Block Deadly Effects Of After Meal Blood SugarDecember 2015
By Michael Downey
Diabetics and prediabetics are prone to accelerated aging due to the systemic damage caused by excess blood sugar. Unfortunately, as humans age, blood sugar tends to rise.1 What researchers are discovering is that people don’t have to be a diabetic to suffer from the extensive health consequences of high blood sugar.2-9
The problem is that after a meal, one’s blood sugar (whether a person is diabetic or not) spikes and the result is the production of deadly byproducts called advanced glycation end products (AGEs).10,11 AGEs are rogue molecules that damage cells, tissues, and organs.11-13
They also trigger inflammation and oxidation, generating even more of these molecules in a vicious, health-robbing cycle.14
Life Extension® has long advised customers about the importance of maintaining a fasting glucose level between 70 to 85 mg/dL.
Compelling data now confirms that a unique form of vitamin B1 called benfotiamine can protect against the ravages of elevated blood sugar.15,16
In the process of helping neutralize the adverse impact of elevated after-meal blood glucose, benfotiamine can help prevent Alzheimer’s disease, vision impairment, cardiovascular disease, kidney damage—and possibly even aging itself!3
Blood Sugar And Tissue Damage
The browning that takes place when foods are cooked at high temperatures (known as the Maillard Reaction) is the result of a sugar-related molecular change known as glycation. This damaging process takes place when a reducing sugar and an amino acid react in the presence of heat.17,18 Put simply, the structure of normal proteins becomes warped.
This same dysfunctional chemical change is occurring every day inside the body.
Within every cell, the sugar that the body uses for fuel is busy at work at every moment reacting with proteins and fats.17,18 The byproducts of this chemical reaction4-7 are called advanced glycation end products.19
Ultimately, these advanced glycation end products deactivate enzymes, disrupt cell signaling, and damage the body’s DNA. This results in intracellular damage and apoptosis (programmed cell death),20 inflammation,9,21 oxidative stress,9,22-24 nerve-cell component damage,25 a depletion of nitric oxide24,26 (which is vital to vascular health), and high cholesterol.28
These effects are implicated in the progression of numerous age-related diseases,28 ranging from neuropathy23 and vision problems29 to kidney30 and cardiovascular disease24,27,31—to even aging itself.2,32
With advancing age, even normal blood sugar levels eventually trigger deadly advanced glycation end products. Studies clearly demonstrate links between major health risks and levels of AGEs in the blood of nondiabetics.33,34
Scientists have speculated that AGE-related changes ultimately contribute to a limitation of the human life span35—suggesting that blocking the pathways of glycation could extend human life expectancy.
Supercharge The Body’s Natural Defenses
One of the natural defenses against advanced glycation end products is vitamin B1, known as thiamine. Vitamin B1 prevents glycation molecules from becoming fully formed in the first place.22,36
The problem is that glucose quickly depletes the body’s limited thiamine supplies.37 And although it might seem logical to use thiamine supplements to block advanced glycation end products, that’s problematic as well.
Because thiamine is water soluble, it has difficulty penetrating the lipid molecules that primarily make up cell membranes. Also, the body has a very low upper-dose limit, which means that taking larger doses of thiamin wouldn’t do any good because it would get excreted in the urine.38,39 Ultimately, tissues simply can’t absorb nearly enough thiamine to prevent cumulative damage caused by advanced glycation end products.40,41
Researchers realized there was an urgent need for a better means of delivering thiamine to the cells—and that’s where the unique form of thiamine called benfotiamine comes in. The major difference is that benfotiamine is a fat-soluble derivative of thiamine. Because it is fat soluble, benfotiamine substantially boosts thiamine absorption into cells and throughout the body.15,40,41
Administration of benfotiamine resulted in a 10 to 40% higher thiamine incorporation into the liver and heart—and a remarkable 5- to 25-fold higher thiamine incorporation into muscle and brain!39 A small clinical study showed that this enhanced bioavailability of benfotiamine caused it to slash the intracellular formation of AGEs in subjects’ blood cells by 40%!42
Benfotiamine has been found to block sugar-induced damage in a number of ways:
- It activates a vital enzyme called transketolase, which converts toxic glucose-induced metabolites into harmless compounds.3,16
- It helps prevent inflammation by inhibiting the activation of nuclear factor-kappaB (NF-kB), a trigger for dangerous inflammatory reactions in the body.16
- A 2012 study showed that benfotiamine boosts glucose breakdown in hyperglycemic (high-glucose) conditions by 70% and up to 49% in normoglycemic (normal-glucose) conditions!43
Benfotiamine is superior to thiamine alone in mitigating the spectrum of diseases such as neurodegenerative diseases and cancer,44 as well as the kidney, eye, and nerve damage seen in diabetic patients.7 Let’s now examine the evidence demonstrating benfotiamine’s potent protection against several of the most common sugar-induced disorders.
