The fat tail of obesity as told by the genome.
OBJECTIVE
Many genes affect pathways that predispose to and protect against obesity. We ask how many different variants affect human obesity and how common are they?


RESULTS
The current generation of genome-wide association scans is moderately powered to detect and replicate associations between single nucleotide polymorphisms, or common copy number variations and common diseases. They are not designed either to find rare germline variants or those somatic changes, unique to an individual, that arise with high frequency in adult stem cells. They do not directly assay the epigenetic reprogramming of outcomes related to maternal or environmental exposures.


CONCLUSIONS
There are more gene variants, more gene-gene and gene-environmental interactions leading to obesity than current genome-wide association scan studies can verify. Those genetic associations that can be validated provide valuable insight into the pathways contributing to human obesity.
Herbert
Alan
A
Department of Genetics and Genomics, Boston University School of Medicine, Boston, Massachusetts 02118, USA. aherbert@bu.edu
D004777:Environment; D044127:Epigenesis, Genetic; D005260:Female; D014644:Genetic Variation; D015894:Genome, Human; D006801:Humans; D008297:Male; D009765:Obesity / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects