Browsing by Subject "ENVIRONMENTAL-INFLUENCES"

Sort by: Order: Results:

Now showing items 1-15 of 15
  • Heim, Anita; Pyhälä, Aili (2020)
    The purpose of this study was to identify, describe and conceptualize the present drivers of food choices and preferences of the Khwe San indigenous peoples by considering influences of their historical and cultural contexts. Data were collected in Eastern Bwabwata National Park in Namibia using a range of qualitative methods: semi-structured and structured interviews and free listing. The various drivers of food choices have been clustered into four levels of the ecological conceptual framework. Key factors, found to be driving participants' food choices, were the following: taste, hunger, health, familiarity and body satisfaction at the individual level; culture and food taboos at the social level; access to food and food storage at the physical level, and; cost and seasonality at the macro level. Many of these factors are directly related to food insecurity and previous experiences of hunger. Current preferences towards traditional foods existed but were not prevailing among all the participants. Interviews with the elderly revealed the historical context of the increasing exposure to modern foods and a contested access to traditional foods and traditional knowledge transmission. Our findings exposed some substantial gaps in the nutritional knowledge of the Khwe that need consideration by future health promotion strategies along with the current perceptions of local food choices. Ensuring access and promoting sustainable management of traditional foods would not only contribute to the health of the Khwe people but also help to maintain a nutritional safety net in their current situation of extreme poverty.
  • Yokoyama, Yoshie; Pitkäniemi, Janne Mikael; Kaprio, Jaakko; Silventoinen, Karri (2013)
  • Savage, Jeanne E.; Rose, Richard J.; Pulkkinen, Lea; Silventoinen, Karri; Korhonen, Tellervo; Kaprio, Jaakko; Gillespie, Nathan; Dick, Danielle M. (2018)
    Early maturation, indexed by pubertal development (PD), has been associated with earlier initiation and greater frequency of adolescent substance use, but this relationship may be biased by confounding factors and effects that change across development. Using a population-based Finnish twin sample (N = 3,632 individuals), we conducted twin modeling and multilevel structural equation modeling of the relationship between PD and substance use at ages 12-22. Shared environmental factors contributed to early PD and heavier substance use for females. Biological father absence was associated with early PD for boys but not girls, and did not account for the relationship between PD and substance use. The association between early PD and heavier substance use was partially due to between-family confounds, although early PD appeared to qualitatively alter long-term trajectories for some substances (nicotine), but not others (alcohol). Mediation by peer and parental factors did not explain this relationship within families. However, higher peer substance use and lower parental monitoring were themselves associated with heavier substance use, strengthening the existing evidence for these factors as targets for prevention/intervention efforts. Early maturation was not supported as a robust determinant of alcohol use trajectories in adolescence and young adulthood, but may require longer term follow-up. Subtle effects of early PD on nicotine and illicit drug use trajectories throughout adolescence and adulthood merit further investigation.
  • Narusyte, Jurgita; Ropponen, Annina; Silventoinen, Karri; Alexanderson, Kristina; Kaprio, Jaakko; Samuelsson, Asa; Svedberg, Pia (2011)
  • Silventoinen, Karri; Su, Jinni; Pulkkinen, Lea; Barr, Peter; Rose, Richard J.; Dick, Danielle M.; Kaprio, Jaakko (2019)
    We analyzed how the effects of genetic and environmental factors on the perceptions of family interaction change from early to late adolescence. The data were collected by postal surveys on Finnish twins (N=4808) at 12, 14 and 17years of age and analyzed using genetic twin modeling. Additive genetic factors explained a modest share of the variation in perceived relational support (a(2)=0.30 in boys and 0.18 in girls) and relational tensions (a(2)=0.13 and 0.14, respectively) at 12years of age, with the proportions becoming larger through 17years of age (a(2)=0.53 in boys and 0.49 in girls for relational support; a(2)=0.35 in boys and 0.33 in girls for relational tensions). Simultaneously, the role of environment shared by co-twins decreased. These findings suggest that the associations between perceived family interaction and other factors in adulthood should be interpreted with caution, because they partly reflect genetic background, whereas in childhood, they may provide more reliable information on parental characteristics.
