Benfotiamine can help diabetics protect delicate microvessels. Much of the damage of diabetes is caused when glucose-derived compounds, called triosephosphates, accumulate in small vessels. Transketolase, turns these toxic compounds into harmless chemicals that can be removed from the body. benfotiamine increases transketolase activity, thus reducing or eliminating the complications associated with diabetes.
Administration of benfotiamine helped to prevent retinopathy in test subjects with diabetes. Study subjects who received benfotiamine for 36 weeks demonstrated completely normalized levels of damaging toxins in the retina, preventing or delaying the onset of diabetic retinopathy.
In a 24-week study, benfotiamine was shown to improve kidney function. This was shown by a 50% reduction of toxin levels in the kidneys, and a reduction in oxidative stress associated with diabetes. Subjects exhibited a 70-80% inhibition in the development of microalbuminuria, protein in the urine that serves as an early sign of kidney dysfunction.
Benfotiamine mitigates oxidative stress in the eyes, the kidneys, the heart, and even the brain that typically occur with diabetes. Researchers conclude that benfotiamine may offer critical protection for the delicate nerves of the eyes, the kidneys, the peripheral limbs, the heart and the brain by shielding them from damage caused by diabetes.
1.
A. In respect of the comment: “…Body weight and moderate hyperglycemia were stabilized by subcutaneous injection of 2 units Ultralente insulin every 2 days…”
http://diabetes.diabetesjournals.org/cgi/content/full/52/8/2110
Where are the UNdrugTREATED control groups: (I) hyperglycemia without insulin?; and (II) hyperglycemia without insulin + Type 2 Diabetes [insulin resistance] protection?
Transient supernormal glycaemia ‘TSG’ occurs in every Human Being as a healthy and natural response to stress [‘adaptive medicine’] and may well increase HgA1c … so what? … when glucose levels surge up for a transient period [and then down again] an above average HgA1c can just as easily be viewed as a marker for a very healthy ‘stress adapted’ Human Being who has the benefit of being ‘insulin-resistant’ ie a criteria for being labelled a ‘type 2 Diabetic’; and
B. What is the most definitive study which substantiates the benefit of reducing HgA1c in drug/insulin treated acute&chronic 'insulin-resistant diabetes' [Type 2] … as compared with treatment-free [drug/insulin] acute&chronic 'insulin-resistant diabetes' [ie in a ZERO drug (repeat zero) treatment control Group]? {ps please note the word written there says: “zero”} ie completely ignoring HgA1c value variability…
... Am seeking a ‘Peer reviewed’ study that clearly disassociates drug/insulin treatment from any changes in Patient behaviour [eg diet/exercise] and/or categorically proves that drug/insulin treated acute&chronic 'insulin-resistant diabetes' is healthier than doing absolutely nothing [‘zero’] ie just accepting the higher HgA1c value and [possibly beneficial] blood glucose value [and possibly beneficial “insulin resistance”]; and
C. What is the most definitive study which provides incontrovertible evidence that the apparent insulin receptor mediated down-regulation [in response to: transient supernormal glycaemia ‘TSG’] is anything substantially other than a stress-adaptive mechanism of 'local' [on a cell-by-cell basis] intracellular cyto-protection from influx of excessive [blood] circulating glucose [ie homeostasis] eg cardio muscle protective?
... My understanding is that insulin receptor mediated down-regulation ‘IRD’ [aka “insulin resistance”] is primarily an adaptive [protective/regulatory/beneficial] reply to transient [and chronically repeated] oral indulgence/stress …
eg "...healthy young students were fed a very high fat diet containing egg yolks, heavy cream, and butter, and within 2 days all of the students had blood sugar levels high enough to be labelled diabetic..."
Sweeney J. Dietary factors that influence the dextrose tolerance test: A preliminary study. Archives of Internal Medicine 1927; 40:818.
“…After World War I, when insulin was first discovered, the medical profession thought diabetes would be totally curable as a medical problem. Diabetes was believed to be due to insulin deficiency, and everyone thought that since insulin would now be given to patients there would be no more problems. It seemed this way for a few years, but terrible things started happening to patients with diabetes who were given insulin to control their blood sugar levels. They developed eye disease, kidney disease, and, most important, accelerating atherosclerosis leading to blood vessel disease and early heart attacks. Their problems were worse than ever. Decades later, when the insulin assay became available and doctors were able to measure insulin levels in their patients’ bloodstreams, they found most interesting results: the insulin levels of type 1 (childhood-onset) diabetics were indeed low, but the levels in type 2 (adult-onset) diabetics were not only not low, but also were higher than those of people without diabetes. It became clear that type 2 diabetes is a disease of insulin resistance, not insulin deficiency. Type 2 diabetics produce plenty of insulin … I can only view today’s treatment of diabetic patients as malpractice…”
(1995) Dr Joel Fuhrman [a board-certified Family Physician practising in Belle Mead, New Jersey who specialises in preventing and reversing chronic conditions of high blood sugar; Dr Fuhrman is an active staff member of Hunterdon Medical Centre and provides nutritionally oriented medical care to Patients as well as nutritional education to other Physicians; Author of “Fasting and Eating for Health” ‘A Medical Doctor’s Program for Conquering Disease’].
Warm thanks, Nicholas Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK c/o www.TheDiabetesBlog.com @ 19:33hrs MON.02.APR.2007.
Posted at 3:02PM on Apr 2nd 2007 by Nicholas Dynes Gracey