Benfotiamine Reverses The Pathways And Memory Loss of Alzheimer’s
Recent studies have indicated that benfotiamine could potentially enhance memory and contribute to the delay in the progression of Alzheimer’s disease.
When benfotiamine treatment was used for eight weeks in a mouse model of Alzheimer’s disease, researchers found that it reduced both amyloid plaque numbers and phosphorylated tau protein levels in the brain. It also helped prevent amyloid plaque from forming in the first place by reducing enzyme activities related to amyloid precursor proteins.45 These changes were validated by a dose-dependent enhancement in memory.45
The study authors concluded that “benfotiamine may be beneficial for clinical Alzheimer’s disease treatment.”45
Then in 2012, scientists determined that benfotiamine was able to do more than just reduce the plaque and tau formation—it could regress it. One of the ways it produced this effect was through a reduction in advanced glycation end products. The study authors wrote that “the use of benfotiamine could provide a safe intervention to reverse biological and clinical processes of Alzheimer’s disease progression.” 46
Defense Against Sugar-Induced Vision Loss
The same blood sugar effects that are associated with blindness in diabetics can cause cataract and retinal damage in nondiabetics as well.47,48 Because of its high vascularity, eye tissue is especially susceptible to damage from advanced glycation end products caused by elevated glucose levels.
In an animal study, benfotiamine supplementation was found to reverse retinal accumulation of AGEs, as well as increasing their urinary excretion.49 This can lead to a number of beneficial effects on the eyes.
Elevated blood sugar and the formation of AGEs can trigger cell death within the retina. However, when researchers applied benfotiamine to retinal blood vessel cells in culture, they found that the benfotiamine was able to prevent this dangerous process. It was also able to reduce DNA damage.50
In the eye, advanced glycation end products increase enzymes called matrix metalloproteinases (MMPs). These protein-dissolving enzymes cause substantial damage to retinal tissue. Scientists found that benfotiamine lowered MMP production to normal levels and increased production of certain proteins that specifically inhibit their activity.51
Inflammatory changes associated with aging, elevated blood glucose, and infections can affect the eyes. Uveitis, a serious inflammation of the middle layer of the eye, is responsible for 10% of all cases of blindness in the United States52 and is characterized by infiltrates of white blood cells, proteins, and inflammatory cytokines that inflict oxidative stress, leading to further inflammation.53 Benfotiamine was found to suppress this process and the expression of inflammatory marker molecules.53
Benfotiamine Protects Against Cardiovascular Damage
The thin layer of endothelial cells that lines blood vessels constantly regulates blood pressure and flow. Advanced glycation end products damage these cells, which can lead to heart attacks, heart failure, and stroke.54,55
Advanced glycation end products damage blood vessels in three ways:
- They reduce endothelial cell replication, a vital process to keep arteries healthy.56
- They trigger an increased level of death among endothelial cells.57
- They produce toxic polyol compounds, which disrupt the functioning of vascular and endothelial cells.58
Remarkably, studies indicate that benfotiamine protects endothelial cells from all three of these damaging effects of AGEs.56-58 This protection ultimately improves the functioning of blood vessels and heart muscle.59,60
An interesting study on humans revealed just what a dramatic impact these effects would have on heart health. In the study, subjects took 1,050 mg of benfotiamine per day for three days. The scientists wanted to determine the effect benfotiamine would have on the changes in endothelial function and blood flow that occur as a result of consuming a meal rich in advanced glycation end products.59 The striking outcome of supplementation revealed that benfotiamine completely prevented endothelial and blood flow impairment!26,61