  • Gialluisi, Alessandro; Andlauer, Till F. M.; Mirza-Schreiber, Nazanin; Moll, Kristina; Becker, Jessica; Hoffmann, Per; Ludwig, Kerstin U.; Czamara, Darina; St Pourcain, Beate; Brandler, William; Honbolygo, Ferenc; Toth, Denes; Csepe, Valeria; Huguet, Guillaume; Morris, Andrew P.; Hulslander, Jacqueline; Willcutt, Erik G.; DeFries, John C.; Olson, Richard K.; Smith, Shelley D.; Pennington, Bruce F.; Vaessen, Anniek; Maurer, Urs; Lyytinen, Heikki; Peyrard-Janvid, Myriam; Leppanen, Paavo H. T.; Brandeis, Daniel; Bonte, Milene; Stein, John F.; Talcott, Joel B.; Fauchereau, Fabien; Wilcke, Arndt; Francks, Clyde; Bourgeron, Thomas; Monaco, Anthony P.; Ramus, Franck; Landerl, Karin; Kere, Juha; Scerri, Thomas S.; Paracchini, Silvia; Fisher, Simon E.; Schumacher, Johannes; Noethen, Markus M.; Mueller-Myhsok, Bertram; Schulte-Koerne, Gerd (2019)
    Developmental dyslexia (DD) is one of the most prevalent learning disorders, with high impact on school and psychosocial development and high comorbidity with conditions like attention-deficit hyperactivity disorder (ADHD), depression, and anxiety. DD is characterized by deficits in different cognitive skills, including word reading, spelling, rapid naming, and phonology. To investigate the genetic basis of DD, we conducted a genome-wide association study (GWAS) of these skills within one of the largest studies available, including nine cohorts of reading-impaired and typically developing children of European ancestry (N = 2562-3468). We observed a genome-wide significant effect (p <1 x 10(-8)) on rapid automatized naming of letters (RANlet) for variants on 18q12.2, within MIR924HG (micro-RNA 924 host gene; rs17663182 p = 4.73 x 10(-9)), and a suggestive association on 8q12.3 within NKAIN3 (encoding a cation transporter; rs16928927, p = 2.25 x 10(-8)). rs17663182 (18q12.2) also showed genome-wide significant multivariate associations with RAN measures (p = 1.15 x 10(-8)) and with all the cognitive traits tested (p = 3.07 x 10(-8)), suggesting (relational) pleiotropic effects of this variant. A polygenic risk score (PRS) analysis revealed significant genetic overlaps of some of the DD-related traits with educational attainment (EDUyears) and ADHD. Reading and spelling abilities were positively associated with EDUyears (p similar to [10(-5)-10(-7)]) and negatively associated with ADHD PRS (p similar to [10(-8)-10(-17)]). This corroborates a long-standing hypothesis on the partly shared genetic etiology of DD and ADHD, at the genome-wide level. Our findings suggest new candidate DD susceptibility genes and provide new insights into the genetics of dyslexia and its comorbities.
