Browsing by Subject "TWINS"

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  • Bozzetto, Lutgarda; Berntzen, Bram; Kaprio, Jaakko; Rissanen, Aila; Taskinen, Marja-Riitta; Pietiläinen, Kirsi H. (2019)
  • 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.
  • Zheng, Guoqiao; Catalano, Calogerina; Bandapalli, Obul Reddy; Paramasivam, Nagarajan; Chattopadhyay, Subhayan; Schlesner, Matthias; Sijmons, Rolf; Hemminki, Akseli; Dymerska, Dagmara; Lubinski, Jan; Hemminki, Kari; Försti, Asta (2020)
    Simple Summary Familial clustering of cancer and identification of high- and low-risk cancer predisposition gene variants implicate that there are families that are at a high to moderate excess risk of cancer. We wanted to test genetically whether there are families protected from cancer. We whole-genome sequenced 51 elderly individuals without any personal or family history of cancer. We identified less high-risk loss-of-function variants in known and suggested cancer predisposition genes in these cancer-free individuals than in the general population. However, our results for low-risk variants were not conclusive. Our study suggests that random environmental causes of cancer are so dominant that a clear demarcation of cancer-free populations using genetic data may not be feasible. However, carrier identification of and counseling about prevalent high-risk cancer predisposition genes is useful. Familial clustering, twin concordance, and identification of high- and low-penetrance cancer predisposition variants support the idea that there are families that are at a high to moderate excess risk of cancer. To what extent there may be families that are protected from cancer is unknown. We wanted to test genetically whether cancer-free families share fewer breast, colorectal, and prostate cancer risk alleles than the population at large. We addressed this question by whole-genome sequencing (WGS) of 51 elderly cancer-free individuals whose numerous (ca. 1000) family members were found to be cancer-free ('cancer-free families', CFFs) based on face-to-face interviews. The average coverage of the 51 samples in the WGS was 42x. We compared cancer risk allele frequencies in cancer-free individuals with those in the general population available in public databases. The CFF members had fewer loss-of-function variants in suggested cancer predisposition genes compared to the ExAC data, and for high-risk cancer predisposition genes, no pathogenic variants were found in CFFs. For common low-penetrance breast, colorectal, and prostate cancer risk alleles, the results were not conclusive. The results suggest that, in line with twin and family studies, random environmental causes are so dominant that a clear demarcation of cancer-free populations using genetic data may not be feasible.
  • Frank, Christoph; Sundquist, Jan; Yu, Hongyao; Hemminki, Akseli; Hemminki, Kari (2017)
    Relatives of cancer patients are at an increased risk of the same (concordant) cancer but whether they are at a risk for different (discordant) cancers is largely unknown - beyond well characterized hereditary cancer syndromes - but would be of major scientific and clinical interest. We therefore decided to resolve the issue by analyzing familial risks when family members were diagnosed with any discordant cancers. We compared the population impact of concordant to discordant familial cancer. The Swedish Family-Cancer Database (FCD) was used to calculate familial relative risks (RRs) for family members of cancer patients, for the 27 most common cancers. Population attributable fractions (PAFs) were estimated for concordant and discordant family histories. Discordant cancers in the family were detected as significant risk factors for the majority of cancers, although the corresponding RRs were modest compared to RRs for concordant cancers. Risks increased with the number of affected family members with the highest RRs for pancreatic (2.31), lung (1.69), kidney (1.98), nervous system (1.79) and thyroid cancers (3.28), when 5 or more family members were diagnosed with discordant cancers. For most cancers, the PAF for discordant family history exceeded that for concordant family history. Our findings suggest that there is an unspecific genetic predisposition to cancer with clinical consequences. We consider it unlikely that shared environmental risk factors could essentially contribute to the risks for diverse discordant cancers, which are likely driven by genetic predisposition. The identification of genes that moderately increase the risk for many cancers will be a challenge.
