The current trends of metabolic syndrome among women of childbearing age demonstrate the need for additional rigorous investigations regarding its long-term effects in these women and their offspring.
Stress fractures are a common overuse problem among military trainees resulting in preventable morbidity, prolonged training, and long-term disability following military service. Femoral neck stress fractures (FNSFs) account for 2% of all stress fractures but result in disproportionate burden in terms of cost and convalescence. The purpose of this study was to describe and investigate FNSF in U.S. Air Force basic trainees and to present new data on risks factors for developing FNSF. We examined 47 cases of FNSF occurring in Air Force basic trainees between 2008 and 2011 and 94 controls using a matched case-control model. Analysis with t tests and conditional logistic regression found the risk of FNSF was not associated with body mass index or abdominal circumference. Female gender (p < 0.001) and slower run time significantly increased risk of FNSF (1.49 OR, p < 0.001; 95% CI 1.19-1.86). A greater number of push-up and sit-up repetitions significantly reduced risk of FNSF (0.55 OR, p = 0.03; 95% CI 0.32-0.93; 0.62 OR, p = 0.04; 95% CI 0.4-0.98) for females. In this study body mass index was not correlated with FNSF risk; however, physical fitness level on arrival to training and female gender were significantly associated with risk of FNSF.
The lack of knowledge about the earliest events in disease development is due to the multi-factorial nature of disease risk. This information gap is the consequence of the lack of appreciation for the fact that most diseases arise from the complex interactions between genes and the environment as a function of the age or stage of development of the individual. Whether an environmental exposure causes illness or not is dependent on the efficiency of the so-called “environmental response machinery” (i.e., the complex of metabolic pathways that can modulate response to environmental perturbations) that one has inherited. Thus, elucidating the causes of most chronic diseases will require an understanding of both the genetic and environmental contribution to their etiology. Unfortunately, the exploration of the relationship between genes and the environment has been hampered in the past by the limited knowledge of the human genome, and by the inclination of scientists to study disease development using experimental models that consider exposure to a single environmental agent. Rarely in the past were interactions between multiple genes or between genes and environmental agents considered in studies of human disease etiology. The most critical issue is how to relate exposure-disease association studies to pathways and mechanisms. To understand how genes and environmental factors interact to perturb biological pathways to cause injury or disease, scientists will need tools with the capacity to monitor the global expression of thousands of genes, proteins and metabolites simultaneously. The generation of such data in multiple species can be used to identify conserved and functionally significant genes and pathways involved in gene-environment interactions. Ultimately, it is this knowledge that will be used to guide agencies such as the U.S. Department of Health and Human Services in decisions regarding biomedical research funding and policy.
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