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American Journal of Epidemiology 2005 161(10):995; doi:10.1093/aje/kwi128
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American Journal of Epidemiology Copyright © 2005 by the Johns Hopkins Bloomberg School of Public Health All rights reserved

LETTERS TO THE EDITOR

RE: "Carbohydrate Intake, Glycemic Index, Glycemic Load, and Dietary Fiber in Relation to Risk of Stroke in Women"

Celia M. Ross

36 Ridgewood Circle, Wilmington, DE 19809

In a recent paper, Oh et al. (1Go) found that a high intake of refined carbohydrates was associated with hemorrhagic stroke. They offered a number of mechanisms to explain this association. There is an additional mechanism that may work in conjunction with the others. A high glucose intake is associated with the accumulation of advanced glycation end products (AGEs) in vessel walls (2Go). AGE accumulation results in vascular abnormalities. Vascular permeability is enhanced by AGEs (3Go). This is due to disruption of the vascular endothelial cadherin complex (4Go), which weakens cell-cell contacts. AGEs are also proinflammatory (5Go) and trigger a reduction of endothelial nitric oxide synthase expression (6Go). These factors contribute to endothelial dysfunction, which is associated with stroke (7Go). Rats bred to model hemorrhagic stroke (stroke-prone spontaneously hypertensive rats (SHRSP)) display greater accumulation of AGEs of the aorta than do Wistar-Kyoto rats (8Go). It is interesting to note that an inhibitor of AGE formation reduces hypertension, one of the risk factors for stroke, in SHRSP rats (9Go).

NOTES

Editor's note: In accordance with Journal policy, Oh et al. were asked whether they wanted to respond to this letter, but they chose not to do so.

References

  1. Oh K, Hu FB, Cho E, et al. Carbohydrate intake, glycemic index, glycemic load, and dietary fiber in relation to risk of stroke in women. Am J Epidemiol 2005;161:161–9.[Abstract/Free Full Text]
  2. Yamada S, Ohkubo C. The influence of frequent and excessive intake of glucose on microvascular aging in healthy mice. Microcirculation 1999;6:55–62.[CrossRef][Web of Science][Medline]
  3. Svensjo E, Cyrino F, Michoud E, et al. Vascular permeability increase as induced by histamine or bradykinin is enhanced by advanced glycation endproducts (AGE). J Diabetes Complications 1999;13:187–90.[CrossRef][Web of Science][Medline]
  4. Otero K, Martinez F, Beltran A, et al. Albumin-derived advanced glycation end-products trigger the disruption of the vascular endothelial cadherin complex in cultured human and murine endothelial cells. Biochem J 2001;359:567–74.[CrossRef][Web of Science][Medline]
  5. Basta G, Lazzerini G, Massaro M, et al. Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses. Circulation 2002;105:816–22.[Abstract/Free Full Text]
  6. Rashid G, Benchetrit S, Fishman D, et al. Effect of advanced glycation end-products on gene expression and synthesis of TNF-alpha and endothelial nitric oxide synthase by endothelial cells. Kidney Int 2004;66:1099–106.[CrossRef][Web of Science][Medline]
  7. Targonski PV, Bonetti PO, Pumper GM, et al. Coronary endothelial dysfunction is associated with an increased risk of cerebrovascular events. Circulation 2003;107:2805–9.[Abstract/Free Full Text]
  8. Mizutani K, Ikeda K, Kawai Y, et al. Biomechanical properties and chemical composition of the aorta in genetic hypertensive rats. J Hypertens 1999;17:481–7.[CrossRef][Web of Science][Medline]
  9. Mizutani K, Ikeda K, Tsuda K, et al. Inhibitor for advanced glycation end products formation attenuates hypertension and oxidative damage in genetic hypertensive rats. J Hypertens 2002;20:1607–14.[CrossRef][Web of Science][Medline]

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