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The high prevalence of CM and peptic ulcer disease comorbidity in our study cohort may be attributed to their shared etiology.
In both sexes, the externalizing factor accounted for little variance in control, indicating a weak association and little shared etiology with externalizing liability.
This frequent comorbidity suggests shared etiology.
Thus, diagnostic homogeneity is no guarantee for uniform pathology and even less so, for shared etiology.
In addition, the observed increase in CHF associated with rosiglitazone may derive from a shared etiology.
Yet these disorders co-occur at above chance levels, suggesting shared etiology.
Similar(33)
Our approach enables exploring shared etiologies of comorbid diseases at the molecular pathway level.
It is well established that there is a clear clinical association between these conditions and sleep disturbances; while preclinical studies are beginning to propose novel mechanisms that underlie these shared etiologies [9, 89].
The direction of the association between the two is what remains unclear, because both have overlapping symptoms, reciprocal effects and shared etiologies [ 35, 79, 83].
9, 26– 29 For example, PC and cardiovascular disease share common risk factors (eg, age, race, and family history), and biological interaction or shared etiologies may cause increased severity of both conditions.
The co-existence of disorders and the development of one problem into another raise important research questions, such as the possibility of shared etiologies and risk factors associated with heterogeneous phenotypes [ 7].
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