 to 0.2) for women, respectively. Being born small for gestational age was not associated with pubertal growth. Age at menarche or voice break was similar in all the gestational age groups. Conclusions Timing of pubertal growth and age at menarche or voice break were similar in participants born preterm and at term. Impact Pubertal growth and pubertal timing were similar in preterm and term participants in a relatively large cohort with a wide range of gestational ages. Previous literature indicates that small for gestational age is a risk for early puberty in term born children. This was not shown in preterm children. While our study had limited power for children born very preterm, all children born preterm were not at increased risk for early puberty.
  • Cousminer, Diana L.; Leinonen, Jaakko T.; Sarin, Antti-Pekka; Chheda, Himanshu; Surakka, Ida; Wehkalampi, Karoliina; Ellonen, Pekka; Ripatti, Samuli; Dunkel, Leo; Palotie, Aarno; Widen, Elisabeth (2015)
    Constitutional delay of growth and puberty (CDGP) is the most common cause of pubertal delay. CDGP is defined as the proportion of the normal population who experience pubertal onset at least 2 SD later than the population mean, representing 2.3% of all adolescents. While adolescents with CDGP spontaneously enter puberty, they are at risk for short stature, decreased bone mineral density, and psychosocial problems. Genetic factors contribute heavily to the timing of puberty, but the vast majority of CDGP cases remain biologically unexplained, and there is no definitive test to distinguish CDGP from pathological absence of puberty during adolescence. Recently, we published a study identifying significant linkage between a locus at the pericentromeric region of chromosome 2 (chr 2) and CDGP in Finnish families. To investigate this region for causal variation, we sequenced chr 2 between the genomic coordinates of 79-124 Mb (genome build GRCh37) in the proband and affected parent of the 13 families contributing most to this linkage signal. One gene, DNAH6, harbored 6 protein-altering low-frequency variants (<6% in the Finnish population) in 10 of the CDGP probands. We sequenced an additional 135 unrelated Finnish CDGP subjects and utilized the unique Sequencing Initiative Suomi (SISu) population reference exome set to show that while 5 of these variants were present in the CDGP set, they were also present in the Finnish population at similar frequencies. Additional variants in the targeted region could not be prioritized for follow-up, possibly due to gaps in sequencing coverage or lack of functional knowledge of non-genic genomic regions. Thus, despite having a well-characterized sample collection from a genetically homogeneous population with a large population-based reference sequence dataset, we were unable to pinpoint variation in the linked region predisposing delayed puberty. This study highlights the difficulties of detecting genetic variants under linkage regions for complex traits and suggests that advancements in annotation of gene function and regulatory regions of the genome will be critical for solving the genetic background of complex phenotypes like CDGP.