• Users Online: 755
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Contacts Login 
Year : 2016  |  Volume : 1  |  Issue : 1  |  Page : 14-23

Genotype, environment, and evolutionary mechanism of diseases

1 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine; Department of Pathology, Wayne State University School of Medicine; Karmanos Cancer Institute, Detroit, USA
2 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit; Division of Graduate Medical Sciences, Boston University School of Medicine, Boston, MA, USA
3 Division of Hematology/Oncology, University of Michigan Comprehensive Cancer Center, Ann Arbor, MI, USA

Correspondence Address:
Henry H. Q. Heng
3226 Scott Hall, 540 E. Canfield, Detroit, MI 48201
Login to access the Email id

Source of Support: None, Conflict of Interest: None

Rights and PermissionsRights and Permissions

Large-scale genomic projects have unexpectedly challenged the current approach of focusing on genes in disease studies. As common gene mutations are difficult to identify for common/complex diseases, and the diagnostic distinction of gene profile between “normal” and “patient” becomes increasingly blurry, the power of gene-focused studies in medicine is actually decreasing. More attention is now being focused on gene–environment interaction. However, such a transition is still within the framework of using molecular descriptions of specific genes for understanding diseases, which is challenging in the clinic, where nonlinear relationships are dominant. In this article, we define diseases as genotype/environment-induced variants that are not compatible with a current environment. This explains (1) why the genotype is not simply the gene mutation profile, but comprised of multiple levels of genetic/nongenetic (including epigenetic) variations, as environmental dynamics require all sorts of system modifications; (2) why many disease conditions represent a trade-off of cellular adaptation, in addition to inherited or environment-induced bio-errors; and (3) why costly variants function as the “insurance policy” for adapting to the unpredictability of environments. This leads to the general mechanism of the majority of diseases: genotype–environment interaction generates variations, which are either essential for future crises or useful for current cellular function. Unfortunately, as a trade-off, these variants also contribute to diseases. This general mechanism can unify diverse specific molecular mechanisms, and suggests that the goal of eliminating all diseases is not only impossible, but also comes with the potential negative consequence of reducing the heterogeneity essential for human survival.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded1122    
    Comments [Add]    

Recommend this journal