Benfotiamine also counters the negative effects of oxidative stress on blood vessels. In a study in which rodents were experimentally induced with vascular endothelial dysfunction, supplemental benfotiamine resulted in improved endothelial integrity and function by enhancement of production of nitric oxide, a compound that helps blood vessels to relax.53,73
Blood sugar and advanced glycation end products greatly contribute to the diminished heart-muscle function known as heart failure, which can be caused by a heart attack or untreated high blood pressure. Scientists have demonstrated that benfotiamine helps normalize the heart muscle’s ability to contract, salvaging damaged heart muscle and improving its capacity to effectively pump blood.60
Benfotiamine Inhibits Sugar-Related Kidney Disease
Kidney disease, or nephropathy, is a known side effect of “natural” aging, but it is also a common and very serious complication of excess blood sugar and especially of diabetes.
Like the eyes, the kidneys are rich in tiny blood vessels known as capillaries. The kidneys are also the site of intensemetabolic activity. These facts make the kidneys particularly vulnerable to the damaging effects of glucose and advanced glycation end products.30
The good news is that evidence indicates that benfotiamine helps protect against sugar-related kidney damage by reducing pathological increases in advanced glycation end products.49,62
In one study, benfotiamine activated the important enzyme transketolase, which rapidly cleared AGEs from the blood before they could damage kidney tissue.62
Another study demonstrated that benfotiamine could help reduce sugar-induced kidney damage as efficiently as the prescription drug fenofibrate.63 The two in combination demonstrated beneficial synergistic effects.63
Benfotiamine has also been found to be helpful during various forms of dialysis treatments.
Hemodialysis, which is a last-resort treatment for patients whose kidneys have failed, quickly depletes the body’s store of thiamine, the very vitamin required to prevent further glucose-related damage. Benfotiamine, which is vastly more bioavailable than thiamine, boosts thiamine levels over 4 times higher than supplementation with thiamine in dialysis patients.64
Peritoneal dialysis is somewhat less stressful to the body than hemodialysis, but it is associated with substantial damage to the delicate tissues lining the abdominal cavity, believed to be caused by glucose and AGEs.65 By reducing the level of AGEs during peritoneal dialysis, benfotiamine decreases markers of inflammation and abnormal new blood vessel formation in the abdominal cavity.65 This protects the delicate abdominal lining, prolonging its usefulness as a dialysis site.
Both types of dialysis also substantially damage DNA throughout the body, increasing the risk of cancer. Benfotiamine treatment has been shown to significantly reduce this DNA damage in dialysis patients by reducing the circulating advanced glycation end products.66-68
These results provide dramatic evidence of the high degree of kidney protection that benfotiamine offers against blood sugar increases and advanced glycation end products.
Just over a decade ago, the health-devastating and faster-aging effects of high blood sugar were associated almost exclusively with diabetics. But healthy individuals are also susceptible to the chronic, age-related diseases triggered by high blood sugar.
Something as simple as eating a heavy meal can ultimately lead to the production of deadly byproducts called advanced glycation end products that damage cells, tissues, and organs—and even cause premature aging.
Fortunately, the discovery of a relative of thiamine (vitamin B1) called benfotiamine has provided a way to powerfully boost intracellular levels of thiamine, the body’s natural defense against the AGEs that cause sugar-related tissue damage.
Numerous studies confirm that benfotiamine blocks the pathways of Alzheimer’s disease, vision loss, cardiovascular disease, and kidney damage.
Benfotiamine, with its impressive safety record, has shown itself to be a powerful factor in slowing glycation-induced aging—potentially maximizing life span—in both diabetic and nondiabetic individuals.
If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.
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