  • Stringer, S.; Minica, C. C.; Verweij, K. J. H.; Mbarek, H.; Bernard, M.; Derringer, J.; van Eijk, K. R.; Isen, J. D.; Loukola, A.; Maciejewski, D. F.; Mihailov, E.; van der Most, P. J.; Sanchez-Mora, C.; Roos, L.; Sherva, R.; Walters, R.; Ware, J. J.; Abdellaoui, A.; Bigdeli, T. B.; Branje, S. J. T.; Brown, S. A.; Bruinenberg, M.; Casas, M.; Esko, T.; Garcia-Martinez, I.; Gordon, S. D.; Harris, J. M.; Hartman, C. A.; Henders, A. K.; Heath, A. C.; Hickie, I. B.; Hickman, M.; Hopfer, C. J.; Hottenga, J. J.; Huizink, A. C.; Irons, D. E.; Kahn, R. S.; Korhonen, T.; Kranzler, H. R.; Krauter, K.; van Lier, P. A. C.; Lubke, G. H.; Madden, P. A. F.; Magi, R.; McGue, M. K.; Medland, S. E.; Meeus, W. H. J.; Miller, M. B.; Montgomery, G. W.; Nivard, M. G.; Nolte, I. M.; Oldehinkel, A. J.; Pausova, Z.; Qaiser, B.; Quaye, L.; Ramos-Quiroga, J. A.; Richarte, V.; Rose, R. J.; Shin, J.; Stallings, M. C.; Stiby, A. I.; Wall, T. L.; Wright, M. J.; Koot, H. M.; Paus, T.; Hewitt, J. K.; Ribases, M.; Kaprio, J.; Boks, M. P.; Snieder, H.; Spector, T.; Munafo, M. R.; Metspalu, A.; Gelernter, J.; Boomsma, D. I.; Iacono, W. G.; Martin, N. G.; Gillespie, N. A.; Derks, E. M.; Vink, J. M. (2016)
    Cannabis is the most widely produced and consumed illicit psychoactive substance worldwide. Occasional cannabis use can progress to frequent use, abuse and dependence with all known adverse physical, psychological and social consequences. Individual differences in cannabis initiation are heritable (40-48%). The International Cannabis Consortium was established with the aim to identify genetic risk variants of cannabis use. We conducted a meta-analysis of genome-wide association data of 13 cohorts (N = 32 330) and four replication samples (N = 5627). In addition, we performed a gene-based test of association, estimated single-nucleotide polymorphism (SNP)-based heritability and explored the genetic correlation between lifetime cannabis use and cigarette use using LD score regression. No individual SNPs reached genome-wide significance. Nonetheless, gene-based tests identified four genes significantly associated with lifetime cannabis use: NCAM1, CADM2, SCOC and KCNT2. Previous studies reported associations of NCAM1 with cigarette smoking and other substance use, and those of CADM2 with body mass index, processing speed and autism disorders, which are phenotypes previously reported to be associated with cannabis use.
  • Silventoinen, Karri; Konttinen, Hanna (2020)
    Obesity has dramatically increased during the last decades and is currently one of the most serious global health problems. We present a hypothesis that obesity is a neuro-behavioral disease having a strong genetic background mediated largely by eating behavior and is sensitive to the macro-environment; we study this hypothesis from the perspective of genetic research. Genetic family and genome-wide-association studies have shown well that body mass index (BMI, kg/m(2)) is a highly heritable and polygenic trait. New genetic variation of BMI emerges after early childhood. Candidate genes of BMI notably express in brain tissue, supporting that this new variation is related to behavior. Obesogenic environments at both childhood family and societal levels reinforce the genetic susceptibility to obesity. Genetic factors have a clear influence on macro-nutrient intake and appetite-related eating behavior traits. Results on the gene-by-diet interactions in obesity are mixed, but emerging evidence suggests that eating behavior traits partly mediate the effect of genes on BMI. However, more rigorous prospective study designs controlling for measurement bias are still needed.
