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LE Magazine January 2007
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Benfotiamine


European Supplement Protects Against Diabetic Complications
By Dale Kiefer

Benfotiamine Optimizes Endothelial and Vascular Function

In clinical studies from around the world, benfotiamine has repeatedly demonstrated remarkable effects in normalizing endothelial function.

Endothelial cells line the interior of blood vessels. These specialized cells are commonly damaged by high blood sugar and diabetes. When blood vessels are unable to relax and dilate in response to increased blood flow demands, the result is the dangerous condition known as endothelial dysfunction. Endothelial dysfunction is believed to contribute to the initiation of atherosclerosis and to underlie much of the damage associated with the complications of diabetes, particularly peripheral vascular disease.

Peripheral vascular disease occurs when blood flow through arteries in the arms and legs is impaired. Dangers of peripheral vascular disease include:

  • Impaired blood flow to the extremities that can cause cramping pain with walking (intermittent claudication)
  • Cuts or abrasions on the feet that fail to heal
  • Ulcers and gangrene of the feet and legs that can necessitate amputation.21

German scientists recently investigated benfotiamine’s effectiveness in supporting healthy endothelial function and peripheral blood flow. In the study, diabetic patients consumed a meal containing large amounts of advanced glycation end products (AGEs) derived from foods cooked at high temperatures. AGEs are known to contribute to endothelial dysfunction. The subjects ate the AGE-rich meal both before and after three days of treatment with benfotiamine. Indicators of endothelial function, oxidative stress, and AGEs were measured after an overnight fast on the test days, and at two, four, and six hours after the test meals.22

The AGE-rich meal alone produced several harmful changes, including:

  • Significantly decreased blood flow to the extremities
  • Increased blood markers of endothelial dysfunction
  • Elevation in oxidative stress
  • Higher levels of AGEs.22

The detrimental changes caused by the AGE-rich meal alone were completely prevented by supplementation with benfotiamine. Benfotiamine promoted numerous improvements, including:

  • Enhanced blood flow in the extremities
  • Improved endothelial function
  • Diminished oxidative stress
  • Normalization of AGE levels.22

This important German study demonstrates that AGEs directly contribute to vastly diminished vascular function in diabetics, and that the use of benfotiamine prevents AGE-induced endothelial dysfunction, impaired blood flow, and increased oxidative stress.22

Two recent studies from Italy validate benfotiamine’s ability to support healthy endothelial function, even in the presence of high blood glucose levels. Independent Italian research teams showed that, in addition to preserving mature endothelial cells lining blood vessels, benfotiamine also protects endothelial progenitor cells, or cells that develop into endothelial cells. These progenitor cells are crucial to the repair and maintenance of healthy endothelial tissue.23,24 While hyperglycemia, or high blood sugar, interferes with the normal development of progenitor cells, the Italian scientists noted that normal development of these cells can be restored by the administration of benfotiamine.23 Similarly, benfotiamine inhibited human epithelial progenitor cell death, which is caused by high glucose levels.24

Benfotiamine’s ability to support the health of endothelial cells may have important implications in helping people to avoid peripheral vascular disease. Scientists now believe that the endothelial dysfunction that occurs with diabetes can easily lead to diabetic peripheral vascular disease.16

Japanese researchers found that peripheral arterial disease affecting the legs’ blood vessels commonly occurs together with endothelial dysfunction. As a result, the legs do not receive the critical supply of blood and oxygen they need to stay healthy and functional.25 Moreover, diabetic patients with peripheral arterial disease have fewer circulating endothelial progenitor cells, which are necessary to keep blood vessels functioning optimally so they can deliver blood to the limbs.26

In a model of peripheral vascular disease, benfotiamine improved endothelial function, which restored circulation to the legs and increased blood and oxygen supply to the tissues. This is especially important in keeping the limbs healthy and avoiding amputation, an all-too-common consequence of vascular dysfunciton. Additionally, benfotiamine reduced the diabetes-induced deficit in endothelial progenitor cells, which led to improved healing responses in the legs of diabetic subjects.24

Diabetes Unleashes a Cascade of Debilitating Health Complications

Diabetes is one of today’s most challenging health afflictions, owing to its explosive growth, devastating effects on the body, and the difficulty of effectively treating the disease and its complications.

