Benfotiamine is a pro-vitamin: taken orally, it is converted into thiamine (Vitamin B1). Benfotiamine is found naturally in plants of the onion family, but the amounts present are miniscule.
Thiamine itself has been used for many years to treat neurological disorders. But this vitamin is poorly absorbed and rapidly metabolized, making it difficult to achieve therapeutic levels in the body. This problem is excalibrated in those individuals who have undergone gastric bypass. Benfotiamine, being fat-soluble, solves this bioavailability problem. It is well absorbed and remains in the body for days. Consequently, benfotiamine can raise thiamine concentrations in the blood and tissues about 5 times higher than oral thiamine consumption can.
Benfotiamine is typically used to prevent:
- diabetes-induced vascular damage
- neuropathy due to diabetes or alcohol consumption
- diabetic damage to eyes and kidneys
- tissue damage and aging due to protein cross-linking
- genetic damage in late-stage kidney disease
- complications of gastric bypass
How does it work?
Benfotiamine supplements serve as a source of thiamine, which in turn plays two biological roles:
- increasing the rate at which glucose is converted to other sugars
- maintaining the ability of nerve fibers to carry information.
Protection of cells against damage by glucose. Glucose is damaging to the body despite being one of the body’s main sources of energy. It has two destructive effects:
- when cells break down glucose to extract its energy, free radicals are produced that damage the surrounding tissues;
- some glucose molecules, instead of being metabolized, react chemically with proteins in the tissues, producing crosslinks (‘AGEs’) that impede or inactivate the proteins. The result is a loss of flexibility and function in skin, muscle, and all other living tissues.
Both of these side effects of glucose consumption are destructive to the body. They are considered major contributors to the aging process as well as to the failure of organs and tissues in diabetes.
But this damage can be limited if glucose levels in the body’s cells can be kept low. And they can be kept low if excess glucose can be rapidly converted to less harmful substances. Thiamine is a biological cofactor that does exactly this — it promotes the conversion of glucose into other, less harmful sugars, as well as promoting the breakdown of glucose into carbon dioxide, water, and energy. Since benfotiamine is converted into thiamine in the body, benfotiamine supplementation is equivalent to dramatically increasing the bioavailability of thiamine.
Nerve conduction and bodybuilding.
In addition to protecting cells from glucose damage, benfotiamine improves nerve function. Bodybuilders, who know from experience that muscles perform better when the nerves controlling them work better, are enthusiastic users of benfotiamine.
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Early Death by Junk Food? High Levels of Phosphate in Sodas and Processed Foods Accelerate the Aging Process in Mice
Here’s another reason to kick the soda habit. New research published online in the FASEB (Federation of American Societies for Experimental Biology) Journal shows that high levels of phosphates may add more “pop” to sodas and processed foods than once thought. That’s because researchers have found that the high levels of phosphates accelerate signs of aging. High phosphate levels may also increase the prevalence and severity of age-related complications, such as chronic kidney disease and cardiovascular calcification, and can also induce severe muscle and skin atrophy.
“Humans need a healthy diet and keeping the balance of phosphate in the diet may be important for a healthy life and longevity,” said M. Shawkat Razzaque, M.D., Ph.D., from the Department of Medicine, Infection and Immunity at the Harvard School of Dental Medicine. “Avoid phosphate toxicity and enjoy a healthy life.”
To make this discovery, Razzaque and colleague examined the effects of high phosphate levels in three groups of mice. The first group of mice was missing a gene (klotho), which when absent, causes mice to have toxic levels of phosphate in their bodies. These mice lived 8 to 15 weeks. The second group of mice was missing the klotho gene and a second gene (NaPi2a), which when absent at the same time, substantially lowered the amount of phosphate in their bodies. These mice lived to 20 weeks. The third group of mice was like the second group (missing both the klotho and NaPi2a genes), except they were fed a high-phosphate diet. All of these mice died by 15 weeks, like those in the first group. This suggests that phosphate has toxic effects in mice, and may have a similar effect in other mammals, including humans.
“Soda is the caffeine delivery vehicle of choice for millions of people worldwide, but comes with phosphorous as a passenger” said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. “This research suggests that our phosphorous balance influences the aging process, so don’t tip it.”
ScienceDaily (Apr. 28, 2010)
Dr. Zarkov’s note: The ‘klotho’ gene plays a central role both in the body’s calcium regulation and in aging. When this gene has low activity or is defective, the aging process is accelerated; when the gene is highly active, the aging process is slowed. Many people have less-than-optimal klotho gene activity, and high vitamin D levels can exacerbate this condition. Judging from mouse experiments, this problem is especially acute in females. But Japanese researchers reported in 2001 that supplementation with zinc orotate provides a ‘rescue’ from the consequences of low klotho activity, even in females.