  • Silventoinen, Karri; Jelenkovic, Aline; Latvala, Antti; Yokoyama, Yoshie; Sund, Reijo; Sugawara, Masumi; Tanaka, Mami; Matsumoto, Satoko; Aaltonen, Sari; Piirtola, Maarit; Freitas, Duarte L.; Maia, Jose A.; Oncel, Sevgi Y.; Aliev, Fazil; 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.; Willemsen, Gonneke; Bartels, Meike; van Beijsterveldt, Catharina E. 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.; Knafo-Noam, Ariel; Mankuta, David; Abramson, Lior; 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.; Nilsen, Thomas S.; Harden, K. Paige; Tucker-Drob, Elliot M.; Franz, Carol E.; Kremen, William S.; Lyons, Michael J.; Lichtenstein, Paul; Jeong, Hoe-Uk; Hur, Yoon-Mi; Boomsma, Dorret I.; Sorensen, Thorkild I. A.; Kaprio, Jaakko (2019)
    Objective The objective of this study was to analyze how parental education modifies the genetic and environmental variances of BMI from infancy to old age in three geographic-cultural regions. Methods A pooled sample of 29 cohorts including 143,499 twin individuals with information on parental education and BMI from age 1 to 79 years (299,201 BMI measures) was analyzed by genetic twin modeling. Results Until 4 years of age, parental education was not consistently associated with BMI. Thereafter, higher parental education level was associated with lower BMI in males and females. Total and additive genetic variances of BMI were smaller in the offspring of highly educated parents than in those whose parents had low education levels. Especially in North American and Australian children, environmental factors shared by co-twins also contributed to the higher BMI variation in the low education level category. In Europe and East Asia, the associations of parental education with mean BMI and BMI variance were weaker than in North America and Australia. Conclusions Lower parental education level is associated with higher mean BMI and larger genetic variance of BMI after early childhood, especially in the obesogenic macro-environment. The interplay among genetic predisposition, childhood social environment, and macro-social context is important for socioeconomic differences in BMI.
  • Masip-Manuel, Guiomar; Silventoinen, Karri; Keski-Rahkonen, Anna; Palviainen, Teemu; Sipilä, Pyry N.; Kaprio, Jaakko; Bogl, Leonie H. (2020)
    Background Obesity susceptibility genes are highly expressed in the brain suggesting that they might exert their influence on body weight through eating-related behaviors. Objectives To examine whether the genetic susceptibility to obesity is mediated by eating behavior patterns. Methods Participants were 3977 twins (33% monozygotic, 56% females), aged 31–37 y, from wave 5 of the FinnTwin16 study. They self-reported their height and weight, eating behaviors (15 items), diet quality, and self-measured their waist circumference (WC). For 1055 twins with genome-wide data, we constructed a polygenic risk score for BMI (PRSBMI) using almost 1 million single nucleotide polymorphisms. We used principal component analyses to identify eating behavior patterns, twin modeling to decompose correlations into genetic and environmental components, and structural equation modeling to test mediation models between the PRSBMI, eating behavior patterns, and obesity measures. Results We identified 4 moderately heritable (h2 = 36–48%) eating behavior patterns labeled “snacking,” “infrequent and unhealthy eating,” “avoidant eating,” and “emotional and external eating.” The highest phenotypic correlation with obesity measures was found for the snacking behavior pattern (r = 0.35 for BMI and r = 0.32 for WC; P < 0.001 for both), largely due to genetic factors in common (bivariate h2 > 70%). The snacking behavior pattern partially mediated the association between the PRSBMI and obesity measures (βindirect = 0.06; 95% CI: 0.02, 0.09; P = 0.002 for BMI; and βindirect = 0.05; 95% CI: 0.02, 0.08; P = 0.003 for WC). Conclusions Eating behavior patterns share a common genetic liability with obesity measures and are moderately heritable. Genetic susceptibility to obesity can be partly mediated by an eating pattern characterized by frequent snacking. Obesity prevention efforts might therefore benefit from focusing on eating behavior change, particularly in genetically susceptible individuals.