In a healthy person, food is converted into glucose, which is subsequently absorbed into the bloodstream. In response to this increase in plasma glucose, the pancreas secretes the hormone insulin, which shepherds glucose molecules into the body’s cells, where they are stored or burned for energy.

In pre-diabetic and diabetic individuals, however, the cells resist insulin and the entry of glucose into the cells. When this happens, specialized cells in the pancreas known as islet cells respond by pumping out more insulin. Over time, the islet cells burn out altogether. The result is hyperglycemia, or high blood sugar, rendering the patient utterly dependent on a constant supply of pharmaceutical insulin.

Despite these challenges, most cells maintain relatively normal concentrations of internal glucose. However, certain cells—most notably endothelial cells, which line the interior of arteries and capillaries—are less capable of self-regulation. They tend to accumulate high levels of internal glucose, which they cannot metabolize efficiently. This causes intermediate glucose breakdown products to pile up, activating metabolic pathways that are implicated in the onset of diabetic complications.

Especially in the small blood vessels that feed the eyes, kidneys, and extremities, the toxic intermediates of glucose breakdown leave a wake of damage. For example, in the retina, this dysfunctional glucose metabolism may lead to blindness. In the kidneys, it may cause irreversible tissue damage, eventually leading to kidney failure. And in the extremities, it may cause vascular disease and nerve pain, possibly requiring amputation.8,10

Benfotiamine Reduces Heart Disease Risk

Individuals with diabetes suffer from a greatly increased risk of heart disease. Benfotiamine may play an important role in strategies to protect heart health in people with high blood sugar.

A recent study conducted by researchers at the University of Wyoming gauged benfotiamine’s ability to prevent heart disease in an experimental model of human type II diabetes. One group was rendered diabetic, while a second control group remained normal. Both groups received benfotiamine therapy for two weeks. Scientists then examined heart cells from both groups, assessing their ability to contract and various biochemical parameters.27

As expected, diabetes was associated with increased oxidative stress, which interfered with the healthy function of heart muscle. Benfotiamine treatment alleviated many of the heart cell changes caused by diabetes, decreasing oxidative stress and restoring heart cell function. The researchers concluded that benfotiamine may guard heart muscle cells against the dysfunction associated with diabetes.27

Supplementing with benfotiamine may thus be crucial in protecting the heart against the adverse effects of diabetes.

Benfotiamine Promotes Kidney Health

Kidney disease, or nephropathy, is one of the most dreaded complications of diabetes. When kidney function deteriorates in people with diabetes, the kidneys may no longer be able to perform their crucial task of filtering urine. As a result, diabetics with advanced nephropathy must resort to kidney dialysis or a kidney transplant. Kidney disease also increases the risk of cardiovascular disease and overall mortality.

In a 24-week study, scientists examined the effects of benfotiamine and thiamine on subjects with diabetes. Both forms of vitamin B1 produced beneficial changes in markers of kidney function and health, including:

  • A 70-80% inhibition in the development of microalbuminuria, protein in the urine that serves as an early sign of kidney dysfunction
  • A normalization of enzyme activity associated with protection against kidney disease
  • A 50% reduction of AGE levels in the kidneys
  • A reduction in oxidative stress associated with diabetes (produced by benfotiamine but not by thiamine).5,10

The scientists noted that while both benfotiamine and thiamine helped prevent the kidney complications associated with diabetes, benfotiamine appears to be a superior choice due to its greater bioavailability in the body.5,10 This research indicates benfotiamine and thiamine may help people with diabetes safeguard the health of their kidneys and protect against the devastating consequences of nephropathy.

