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Dress Women's Agata Joie Sandal Black Womens nHBfY

Black Womens Joie Agata Women's Dress Sandal Posted on 12/01/10

MB, a 48-year-old African American woman, presented to her nurse practitioner to follow up on a recent blood test that indicated moderately elevated levels of fasting blood glucose (118 mg/dL) and hemoglobin A1c (6.2%). Over the previous year, MB had gained 25 pounds, which increased her body mass index to 29.8. The nurse practitioner explained to MB that her fasting glucose and body weight put her at risk for developing type 2 diabetes. They discussed dietary changes and an exercise program as preventive measures. During this conversation, MB expressed an interest in learning about the negative health outcomes associated with type 2 diabetes.

"From articles that I've read about diabetes in health magazines and on the Internet," she said, "I know that having too much sugar in the blood is a sign of trouble. But I don't understand what could happen to my body if my glucose levels stay high. And I'm betting that if I know the risks, I'll be more mindful about exercising and eating the right foods. So, for people with diabetes, what are the risks of too much blood glucose?"

Discussion

As reported in the 2007 National Health and Nutrition Examination Survey (NHANES), more than 23 million people in the US, almost 8% of the population, had diabetes.Joie Dress Sandal Womens Women's Agata Black 1 The NHANES report ranked diabetes as the seventh leading cause of death in the US. The risk for developing type 2 diabetes, which accounts for 90% to 95% of all diabetes cases, is especially high in minority racial and ethnic groups including African Americans, Hispanic/Latino Americans, American Indians, and some groups of Asian Americans. In a 2010 analysis conducted by the Centers for Disease Control and Prevention, researchers predicted that more than 30% of Americans will have diabetes by 2050 if recent trends of its increasing incidence continue.2

Hyperglycemia, the physiological hallmark of type 2 diabetes, is caused by the combination of insulin resistance -- especially in skeletal muscle and adipose tissue -- and inadequate compensatory secretion of insulin from the pancreas. Through a number of mechanisms that have yet to be fully elucidated, chronically elevated blood glucose can damage vascular and neural tissue. The resulting microvascular complications are retinopathy, which can lead to blindness; nephropathy and associated renal failure; peripheral neuropathy, which increases risks of foot ulcers and amputation; and autonomic neuropathy, which often causes genitourinary and gastrointestinal symptoms. The main macrovascular complications of diabetes-related hyperglycemia are coronary heart disease (CHD) and cerebrovascular disease.

Published in 2010, 2 large-scale studies provide updated evidence that links diabetes-related hyperglycemia and macrovascular disease. The Lancet published a meta-analysis of 102 community-based studies that followed nearly 700,000 people over a median of 10.8 years.3 Study participants who had diabetes at baseline were significantly more likely than their healthy counterparts to develop non-fatal or fatal vascular diseases. Risks of CHD and ischemic stroke were approximately 2 times greater among those diagnosed with diabetes. The disease was also associated with a 73% increase in the risk of death due to vascular diseases. For study participants with fasting glucose concentrations in the normal range (70-101 mg/dL), the risk of developing vascular disease was negligible. In contrast, at a fasting glucose concentration of 126 mg/dL, CHD risk increased by 78%. Above 101 mg/dL, every 18 mg/dL increase in fasting glucose was associated with a 12% increase in CHD risk.   

Another 2010 article, which was published in The New England Journal of Medicine, provided new evidence on the association between HbA1c levels and vascular disease risk.4 The article reported the latest findings from the Atherosclerosis Risk in Communities (ARIC) study, which has followed nearly 16,000 people since 1987. In the 2010 study, which followed a cohort of 11,092 adults over approximately 14 years, the incidence of newly diagnosed diabetes was 6% among participants whose HbA1c values were lower than 5% at baseline. Diabetes incidence increased to 79% among participants whose HbA1c values exceeded 6.5%. At HbA1c values between 5.0% and 5.5%, which served as a reference level, CHD risk was negligible. However, among study participants whose HbA1c values exceeded 6.5%, the risk of developing CHD increased by 95%. The risk of ischemic stroke was approximately 3 times greater for patients with HbA1c values above 6.5%.

Combined with reports from the landmark United Kingdom Prospective Diabetes Study,5 the 2010 studies summarized above provide compelling evidence for high risks of macrovascular disease in patients with diabetes whose hyperglycemia is not controlled. This information can aid health care professionals in educating patients about their risks and in encouraging adherence to effective lifestyle and pharmaceutical interventions.

References

  1. Centers for Disease Control and Prevention. National Diabetes Fact Sheet, 2007. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2007.pdf. Accessed November 22, 2010.
  2. Boyle JP, Thompson TJ, Gregg, EW, Barker LE, Williamson DF. Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence. Popul Health Metr. 2010;8(1):29. [Epub ahead of print]
  3. The Emerging Risk Factors Collaboration. Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies. Lancet. 2010;375:2215-2222.
  4. Selvin E, Steffes MW, Zhu H, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. N Engl J Med. 2010;362:800-811.
  5. Stratton IM, Adler AI, Neil HA, et al.Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000;321:405-412.