Metabolic syndrome (MetS) is a common complex trait consisting of the clustering 
of abdominal obesity, hypertension, dyslipidemia, and dysglycemia. MetS is found 
in about 25% of the population in the United States and is associated with 
increased risk for type 2 diabetes and cardiovascular disease. Despite research 
into possible genetic influences for MetS, no consistently reproducible genetic 
markers have been obtained, partially due to lack of agreement on the definition 
of the phenotype. Because phenotypic precision is essential for genomic 
interrogation, the evolving discipline of clinical phenomics, which uses 
objective and systematic acquisition of phenotypic data (ie, "deep 
phenotyping"), may help evaluate the genetic influences of MetS. This article 
reviews evidence that MetS has a genetic component and the potential 
applicability of clinical phenomics for the genetic evaluation of MetS using the 
example of hierarchical cluster analysis of phenotypic components of 
lipodystrophy syndromes, which serve as monogenic models of MetS.