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Autism Coach

Benfotiamine - Vitamin B1


Benfotiamine - Vitamin B1

0.25 LBS
Calculated at checkout

Product Description

Benfotiamine is a fat-soluble form of thiamine (vitamin B1) with high bioavailability that was developed in Japan in the 1960's. It is especially useful for people needing high levels of thiamine or with impaired absorption of this essential B-vitamin. Oral benfotiamine passively diffuses through the intestinal mucosa and is rapidly converted to active thiamine. Its absorption is much more efficient than water-soluble thiamine which requires active transport. Benfotiamine intake attains higher plasma and tissue thiamine levels and maintains these levels longer than common forms of thiamine. Bioavailability of benfotiamine is up to 3.6 times greater than water-soluble thiamine salts and is associated with a 120-fold greater increase in the levels of metabolically active thiamine diphosphate. It does not accumulate in the body.

Benfotiamine increases blood levels of thiamine pyrophosphate (TPP), the primary thiamin co-enzyme and is also used to help maintain healthy cells in the presence of blood glucose, Befotiamine prevents glycation by inhibiting several metabolic pathways that result in glucose-induced damage to cells and tissues through the formation of Advanced Glycation End-products (AGEs).
Damage to cells and tissues from Glycation have been found in individuals diagnosed with autism, diabetes, and dementia. An accumulation AGES has been reported in the brains of individuals within the autism spectrum.

Benfotiamine can also provide support for neuropathy, retinopathy and nephropathy associated with diabetes2 and neuropathy associated with chemotherapy, sciatica, fibromyalgia and shingles.

Phenolic compounds in foods can also deplete levels of B1 and individuals with impaired ability to metabolize phenols may benefit from Benfotiamine.

B1 is required in the metabolism of phenols. Chronic low B1 deficiency (pellegra) can cause issues with the nervous and digestive systems. Some individuals within the autism spectrum have low levels of Vitamin B1.

What is Glycation?

Glucose is the primary source of energy for cells in the body and brain. The body attempts to maintain a precise level of glucose in the blood, just enough for cells to obtain the energy they need to function but no more. Too much glucose in the bloodstream damages tissues and DNA throughout the body in a process called glycation. The original patent filed inthe United States on benfotiamine, included data from LD-50tests on lab mice indicating that benfotiamine is significantlyless toxic than common vitamin B-1 (typically, thiamine hydrochloride).

Glycation is the random bonding of glucose to proteins it meets up with. This random bonding of glucose to proteins results in cross-linking of glucose to cells and tissues in the body which reduces the efficiency with which cells and tissues can function and repair themselves. Glycation is believed to be one of the primary causes of aging. When glucose cross-links with the collagen in skin, it produces wrinkles. As people age, their cells and tissues change in ways that lead to the bodys decline and death. The cells become less efficient and less able to replace damaged materials. At the same time tissues stiffen. For example, the lungs and the heart muscle expand less successfully, the blood vessels become increasingly rigid and the ligaments and tendons tighten. Older people are also more likely to develop cataracts, atherosclerosis, and cancer, among other disorders. Glucose binds to nucleic acids such as DNA, genes. Over time, the body becomes less and less efficient at maintaining and repairing the wear and tear on a cellular level due to the processes of daily life due to the attachment of glucose to cells and tissues.

Insulin is a hormone secreted by the pancreas that signals to cells in the body to take up glucose. If there are excessive levels of glucose in the blood on a regular basis, the pancreas has to regularly secrete more insulin for the cells to take up the glucose. Over time, these cells may become resistant to taking up glucose through excessive insulin signalling. This, in turn, forces the pancreas to secrete more insulin in an attempt to reduce the level of glucose in the blood. Over-taxing the cells of the body and the pancreas often proves to be unsustainable over time. When too much glucose bathes the pancreas itself, it may result in cross-linking of glucose to beta cells that kills these cells off and reduces the ability of the pancreas to produce the insulin needed by the body, eventually leading to diabetes.

