For long it is known that shorter adult height is associated with an increased risk of coronary artery disease. This association is mainly explained by
by the association between shorter height and an adverse lipid profile.
A collaborative effort with national and international colleagues led by Nilesh Samani (University of Leicester) studied the association between height-associated
genetic variants and CAD.
The main advantage of our genetic approach is that it reduces the likelihood of known and unknown demographic, lifestyle, socioeconomic, or behavioral
confounders that have an independent effect on height and the risk of CAD and could give rise to a false association between the two factors.
It is possible that the association between the studied genetic variants and height and the association with CAD are through completely different mechanisms. However, the more likely scenario on the basis of our findings is that height variants affect biologic pathways, which on the one hand determine achieved height and on the other hand
influence the risk of CAD. It is also possible that genetically determined height itself alters lifestyle or behavior, which then affects the risk of CAD.
The study is published online in the New England Journal of Medicine.
