Life Extension Update
Benfotiamine prevents endothelial dysfunction after AGE-rich meal
A report published in the September, 2006 issue of the American Diabetes Association journal Diabetes Care revealed the finding of researchers in Germany that type 2 diabetics who consumed benfotiamine before a meal rich in damaging advanced glycation end products (AGEs) were prevented from experiencing the impairment in endothelial function that would have otherwise occurred. Dysfunction of the lining of the blood vessels, or endothelium, accompanies conditions associated with increased cardiovascular risk such as smoking, abnormal lipids, arterial hypertension, obesity, coronary artery disease, congestive heart failure, and both types of diabetes. Endothelial dysfunction that follows a meal occurs in patients with cardiovascular disease and diabetes, and can also occur in healthy individuals.
For the current research, 13 type 2 diabetics were provided with a meal containing high amounts of AGEs: damaging molecules formed in food during cooking that are partially retained in the body after consuming them, and which are also endogenously produced. On the following three days the subjects were given 1,050 milligrams per day benfotiamine, a fat soluble form of vitamin B1 which has greater bioavailability than thiamine, the commonly consumed form of the vitamin. Following treatment with benfotiamine, participants were again provided with a high AGE meal. After each AGE-rich meal, endothelial function was assessed at the macrovascular and microvascular level as well as via serum markers, and markers of inflammation and oxidative stress were measured.
While the initial high AGE meal adversely affected flow mediated dilatation of the arteries (an assessment of macrovascular endothelial function), this impairment was completely prevented following treatment with benfotiamine. Benfotiamine also prevented the effect of the high AGE meal on microvascular endothelial dysfunction, and blood markers of the condition were reduced. Thiobarbituric acid reacting substances, which indicate oxidative stress and which were initially increased after the AGE-rich meal, were reduced by treatment with benfotiamine. Additionally, serum AGEs decreased.
“Our study confirms micro- and macrovascular endothelial dysfunction accompanied by increased oxidative stress following a real-life, heat-processed, AGE-rich meal in individuals with type 2 diabetes and suggests benfotiamine as a potential treatment,” the authors conclude.
Glycation and oxidative stress are central to the damage caused by diabetes. Unfortunately, neither of them figures into conventional treatment for diabetes, which is generally concerned only with blood sugar control.
Glycation occurs when glucose reacts with protein, resulting in sugar-damaged proteins called advanced glycation end products (AGEs) (Kohn RR et al 1984; Monnier VM et al 1984). One well-known AGE among diabetics is glycated hemoglobin (HbA1c). HbA1c is created when glucose molecules bind to hemoglobin in the blood. Measuring HbA1c in the blood can help determine the overall exposure of hemoglobin to glucose, which yields a picture of long-term blood glucose levels.
Glycated proteins cause damage to cells in numerous ways, including impairing cellular function, which induces the production of inflammatory cytokines (Wright E Jr. et al 2006) and free radicals (Forbes JM et al 2003; Schmidt AM et al 2000). In animal studies, inhibiting glycation protects against damage to the kidney, nerves, and eyes (Forbes JM et al 2003; Sakurai S et al 2003). In a large human trial, therapies that resulted in each 1 percent reduction in HbA1c correlated with a 21 percent reduction in risk for any complication of diabetes, a 21 percent reduction in deaths related to diabetes, a 14 percent reduction in heart attack, and a 37 percent reduction in microvascular complications (Stratton IM et al 2000).
High levels of blood glucose and glycation also produce free radicals that further damage cellular proteins (Vincent AM et al 2005) and reduce nitric oxide levels. Nitric oxide is a potent vasodilator that helps keep arteries relaxed and wide open. Oxidative stress in diabetes is also linked to endothelial dysfunction, the process that characterizes atherosclerotic heart disease. According to studies, diabetes encourages white blood cells to stick to the endothelium, or the thin layer of cells that line the inside of arteries. These white blood cells cause the local release of pro-inflammatory chemicals that damage the endothelium, accelerating atherosclerosis (Lum H et al 2001). Diabetes is closely associated with severe coronary heart disease and increased risk of heart attack.
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