If the neurons in the brain become insulin resistant, they do not absorb enough glucose to produce the energy they need to survive, and some researchers theorize insulin resistance of neurons may lead to them slowly starving, resulting in neuronal die-off that takes place in Alzheimers and possibly other neurodegenerative conditions.
Studies of the brain show that the tissue making up the sheath that separates the brain from the skull accumulates glycation products too. The amount of glycationproducts increases directly with age, this process is accelerated in diabetes.

The pancreas chronically producing high levels of insulin that can also signal the liver to produce cholesterol and act on the kidneys to contribute to high blood pressure.

Aging is associated with organism decay and an exponential increase in a wide range of degenerative diseases. The increase in these diseases is associated with a loss of reserve capacity of the mitochondria, the energy producing center of each cell. A strong relationship exists between aging and mitochondrial dysfunction as well as an accumulation of altered proteins. This is exactly what the glycation process does it alters the integrity of the proteins that make up our body, particularly those proteins that make up mitochondria. A significant number of individuals within the autism spectrum have been diagnosed with mitochondrial dysfunction.
Suggested Use

1 capsule daily with food.

Supplement Facts

lterations of circulating endogenous secretory RAGE and S100A9 levels indicating dysfunction of the AGE-RAGE axis in autism.

Department of Applied Health and Behavioural Sciences, Section of Psychiatry, University of Pavia, Pavia, Italy.


An excess accumulation of advanced glycation end products (AGEs) has been reported in autism brains. Through their interaction with their putative receptor RAGE, AGEs can promote neuroinflammation, oxidative stress and neuronal degeneration. To shed more light on the possible alterations of the AGEs-RAGE axis in autism, hereto we measured plasma levels of endogenous secretory RAGE (esRAGE) and its proinflammatory ligand S100A9 in 18 young adults with autistic spectrum disorder (ASD) and 18 age- and gender-matched healthy comparison subjects. The Childhood Autism Rating Scale (CARS) was used to assess the severity of autistic symptoms. Significantly reduced levels of esRAGE (P = 0.0023) and elevated concentrations of S100A9 (P = 0.0012) were found in ASD patients as compared to controls. In autistic patients, there was a statistically significant positive correlation between CARS scores and S100A9 levels (r = 0.49, P = 0.035), but no significant correlation was seen between esRAGE and S100A9 values (r = -0.23, P = 0.34). Our results of a significantly reduced peripheral level of esRAGE coupled with elevated S100A9 point to a subtle but definite dysfunction of the AGEs/RAGE axis in autism that could play a role in the pathophysiology of this disorder.

2. The multifaceted therapeutic potential of benfotiamine.

Department of Pharmacology, SB College of Pharmacy, Sivakasi 626130, India.


Thiamine, known as vitamin B(1), plays an essential role in energy metabolism. Benfotiamine (S-benzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine. Once absorbed, benfotiamine is dephosphorylated by ecto-alkaline phosphatase to lipid-soluble S-benzoylthiamine. Transketolase is an enzyme that directs the precursors of advanced glycation end products (AGEs) to pentose phosphate pathway. Benfotiamine administration increases the levels of intracellular thiamine diphosphate, a cofactor necessary for the activation transketolase, resulting in the reduction of tissue level of AGEs. The elevated level of AGEs has been implicated in the induction and progression of diabetes-associated complications. Chronic hyperglycemia accelerates the reaction between glucose and proteins leading to the formation of AGEs, which form irreversible cross-links with many macromolecules such as collagen. In diabetes, AGEs accumulate in tissues at an accelerated rate. Experimental studies have elucidated that binding of AGEs to their specific receptors (RAGE) activates mainly monocytes and endothelial cells and consequently induces various inflammatory events. Moreover, AGEs exaggerate the status of oxidative stress in diabetes that may additionally contribute to functional changes in vascular tone control observed in diabetes. The anti-AGE property of benfotiamine certainly makes it effective for the treatment of diabetic neuropathy, nephropathy and retinopathy. Interestingly, few recent studies demonstrated additional non-AGE-dependent pharmacological actions of benfotiamine. The present review critically analyzed the multifaceted therapeutic potential of benfotiamine.




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