Decanalization and the origin of complex disease

Complex genetic disease is caused by the interaction between genetic and environmental variables and is the predominant cause of mortality globally. Recognition that susceptibility arises through the combination of multiple genetic pathways that influence liability factors in a nonlinear manner suggests that a process of 'decanalization' contributes to the epidemic nature of common genetic diseases. The rapid evolution of the human genome combined with marked environmental and cultural perturbation in the past two generations might lead to the uncovering of cryptic genetic variation that is a major source of disease susceptibility.

[1]  Peter M Visscher,et al.  Prediction of individual genetic risk to disease from genome-wide association studies. , 2007, Genome research.

[2]  J. Diamond,et al.  The double puzzle of diabetes , 2003, Nature.

[3]  Kenny Q. Ye,et al.  Strong Association of De Novo Copy Number Mutations with Autism , 2007, Science.

[4]  John D. Storey,et al.  A Genome-Wide Gene Expression Signature of Environmental Geography in Leukocytes of Moroccan Amazighs , 2008, PLoS genetics.

[5]  J. Renauld.  New insights into the role of cytokines in asthma , 2001, Journal of clinical pathology.

[6]  Simon C. Potter,et al.  Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls , 2007, Nature.

[7]  Robert C Elston,et al.  The genetic basis of complex traits: rare variants or "common gene, common disease"? , 2007, Methods in molecular biology.

[8]  Majid Ezzati,et al.  Estimates of global mortality attributable to smoking in 2000 , 2003, The Lancet.

[9]  S. Kahn,et al.  Mechanisms linking obesity to insulin resistance and type 2 diabetes , 2006, Nature.

[10]  Thomas W. Mühleisen,et al.  Large recurrent microdeletions associated with schizophrenia , 2008, Nature.

[11]  Wim E Crusio.  Flanking gene and genetic background problems in genetically manipulated mice , 2004, Biological Psychiatry.

[12]  David M. Evans,et al.  Genome-wide association analysis identifies 20 loci that influence adult height , 2008, Nature Genetics.

[13]  P. Ridker,et al.  Novel Association of ABO Histo-Blood Group Antigen with Soluble ICAM-1: Results of a Genome-Wide Association Study of 6,578 Women , 2008, PLoS genetics.

[14]  Elaine Holmes,et al.  Metabolic changes in schizophrenia and human brain evolution , 2008, Genome Biology.

[15]  J. Gulcher,et al.  Refining the impact of TCF7L2 gene variants on type 2 diabetes and adaptive evolution , 2007, Nature Genetics.

[16]  G. Gibson,et al.  Association Between Nucleotide Variation in Egfr and Wing Shape in Drosophila melanogaster , 2004, Genetics.

[17]  W. G. Hill,et al.  Data and Theory Point to Mainly Additive Genetic Variance for Complex Traits , 2008, PLoS genetics.

[18]  N. Barton,et al.  WILL POPULATION BOTTLENECKS AND MULTILOCUS EPISTASIS INCREASE ADDITIVE GENETIC VARIANCE? , 2006, Evolution; international journal of organic evolution.

[19]  Mark M Iles,et al.  What Can Genome-Wide Association Studies Tell Us about the Genetics of Common Disease , 2008, PLoS genetics.

[20]  T. Linksvayer,et al.  The conversion of variance and the evolutionary potential of restricted recombination , 2006, Heredity.

[21]  Mark I. McCarthy,et al.  Assessing the Combined Impact of 18 Common Genetic Variants of Modest Effect Sizes on Type 2 Diabetes Risk , 2008, Diabetes.

[22]  S. Rice.  THE EVOLUTION OF CANALIZATION AND THE BREAKING OF VON BAER'S LAWS: MODELING THE EVOLUTION OF DEVELOPMENT WITH EPISTASIS , 1998, Evolution; international journal of organic evolution.

[23]  David N. Messina,et al.  Evolutionary and Biomedical Insights from the Rhesus Macaque Genome , 2007, Science.

[24]  Eric M. Morrow,et al.  Identifying Autism Loci and Genes by Tracing Recent Shared Ancestry , 2008, Science.

[25]  R. Germain,et al.  Variability and Robustness in T Cell Activation from Regulated Heterogeneity in Protein Levels , 2008, Science.

[26]  Greg Gibson,et al.  Uncovering cryptic genetic variation , 2004, Nature Reviews Genetics.

[27]  L. Liang,et al.  Genome-Wide Scan on Total Serum IgE Levels Identifies FCER1A as Novel Susceptibility Locus , 2008, PLoS genetics.

[28]  E. Klein,et al.  Major depression as a disorder of serotonin resistance: inference from diabetes mellitus type II. , 2007, International Journal of Neuropsychopharmacology.

[29]  D. Goldstein,et al.  Human Genetics: The Hidden Text of Genome-wide Associations , 2007, Current Biology.

[30]  J. True,et al.  Developmental system drift and flexibility in evolutionary trajectories , 2001, Evolution & development.

[31]  D. Haegert.  Analysis of the threshold liability model provides new understanding of causation in autoimmune diseases. , 2004, Medical Hypotheses.

[32]  G. Wagner,et al.  The Population Genetic Theory of Hidden Variation and Genetic Robustness , 2004, Genetics.

[33]  T. Flatt.  The Evolutionary Genetics of Canalization , 2005, The Quarterly Review of Biology.

[34]  Judy H. Cho,et al.  Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease , 2008, Nature Genetics.

[35]  S. Rice.  Theoretical Approaches to the Evolution of Development and Genetic Architecture , 2008, Annals of the New York Academy of Sciences.

[36]  Ryan D. Hernandez,et al.  Natural selection on protein-coding genes in the human genome , 2005, Nature.

[37]  A. Rienzo,et al.  An Evolutionary Framework for Common Disease , 2007 .

[38]  Garth A. Gibson,et al.  Canalization in evolutionary genetics: a stabilizing theory? , 2000, BioEssays : news and reviews in molecular, cellular and developmental biology.

[39]  D. Strachan.  Family size, infection and atopy: the first decade of the 'hygiene hypothesis' , 2000, Thorax.

[40]  J. Hugot,et al.  For Personal Use. Only Reproduce with Permission from the Lancet Publishing Group. Cold Chain and Crohn's Disease Crohn's Disease: the Cold Chain Hypothesis , 2022 .

[41]  Adrian Gherman,et al.  Population Bottlenecks as a Potential Major Shaping Force of Human Genome Architecture , 2007, PLoS genetics.

[42]  S. Chanock,et al.  Common variants of FUT2 are associated with plasma vitamin B12 levels , 2008, Nature Genetics.

[43]  P. Phillips.  Epistasis — the essential role of gene interactions in the structure and evolution of genetic systems , 2008, Nature Reviews Genetics.

[44]  Michael Dean,et al.  Balanced polymorphism selected by genetic versus infectious human disease. , 2003, Annual review of genomics and human genetics.

[45]  Taghreed Adam,et al.  The burden and costs of chronic diseases in low-income and middle-income countries , 2007, The Lancet.

[46]  M. McCarthy,et al.  Genome-wide association studies: potential next steps on a genetic journey. , 2008, Human molecular genetics.

[47]  W. Cookson,et al.  The alliance of genes and environment in asthma and allergy , 1999, Nature.

[48]  M. Permutt,et al.  Post Genome-Wide Association Studies of Novel Genes Associated with Type 2 Diabetes Show Gene-Gene Interaction and High Predictive Value , 2008, PloS one.