  • Yokoyama, Yoshie; Pitkäniemi, Janne Mikael; Kaprio, Jaakko; Silventoinen, Karri (2013)
  • Bijwaard, Govert E.; Myrskylä, Mikko; Tynelius, Per; Rasmussen, Finn (2017)
    A negative educational gradient has been found for many causes of death. This association may be partly explained by confounding factors that affect both educational attainment and mortality. We correct the cause-specific educational gradient for observed individual background and unobserved family factors using an innovative method based on months lost due to a specific cause of death re-weighted by the probability of attaining a higher educational level. We use data on men with brothers from the Swedish Military Conscription Registry (1951-1983), linked to administrative registers. This dataset of some 700,000 men allows us to distinguish between five education levels and many causes of death. The empirical results reveal that raising the educational level from primary to tertiary would result in an additional 20 months of survival between ages 18 and 63. This improvement in mortality is mainly attributable to fewer deaths from external causes. The highly educated gain more than nine months due to the reduction in deaths from external causes, but gain only two months due to the reduction in cancer mortality and four months due to the reduction in cardiovascular mortality. Ignoring confounding would lead to an underestimation of the gains by educational attainment, especially for the less educated. Our results imply that if the education distribution of 50,000 Swedish men from the 1951 cohort were replaced with that of the corresponding 1983 cohort, 22% of the person-years that were lost to death between ages 18 and 63 would have been saved for this cohort. (C) 2017 Elsevier Ltd. All rights reserved.
  • Wacklin, Pirjo; Tuimala, Jarno; Nikkila, Janne; Tims, Sebastian; Makivuokko, Harri; Alakulppi, Noora; Laine, Pia; Rajilic-Stojanovic, Mirjana; Paulin, Lars; de Vos, Willem M.; Matto, Jaana (2014)
  • Heikkinen, Sanna M. M.; Madanat-Harjuoja, Laura-Maria; Seppä, Karri J. M.; Rantanen, Matti E.; Hirvonen, Elli M.; Malila, Nea K.; Pitkäniemi, Janne M. (2020)
    This registry-linkage study evaluates familial aggregation of cancer among relatives of a population-based series of early-onset (
  • Jelenkovic, Aline; Sund, Reijo; Yokoyama, Yoshie; Latvala, Antti; Sugawara, Masumi; Tanaka, Mami; Matsumoto, Satoko; Freitas, Duarte L.; Maia, Jose Antonio; Knafo-Noam, Ariel; Mankuta, David; Abramson, Lior; Ji, Fuling; Ning, Feng; Pang, Zengchang; Rebato, Esther; Saudino, Kimberly J.; Cutler, Tessa L.; Hopper, John L.; Ullemar, Vilhelmina; Almqvist, Catarina; Magnusson, Patrik K. E.; Cozen, Wendy; Hwang, Amie E.; Mack, Thomas M.; Nelson, Tracy L.; Whitfield, Keith E.; Sung, Joohon; Kim, Jina; Lee, Jooyeon; Lee, Sooji; Llewellyn, Clare H.; Fisher, Abigail; Medda, Emanuela; Nistico, Lorenza; Toccaceli, Virgilia; Baker, Laura A.; Tuvblad, Catherine; Corley, Robin P.; Huibregtse, Brooke M.; Derom, Catherine A.; Vlietinck, Robert F.; Loos, Ruth J. F.; Burt, S. Alexandra; Klump, Kelly L.; Silberg, Judy L.; Maes, Hermine H.; Krueger, Robert F.; McGue, Matt; Pahlen, Shandell; Gatz, Margaret; Butler, David A.; Harris, Jennifer R.; Brandt, Ingunn; Nilsen, Thomas S.; Harden, K. Paige; Tucker-Drob, Elliot M.; Franz, Carol E.; Kremen, William S.; Lyons, Michael J.; Lichtenstein, Paul; Bartels, Meike; van Beijsterveldt, Catharina E. M.; Willemsen, Gonneke; Oncel, Sevgi Y.; Aliev, Fazil; Jeong, Hoe-Uk; Hur, Yoon-Mi; Turkheimer, Eric; Boomsma, Dorret; Srensen, Thorkild I. A.; Kaprio, Jaakko; Silventoinen, Karri (2020)
    Genetic factors explain a major proportion of human height variation, but differences in mean stature have also been found between socio-economic categories suggesting a possible effect of environment. By utilizing a classical twin design which allows decomposing the variation of height into genetic and environmental components, we tested the hypothesis that environmental variation in height is greater in offspring of lower educated parents. Twin data from 29 cohorts including 65,978 complete twin pairs with information on height at ages 1 to 69 years and on parental education were pooled allowing the analyses at different ages and in three geographic-cultural regions (Europe, North America and Australia, and East Asia). Parental education mostly showed a positive association with offspring height, with significant associations in mid-childhood and from adolescence onwards. In variance decomposition modeling, the genetic and environmental variance components of height did not show a consistent relation to parental education. A random-effects meta-regression analysis of the aggregate-level data showed a trend towards greater shared environmental variation of height in low parental education families. In conclusion, in our very large dataset from twin cohorts around the globe, these results provide only weak evidence for the study hypothesis.
