Preventing Glucose-Induced Cardiovascular Damage - Michaels

Preventing Glucose-Induced Cardiovascular Damage

Conditions Associated With Elevated Blood Glucose and Advanced Glycation End Products

Elevated cholesterol and atherosclerosis49,50 Symptoms of carotid artery atherosclerosis (major risk for stroke)51 Risk of developing high risk cardiac rhythm disturbances following heart attack52 Cataracts of the eye35 Overall risk of developing cancer53 Risk of developing fatal cancer54 Increased prostate size in benign prostatic hyperplasia (BPH)55 Abnormal elevation in liver enzymes, markers of liver damage56 Incidence and severity of obstructive sleep apnea57

Blood vessels are lined by a thin layer of cells called the endothelium which constantly regulates blood pressure and flow. Damage to the endothelium, which occurs in response to elevated glucose levels, is an important first step in producing heart attacks, heart failure, and stroke.

Studies now show that benfotiamine can prevent endothelial dysfunction and substantially improve blood vessel and heart muscle function, even in the face of glucose-induced tissue damage.

The process of healthy endothelial cell replication is vital to maintaining healthy arteries. Excess levels of glucose can reduce endothelial cell replication. The addition of benfotiamine to endothelial cells grown in a high-glucose environment corrects the defective replication. Benfotiamine accomplishes this through normalization of advanced glycation end product production.

High glucose levels also trigger early death of endothelial cells through the process called apoptosis; benfotiamine supplementation reverses increased apoptosis in cultures of endothelial cells by several mechanisms.

The body produces toxic alcohol-like compounds called polyols during periods of high blood sugar. Polyols disrupt endothelial and cardiovascular cell function. Benfotiamine reduces production of polyols, accelerates the rate of glucose breakdown, and reduces free glucose levels within cells. All of these effects further contribute to protection of endothelial cell function.

After a heart attack, or as a result of persistently high blood pressure, heart muscle cells beat more weakly than they should, resulting in heart failure. High glucose levels and advanced glycation end products substantially contribute to this diminished heart muscle function. Studies show that benfotiamine abolishes many of the abnormalities in heart muscle cell contractility, which may "rescue" impaired heart muscle and improve its ability to pump blood effectively. Benfotiamine activates important cell survival signaling pathways in heart muscle cells failing under the effects of elevated glucose.

Atherosclerosis

Not all advanced glycation end products (AGEs) are produced internally in the body. Consuming a meal rich in AGEs (such as one abundant in browned meats or caramelized sugars) can increase blood levels of AGEs and impair endothelial function. Supplementation with benfotiamine, 1,050 mg/day for 3 days, completely prevented the changes in endothelial function and blood flow produced by such a meal in a group of human subjects.

In addition to its effective control of AGE-related endothelial dysfunction, benfotiamine exerts powerful direct antioxidant effects. In rats with experimentally induced vascular endothelial dysfunction, benfotiamine reduced oxidative stress and enhanced favorable generation of nitric oxide, a compound that contributes to blood vessel relaxation.33,34 The result was an improvement in endothelial integrity and function.

All of these endothelium-protecting effects make benfotiamine an essential nutrient in your fight against the devastating effects of elevated blood glucose on your cardiovascular system.
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Read the complete article here.

Don’t believe everything you read (including in scientific journals)

Don’t believe everything you read (including in scientific journals)

News broke last week (see here for an example) that a University of Connecticut researcher had be found to have falsified data concerning his research into the antioxidant resveratrol (found in, among other things, red wine and red grapes). This week the British Medical Journal reports on the fact that a doctor and flu vaccine researcher based at Leicester University in the UK has been suspended for a range of misdemeanours including forging colleagues signatures and recruiting himself into a study under a disguised name.

It would be comforting to think of these events as isolated incidences in the scientific community. However, according to a recent piece in the British Medical Journal, scientific misconduct is ‘worryingly prevalent’, at least in the UK [1].

The BMJ sent out a questionnaire to more than 9,000 researchers and reviewers asking if they has knowledge of colleagues “inappropriately adjusting, excluding, altering, or fabricating data” for the purpose of publication. Of those who responded, 13 per cent admitted they had such knowledge. 6 per cent admitted they were aware of misconduct within their own institutions which remained insufficiently investigated.

On January 12, the Committee on Publication Ethics (COPE) held a summit to address the problem of research misconduct in the UK. Referring to the BMJ survey, the Chair of COPE Dr Elizabeth Wagner is quoted as saying “This survey chimes with our experience from COPE where we see many cases of institutions not cooperating with journals and failing to investigate research misconduct properly.”

In a recent editorial in the BMJ [2], Dr Wagner and the BMJ’s editor Fiona Godlee wrote: “There are enough known or emerging cases to suggest that the UK’s apparent shortage of publicly investigated examples has more to do with a closed, competitive, and fearful academic culture than with Britain’s researchers being uniquely honest.”

My feeling is if the culture wasn’t so ‘closed, competitive, and fearful’ we’d probably see that misconduct is even more prevalent than the recent BMJ survey suggests. And that’s a problem because we really do need to rely on the integrity of research findings in making truly informed decisions about health and the management of disease.

Personally, I’m delighted that institutions such as the BMJ and COPE are shining a light onto this issue and thinking about how we might curb research misconduct.

References:
1. Tavare A. Scientific misconduct is worryingly prevalent in the UK, shows BMJ survey. BMJ 2012;344:e377
2. Godlee F, et al. Research misconduct in the UK. BMJ 2012;344:d8357