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