The Metabolic Syndrome: A Modern Plague Spread by Modern Technology

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73419/1/j.1751-7176.2009.00191.x.pd

Unexpected syncope and death during intense physical training:evolving role of molecular genetics

Special operations forces (SOF) undergo an unparalleled degree of physical training. The medical officer responsible for these personnel must often deal with episodes of syncope that cannot be readily explained. In the past, loss of consciousness during heavy physical exertion was attributed to inadequate fluid intake resulting in dehydration or abnormalities in temperature regulation. However, many of those diagnoses, in retrospect were probably incorrect. The occurrence of exercise-related syncope in multiple members of the same family suggested that there could be a genetic basis for the unexpected loss of consciousness during exercise. Intensive clinical examinations of these patients, coupled with current advances in molecular genetics, have shown this to be the case. We review some of the more common genetic abnormalities associated with exertion-related syncope. These syndromes should be considered by the medical officer presented with a patient having syncope of indeterminate cause

Vascular reactivity and high dietary eicopentaenoic acid

Epidemiologic studies suggest that high dietary intake of eicosapentaenoic acid (EPA), a precursor of the trienoic prostaglandins, is associated with a low incidence and reduced extent of myocardial infarction. Vascular reactivity of isolated aortic strips from rats maintained for 3 weeks on a control diet or on a diet supplemented with menhaden fish oil (17% EPA) was examined with norepinephrine, sodium arachidonate, KCl, PGF2[alpha] and nitroprusside. Aortic strips from rats fed the fish oil diet were significantly less responsive to the contractile effects of norepinephrine and arachidonate compared to those from control diet rats. Treatment of aortic strips with indomethacin decreased responsiveness to norepinephrine. The magnitude of the decrease was greater in control rats resulting in a similar vascular response between the 2 groups after blockade. Contractions to arachidonate were abolished by indomethacin. There were no differences in vascular responses to KCl, PGF2[alpha] and nitroprusside in aortic strips from control diet rats and those from the fish oil diet rats. Aortic strips from the fish oil diet rats contained more EPA than those from the control diet rats. Thus, the contractile effect of norepinephrine in isolated rat aortic strips is normally augmented by intrinsic prostaglandins, and this augmentation is diminished by dietary intake of EPA.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/23822/1/0000061.pd

Cognitive Dysfunction and Diabetes Mellitus

The deleterious effects of diabetes mellitus on the retinal, renal, cardiovascular, and peripheral nervous systems are widely acknowledged. Less attention has been given to the effect of diabetes on cognitive function. Both type 1 and type 2 diabetes mellitus have been associated with reduced performance on numerous domains of cognitive function. The exact pathophysiology of cognitive dysfunction in diabetes is not completely understood, but it is likely that hyperglycemia, vascular disease, hypoglycemia, and insulin resistance play significant roles. Modalities to study the effect of diabetes on the brain have evolved over the years, including neurocognitive testing, evoked response potentials, and magnetic resonance imaging. Although much insightful research has examined cognitive dysfunction in patients with diabetes, more needs to be understood about the mechanisms and natural history of this complication in order to develop strategies for prevention and treatment