source: www.vanuatumedical.com As we age, a non-enzymatic reaction between sugars in the blood and amino groups in our body’s proteins, fats, and DNA, produces compounds called advanced glycation end-products (appropriately called AGEs). AGEs bond to one another, creating crosslinks

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source: www.vanuatumedical.com
As we age, a non-enzymatic reaction between sugars in the blood and amino groups in our body’s proteins, fats, and DNA, produces compounds called advanced glycation end-products (appropriately called AGEs). AGEs bond to one another, creating crosslinks between proteins that disrupt normal cellular activity. By stiffening collagen and elastin (the key proteins of the extracellular matrix in all tissues), AGEs promote high blood pressure, atherosclerosis, and heart failure. In the kidneys, AGEs target nephrons, the filtering units that remove wastes from the blood.
Not only do AGEs wreak havoc on extracellular matrix proteins, they also activate AGE receptors (called RAGEs) on cells throughout the body. RAGEs trigger the release of a wide variety of compounds involved in inflammation and the creation of stiff fibrous tissue, compromising function in the heart, blood vessels, kidneys and brain.
In addition to chronological aging, AGE formation is greatly increased by high blood sugar levels and plays a central role in all diabetes-related disease complications.
AGE accumulation is also accelerated by insulin resistance, high cholesterol, smoking, and a diet lacking in vitamin, mineral and antioxidant-rich fruits and vegetables. In fact, a diet made up of highly processed foods, especially foods processed at high heat, is loaded with AGEs, which our bodies absorb from the food.
Fortunately, test tube, animal and human studies demonstrate that AGE crosslinks can be effectively—and safely—broken by ALT-711 (alagebrium), preventing and reversing AGE-related pathology. In diabetic animals, ALT-711 has been shown to reduce the body’s load of AGEs, promoting AGE excretion in the urine, and to improve the heart muscle’s pumping ability, decrease stiffness in the aorta (the artery through which blood flows into the body from the heart), decrease proteinuria (protein in the urine, a sign of kidney damage), reverse ED (erectile dysfunction) and extend survival.
In men who still had high blood pressure (systolic blood pressure >140 mmHg, diastolic blood pressure <90 mmHg or pulse pressure >60 mmHg), even after treatment with antihypertensive drugs, ALT-711 (210 mg twice daily for 8 weeks) decreased arterial stiffness by 37% and reduced blood pressure by an average of 6.8 mmHg. The men’s blood flow (measured by flow-mediated dilation) increased from an average of 4.6 to 7.1, plus levels of a number of compounds that indicate blood vessel damage and thickening greatly decreased.
When given to elderly patients (mean age 71) with diastolic heart failure, ALT-711 (420 mg/day for a period of 16 weeks) significantly decreased left ventricular mass (the major pumping chamber on the left side of the heart). Patients’ quality of life increased almost 25% as measured by the Minnesota Living with Heart Failure assay.
Other recent studies indicate that ALT-711’s multiple benefits are related not only to its ability to break AGE-related crosslinks, but also to its effects on cell receptors (RAGE), which result in lowered oxidative stress (free radical damage) and diminished pro-fibrotic cytokine production.
In Phase 2 clinical trials involving approximately 800 patients, ALT-711 has been found to be so safe and well-tolerated that it produced fewer side effects than placebo!
For all of us as we grow older, but especially for those with diabetes, metabolic syndrome or cardiovascular disease, ALT-711 (alagebrium) offers effective, safe therapy for the prevention, retardation, and reversal of the diseases of AGE-ing.
REFERENCES
Pizzorno L, ALT-711 – Effective New Anti-Aging Therapy, Smart Publications http://www.smart-publications.com
Pizzorno L, ALT-711: Cross Link Breaker Delivers Effective Anti-AGE-ing Therapy, http://www.lmreview.com/#AGEs
Author: dragon web profit

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