  • Silventoinen, Karri; Gouveia, Elvio; Jelenkovic, Aline; Maia, Jose; Antunes, Antonio M.; Pinheiro de Carvalho, Miguel A. A.; Brehm, Antonio M.; Thomis, Martine; Lefevre, Johan; Kaprio, Jaakko; Freitas, Duarte (2017)
    Background: It is well known that metabolic risk factors of cardiovascular diseases are correlated, but the background of this clustering in children is more poorly known than in adults. Thus, we studied the contribution of genetic and environmental factors to the clustering of metabolic traits in childhood and adolescence. Data and Methods: Nine metabolic traits were measured in 214 complete twin pairs aged 3-18 years in the Autonomous Region of Madeira, Portugal, in 2007 and 2008. The variation of and covariations between the traits were decomposed into genetic and environmental components by using classical genetic twin modeling. Results: A model, including additive genetic and environmental factors unique for each twin individual, explained the variation of metabolic factors well. Under this model, the heritability estimates varied from 0.47 (systolic blood pressure in children under 12 years of age) to 0.91 (high-density lipoprotein [HDL] cholesterol in adolescents 12 years of age or older). The most systematic correlations were found between adiposity (body mass index and waist circumference) and blood lipids (HDL cholesterol, low-density lipoprotein cholesterol, and triglycerides), as well as blood pressure. These correlations were mainly explained by common genetic factors. Conclusions: Our results suggest that obesity, in particular, is behind the clustering of metabolic factors in children and adolescents. Both general and abdominal obesity partly share the same genetic background as blood lipids and blood pressure. Obesity prevention early in childhood is important in reducing the risk of metabolic diseases in adulthood.
  • Kaprio, Jaakko; Bollepalli, Sailalitha; Buchwald, Jadwiga; Iso-Markku, Paula; Korhonen, Tellervo; Kovanen, Vuokko; Kujala, Urho; Laakkonen, Eija K.; Latvala, Antti; Leskinen, Tuija; Lindgren, Noora; Ollikainen, Miina; Piirtola, Maarit; Rantanen, Taina; Rinne, Juha; Rose, Richard J.; Sillanpää, Elina; Silventoinen, Karri; Sipilä, Sarianna; Viljanen, Anne; Vuoksimaa, Eero; Waller, Katja (2019)
    The older Finnish Twin Cohort (FTC) was established in 1974. The baseline survey was in 1975, with two follow-up health surveys in 1981 and 1990. The fourth wave of assessments was done in three parts, with a questionnaire study of twins born during 1945-1957 in 2011-2012, while older twins were interviewed and screened for dementia in two time periods, between 1999 and 2007 for twins born before 1938 and between 2013 and 2017 for twins born in 1938-1944. The content of these wave 4 assessments is described and some initial results are described. In addition, we have invited twin-pairs, based on response to the cohortwide surveys, to participate in detailed in-person studies; these are described briefly together with key results. We also review other projects based on the older FTC and provide information on the biobanking of biosamples and related phenotypes.
  • Yokoyama, Yoshie; Jelenkovic, Aline; Sund, Reijo; Sung, Joohon; Hopper, John L.; Ooki, Syuichi; Heikkila, Kauko; Aaltonen, Sari; Tarnoki, Adam D.; Tarnoki, David L.; Willemsen, Gonneke; Bartels, Meike; van Beijsterveldt, Toos C. E. M.; Saudino, Kimberly J.; Cutler, Tessa L.; Nelson, Tracy L.; Whitfield, Keith E.; Wardle, Jane; Llewellyn, Clare H.; Fisher, Abigail; He, Mingguang; Ding, Xiaohu; Bjerregaard-Andersen, Morten; Beck-Nielsen, Henning; Sodemann, Morten; Song, Yun-Mi; Yang, Sarah; Lee, Kayoung; Jeong, Hoe-Uk; Knafo-Noam, Ariel; Mankuta, David; Abramson, Lior; Burt, S. Alexandra; Klump, Kelly L.; Ordonana, Juan R.; Sanhez-Romera, Juan F.; Colodro-Conde, Lucia; Harris, Jennifer R.; Brandt, Ingunn; Nilsen, Thomas Sevenius; Craig, Jeffrey M.; Saffery, Richard; Ji, Fuling; Ning, Feng; Pang, Zengchang; Dubois, Lise; Boivin, Michel; Brendgen, Mara; Dionne, Ginette; Vitaro, Frank; Martin, Nicholas G.; Medland, Sarah E.; Montgomery, Grant W.; Magnusson, Patrik K. E.; Pedersen, Nancy L.; Aslan, Anna K. Dahl; Tynelius, Per; Haworth, Claire M. A.; Plomin, Robert; Rebato, Esther; Rose, Richard J.; Goldberg, Jack H.; Rasmussen, Finn; Hur, Yoon-Mi; Sorensen, Thorkild I. A.; Boomsma, Dorret I.; Kaprio, Jaakko; Silventoinen, Karri (2016)
