Overview

Glycation is an insidious and potentially devastating process by which sugars form chemical bonds with proteins in the body, gumming them up and often permanently damaging the body’s vital tissues. This process happens at an accelerated rate for those with chronically high blood sugar, but it happens to all of us as we age nonetheless. Read more.

The damage can, however, be prevented at many stages before it reaches a point that is irreversible .

Insulin Resistance

At the very beginning of the process is insulin resistance. Insulin is a hormone released typically after a meal, which sends signals to the body's cells to open up their walls and let the blood sugar in. Generally as our telomeres shorten and we age, but particularly if our refined carbohydrate consumption has been higher than what we were designed to handle, the cells' sensitivity to insulin throughout the entire body diminishes. When this happens, the cell walls tend to stay closed and the blood sugar tends to stay out. This results in less energy for the body, more sugar in the blood, a reaction by the body to produce more insulin in response, and a viscous cycle. All of this spells more glycation reactions.

AGEs and Intermediaries

The body is equipped to handle the byproducts of these initial glycation reactions. But if allowed to continue, they go through several intermediate states where these sugar-protein clusters grow larger and more complex into what are known as Amadori Products, Schiff Bases and Reactive intermediaries. At this point the body can still break these molecules down and eliminate them. But if this fails to happen, due to inadequate natural stores of anti-glycation compounds, elevated blood sugar levels, or to general dysfunction of glycation defenses associated with older cells with shorter telomeres, then they become even larger and more complex molecules which take on different forms but are generally referred to as Advanced Glycation End Products (AGEs). In most areas of the body, even these molecules do not pose a direct immediate threat of permanent damage. This is because almost all dividing cells in the body are part of a pool of cells that are constantly discarded and reborn from underlying stem cells. So in these cases the intracellular AGE accumulation will be discarded along with the cells eventually. However, in non-dividing cells, particularly those in the nervous system, in extracellular proteins such as collagen in the skin, and particularly in long-lived extracellular proteins such as the lens of the eye, the body is particularly vulnerable to the gradual accumulation of AGEs. The accumulation is generally irreversible and the effects are often crippling.

Targeting Each Stage

All of this gives us an opportunity. If we simultaneously target the process at every one of these points we can provide a formidable defense to the ravages of cross-linking. Below you can see a chart of the road from insulin resisitance to eventual AGE formation, and all the intervention points our product takes advantage of to stop it along the way:

Components of Glycation Guard

Benfotiamine

A number of in vitro studies showed that when thiamine (B1) was applied directly to cells in culture that had been exposed to high glucose levels, it significantly reduced total AGE formation, increased cell survival and restored reproductive activity to normal levels. However B1 has low bioavailablity. Benfotiamine is thiamin’s fat-soluble cousin, and is much more able to penetrate the fatty-acid-rich cell membranes. It has a 420% better overall bioavilability than thiamine as a result.

Because of this improved bioavailability, benfotiamine has been shown to inhibit intracellular AGE formation in real human subjects in a way that is markedly superior to thiamine. In one study in particular, the levels of two key AGE molecules(CML and Methlyglyoxal-derived AGEs) in red blood cells dropped an amazing 40% and 69% respectively after only 4 weeks of treatment.

More exciting than the direct measurements of glycation in vitro is that we are also seeing these glycation reduction numbers borne out in the real experiences of human subjects of in vivo studies. Benfotiamine supplementation has greatly reduced nerve pain associated with glycation in humans, increased vibration perception, dramatically increased nerve conduction velocity, restored normal blood vessel relaxation and accelerated pressure sore healing, improved kidney function and improved heart cell nerve conductivity function. Read more.

Carnosine

The chemical structure of L-carnosine is very similar to that of the proteins attacked by sugars, and it uses this to offer itself up for cross linking with sugar instead of the body’s tissues. In addition, it tags affected (glycated) proteins for removal from the cells they can affect before they can cause further harm. The result is that Carnosine is a highly effective inhibitor of glycation in vivo.

Alpha Lipoic Acid

Alpha lipoic acid (ALA) reduces many of the secondary harmful effects of glycation, such as increased oxidation, increased cell adhesion, and NF-kappaB expression. It also improves insulin sensitivity in skeletal muscle and liver, improves glucose use and transport and was shown to protect against glycation of the retina.

N-Acetyl-Cysteine

N-Acetyl-Cysteine (NAC) has been found to reduce glycation, nerve damage caused by glycation, and help prevent insulin resistance. It has also been shown to improve blood flow to peripheral areas that have been restricted as a result of glycation.

Cinnamon

Cinnamon has long been known to normalize blood sugar, improve insulin sensitivity and normalize blood lipid profiles. One study tested different sweet foods’ impact on immediate blood sugar levels and were surprised to find that apple pie with cinnamon actually lowered blood sugar levels, and attributed it to the cinnamon. Another study suggested that this effect is due to a particular polymer in cinnamon that penetrates the cell and reacts with kinase in a way that mimics insulin.

Pyridoxal-5-Phospate

Pyridoxal-5-Phospate (P5P), the active form of B6, has been found to significantly reduce glycation and AGE formation. In the complex set of chemical reactions from blood sugar to AGE formation, P5P intervenes at the very first stage – initial sugar attachment. As an inhibitor of the glycation of lipids in particular, several studies found P5P along with Pyridoxal to be more effective than any of the other compounds tested, including carnosine, aminoguanidine and pyridoxamine.

Chromium

Chromium is the mineral component of the glucose tolerant factor (GTF) molecule, required for the proper entrance of blood sugar into the cells. So, in other words, chromium helps insulin perform its job of getting blood sugar into the cells, making it more effective. As a result chromium increases insulin sensitivity, reduces insulin levels (because the body needs less of it) , and reduces blood sugar and fat by allowing them to more readily enter muscle and adipose cells. Due to the increased efficacy in converting the glucose and fat into energy, its use has been associated with lower body fat and higher muscle mass.

Glycation Guard Supplement Facts