  • Manrique, Pilar; Bolduc, Benjamin; Walk, Seth T.; van der Oost, John; de Vos, Willem M.; Young, Mark J. (2016)
    The role of bacteriophages in influencing the structure and function of the healthy human gut microbiome is unknown. With few exceptions, previous studies have found a high level of heterogeneity in bacteriophages from healthy individuals. To better estimate and identify the shared phageome of humans, we analyzed a deep DNA sequence dataset of active bacteriophages and available metagenomic datasets of the gut bacteriophage community from healthy individuals. We found 23 shared bacteriophages in more than one-half of 64 healthy individuals from around the world. These shared bacteriophages were found in a significantly smaller percentage of individuals with gastrointestinal/irritable bowel disease. A network analysis identified 44 bacteriophage groups of which 9 (20%) were shared in more than one-half of all 64 individuals. These results provide strong evidence of a healthy gut phageome (HGP) in humans. The bacteriophage community in the human gut is a mixture of three classes: a set of core bacteriophages shared among more than one-half of all people, a common set of bacteriophages found in 20-50% of individuals, and a set of bacteriophages that are either rarely shared or unique to a person. We propose that the core and common bacteriophage communities are globally distributed and comprise the HGP, which plays an important role in maintaining gut microbiome structure/function and thereby contributes significantly to human health.
  • Rokholm, Benjamin; Silventoinen, Karri; Angquist, Lars; Skytthe, Axel; Kyvik, Kirsten Ohm; Sorensen, Thorkild I. A. (2011)
  • Hovatta, Iiris; de Mello, Vanessa D. F.; Kananen, Laura; Lindstrom, Jaana; Eriksson, Johan G.; Ilanne-Parikka, Pirjo; Keinanen-Kiukaanniemi, Sirkka; Peltonen, Markku; Tuomilehto, Jaakko; Uusitupa, Matti (2012)
  • Dicksved, Johan; Ellstrom, Patrik; Engstrand, Lars; Rautelin, Hilpi (2014)
  • Kokkinen, Lauri; Muntaner, Carles; Kouvonen, Anne; Koskinen, Aki; Varje, Pekka; Vaananen, Ari (2015)
    Objectives: Epidemiological studies have shown an association between educational credentials and mental disorders, but have not offered any explanation for the varying strength of this association in different historical contexts. In this study, we investigate the education-specific trends in hospitalisation due to psychiatric disorders in Finnish working-age men and women between 1976 and 2010, and offer a welfare state explanation for the secular trends found. Setting: Population-based setting with a 25% random sample of the population aged 30-65 years in 7 independent consecutive cohorts (1976-1980, 1981-1985, 1986-1990, 1991-1995, 1996-2000, 2001-2005, 2006-2010). Participants: Participants were randomly selected from the Statistics Finland population database (n=2 865 746). These data were linked to diagnosis-specific records on hospitalisations, drawn from the National Hospital Discharge Registry using personal identification numbers. Employment rates by educational credentials were drawn from the Statistics Finland employment database. Primary and secondary outcome measures: Hospitalisation and employment. Results: We found an increasing trend in psychiatric hospitalisation rates among the population with only an elementary school education, and a decreasing trend in those with higher educational credentials. The employment rate of the population with only an elementary school education decreased more than that of those with higher educational credentials. Conclusions: We propose that restricted employment opportunities are the main mechanism behind the increased educational inequality in hospitalisation for psychiatric disorders, while several secondary mechanisms (lack of outpatient healthcare services, welfare cuts, decreased alcohol duty) further accelerated the diverging long-term trends. All of these inequality-increasing mechanisms were activated by welfare state retrenchment, which included the liberalisation of financial markets and labour markets, severe austerity measures and narrowing down of public sector employment commitment.