    We analyzed birth order differences in means and variances of height and body mass index (BMI) in monozygotic (MZ) and dizygotic (DZ) twins from infancy to old age. The data were derived from the international CODATwins database. The total number of height and BMI measures from 0.5 to 79.5 years of age was 397,466. As expected, first-born twins had greater birth weight than second-born twins. With respect to height, first-born twins were slightly taller than second-born twins in childhood. After adjusting the results for birth weight, the birth order differences decreased and were no longer statistically significant. First-born twins had greater BMI than the second-born twins over childhood and adolescence. After adjusting the results for birth weight, birth order was still associated with BMI until 12 years of age. No interaction effect between birth order and zygosity was found. Only limited evidence was found that birth order influenced variances of height or BMI. The results were similar among boys and girls and also in MZ and DZ twins. Overall, the differences in height and BMI between first-and second-born twins were modest even in early childhood, while adjustment for birth weight reduced the birth order differences but did not remove them for BMI.
  • Stephenson, Mallory; Barr, Peter; Ksinan, Albert; Aliev, Fazil; Latvala, Antti; Viken, Richard; Rose, Richard; Kaprio, Jaakko; Dick, Danielle; Salvatore, Jessica E. (2020)
    Background and aims Research on adolescent predictors of later alcohol misuse is typically conducted on samples of singletons, and associations may be confounded by between-family differences. To address potential confounding, we applied a co-twin comparison design to evaluate whether differences between co-twins in a wide array of adolescent risk factors predicted differences in young adult alcohol misuse. Design Longitudinal study in which associations between characteristics of the sample as adolescents were used to predict young adult alcohol misuse in individual-level analyses and co-twin comparisons. Setting Finland. Participants A total of 3402 individuals (1435 complete twin pairs; 36% monozygotic; 57% female) from the FinnTwin12 study. Measurements The young adult alcohol misuse outcome was a composite score of alcohol use and intoxication frequency. Adolescent predictors included factor scores representing academic performance, substance use, externalizing problems, internalizing problems, peer environment, physical health and relationship with parents; and single measures tapping alcohol expectancies, life events and pubertal development. Findings In individual-level analyses, individuals with higher adolescent substance use, externalizing problems, time with friends, peer deviance, sports involvement, sleeping difficulties, parental discipline, positive alcohol expectancies and difficulty of life events reported higher alcohol misuse in young adulthood (Ps <0.019, R-2 = 0.0003-0.0310%). Conversely, those with higher adolescent internalizing problems, parent-child relationship quality and time with parents reported lower alcohol misuse (Ps <0021, R-2 = 0.0018-0.0093%). The associations with adolescent substance use and alcohol expectancies remained significant in co-twin comparisons (Ps <0.049, R-2 = 0.0019-0.0314%). Further, academic performance emerged as a significant predictor, such that individuals with higher grades compared with their co-twin reported higher young adult alcohol misuse (Ps <0.029, R-2 = 0.0449-0.0533%). Conclusions Adolescent substance use, positive alcohol expectancies and higher academic performance appear to be robust predictors of later alcohol misuse.