Sub-Areas to Risk Factors and Susceptibility:
(Journal Article): The increase in risk of diabetes mellitus from exposure to second-generation antipsychotic agents
Citrome LL (New York University School of Medicine, Department of Psychiatry, New York; Nathan S. Kline Institute for Psychiatric Research, Clinical Research and Evaluation Facility, Orangeburg, New York, USA,
citrome@nki.rfmh.org
)
IN:
Drugs Today (Barc)
2004; 40(5):445-464
Impact Factor(s) of Drugs Today (Barc): 0.936 (2004), 0.525 (2003), 0.626 (2001)
ABSTRACT: This is a review of the evidence for a link between exposure to second-generation antipsychotic agents and the development of type 2 diabetes mellitus. Most of this evidence comes from case series and retrospective pharmacoepidemiological studies. Exposure to second-generation antipsychotic agents increases the risk for diabetes mellitus compared to no exposure to antipsychotic drugs. The risk with second-generation antipsychotic agents compared to exposure to first-generation antipsychotics is smaller and not consistent. The differential risk among the second-generation antipsychotic agents has not yet been adequately established. Other risk factors for diabetes mellitus, such as advancing age, non-White ethnicity, family history, obesity, lack of physical activity and the diagnosis of schizophrenia, probably contribute more to the risk than exposure to any single antipsychotic drug. Clinicians are urged to manage risk by regularly monitoring all patients receiving second-generation antipsychotic agents for the emergence of diabetes mellitus.
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(Journal Article): Sedentary death syndrome
Lees SJ, Booth FW (Dept. of Biomedical Sciences, Univ. of Missouri-Columbia, Columbia, MO, USA)
IN:
Can J Appl Physiol
2004; 29(4):447-460
Impact Factor(s) of Can J Appl Physiol: 1.126 (2004), 1.211 (2003), 1.386 (2001)
ABSTRACT: Sedentary death syndrome (SeDS) is a major public health burden due to its causing multiple chronic diseases and millions of premature deaths each year. Despite the impact of physical inactivity, very little is known about the actual causes of physical inactivity-induced chronic diseases. It is important to study the mechanisms underlying molecular changes related to physical inactivity in order to better understand the scientific basis of individualized exercise prescription and therapies for chronic diseases, and to support improved public health efforts by providing molecular proof that physical inactivity is an actual cause of chronic diseases. Physical activity has a genetic basis. A subpopulation of genes, which have functioned to support physical activity for survival through most of humankind's existence, require daily exercise to maintain long-term health and vitality. Type 2 diabetes (T2D) is an example of a SeDS condition, as it is almost entirely preventable with physical activity. To determine the true role of physical inactivity in the development and progression of T2D, information is presented which indicates that comparisons should be made to physically active controls, rather than sedentary controls, as this population is the healthiest. Use of sedentary subjects as the control group has led to potentially misleading interpretations. If physically active individuals were designated as the control group, a different interpretation would have been drawn. It is thought that there is no difference in GLUT4 concentration between T2D and sedentary groups. However, GLUT4 expression is higher in active controls than in sedentary and T2D groups. Therefore, to obtain causal mechanisms for SeDS in order to allow for scientifically based prevention and therapy strategies, physically active subjects must serve as the control group.
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