Conditions were added as two distinct common causes to SC fat
Conditions were added as two distinct common causes to SC fat cell size and OM fat cell size. Almost all the undirected edges were oriented based on current PD150606 cost literature as follows. Edges directed from the age variable were oriented based on the well-documented impact of ageing on visceral adipose tissue accumulation, blood pressure and plasma LDL-cholesterol levels [20,21]. The edge between age and tea consumption is based on the 2004 Canadian Community Health Survey, which showed a steady increase in tea consumption from 19 to more than 71 years of age [22]. The edge between tea consumption and blood pressure was oriented based on literature showing lower cardiovascular disease risk in tea consumers [23] and a direct effect of black teaconsumption on peripheral blood flow and arterial stiffness [24]. The edge between PubMed ID: age and the number of live children was attributed to the slight decrease in Canadian birth rates observed between 1961-66 and 1981-86 [25], which corresponds approximately to the period in which women of the study had their children. Accordingly, older women of the sample were more likely to have delivered slightly more children. Orientation of the edge between the number of pregnancies and the number of live children is self-explanatory. The edge between the number of live children and OM fat cell size was derived from literature supporting that post-pregnancy weight retention is an important risk factor for obesity [26]. The finding of a specific association between the number of children and OM fat cell size was novel and warrants further investigation. The edges between OM and SC fat cell sizes and the variables obesity or visceral fat is self explanatory since the excess adipose tissue mass of obese or abdominal obese individuals is constituted of larger fat cells. Associations between fat cell size and obesity have been previously observed [27]. The edges between visceral fat or large OM fat cells and metabolic variables such as LDL-cholesterol, triglycerides and blood pressure wasAussem et al. BMC Bioinformatics 2010, 11:487 6 oforiented based on the `portal vein hypothesis’, which states that visceral fat is a causal agent for metabolic disturbances [28]. However, this hypothesis has not yet been fully proven as operative and has been challenged by a number of investigators. Further studies are required to firmly establish causality. However, the fact that the association between visceral fat and metabolic disturbances is independent from overall obesity is wellaccepted [29,30]. The edges between the various components of body composition (i.e., bone density, lean body mass and obesity) were logical but it was difficult to provide causal direction between these variables. Indeed, many genetic, epigenetic, developmental and environmental factors can contribute to determine body built of a given individual. Moreover, the sizes of all compartments generally evolve in a more or less coordinated manner throughout the individual’s existence [31,32]. It was expected that the variable 5-yr maximal weight would be a strong correlate of the level of obesity and lean body mass since these variables are the main components of body composition [32] and that most patients reported a stable weight in the five years preceding their inclusion in the study. The edges around the number of hours of work and the number of meals out per week were oriented based on the demonstration that in.