Damaging Consequences of Vitamin B1 Deficiency

Intake of simple carbohydrates, which the body processes mainly into glucose, automatically increases the need for dietary thiamine. As a result, people often suffer vitamin B1 deficiency when they routinely consume a high-calorie, high-carbohydrate diet with inadequate nutritional value.28 Alcoholism may also lead to vitamin B1 deficiency, resulting in a condition known as Wernicke’s encephalopathy.10

Other conditions that may be associated with thiamine deficiency are gastrectomy (surgical removal of all or part of the stomach) and bariatric surgery (used to treat obesity), which contribute to difficulties with nutrient absorption.10

Benfotiamine Helps to Avert Vision Loss

While diabetes threatens whole-body health, the eyes are particularly vulnerable to damage. Damage to small blood vessels caused by diabetes can result in retinopathy (a disease of the eye’s retina, which collects visual information) and even blindness.

Scientists in Germany discovered that 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 AGEs in the retina, leading the research team to conclude that benfotiamine may help prevent or delay the onset and progression of diabetic retinopathy.8

Benfotiamine appears to provide essential protection to the eyes, helping prevent vision-robbing diabetic retinopathy.

Conclusion

For decades, benfotiamine has been safely used as a prescription drug in Europe, where this natural vitamin B1 derivative has demonstrated efficacy in preventing many serious complications of prolonged hyperglycemia.

Consumers in America can now readily access benfotiamine as a low-cost dietary supplement. Laboratory investigations and controlled studies have confirmed that benfotiamine alleviates and may even reverse diabetic neuropathy, kidney disease, cardiac impairment, endothelial dysfunction, peripheral vascular disease, and diabetic retinopathy. With its proven ability to confer broad-spectrum support for the blood vessels, nerves, kidneys, eyes, and heart, benfotiamine should be considered a first-line defense against the debilitating consequences of diabetes and high blood sugar.

References

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2. Stracke H, Hammes HP, Werkmann D, et al. Efficacy of benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.

3. Haupt E, Ledermann H, Kopcke W. Benfotiamine in the treatment of diabetic polyneuropathy—a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacol Ther. 2005 Feb;43(2):71-7.

4. Sanchez-Ramirez GM, Caram-Salas NL, Rocha-Gonzalez HI, et al. Benfotiamine relieves inflammatory and neuropathic pain in rats. Eur J Pharmacol. 2006 Jan 13;530(1-2):48-53.

5. Babaei-Jadidi R, Karachalias N, Ahmed N, Battah S, Thornalley PJ. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003 Aug;52(8):2110-20.

6. Woelk H, Lehrl S, Bitsch R, Kopcke W. Benfotiamine in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov;33(6):631-8.

7. Winkler G, Pal B, Nagybeganyi E, et al. Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.

8. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.

9. Arora S, Lidor A, Abularrage CJ, et al. Thiamine (vitamin B(1)) improves endothelium-dependent vasodilatation in the presence of hyperglycemia. Ann Vasc Surg. 2006 May 31.

10. [No authors listed]. Benfotiamine.Monograph. Altern Med Rev. 2006;11(3):238-42.

11. Pomero F, Molinar MA, La SM, et al. Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.

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13. Beltramo E, Berrone E, Buttiglieri S, Porta M. Thiamine and benfotiamine prevent increased apoptosis in endothelial cells and pericytes cultured in high glucose. Diabetes Metab Res Rev. 2004 Jul;20(4):330-6.

14. Thomas MC, Baynes JW, Thorpe SR, Cooper ME. The role of AGEs and AGE inhibitors in diabetic cardiovascular disease. Curr Drug Targets. 2005 Jun;6(4):453-74.

15. Cameron NE, Gibson TM, Nangle MR, Cotter MA. Inhibitors of advanced glycation end product formation and neurovascular dysfunction in experimental diabetes. Ann NY Acad Sci. 2005 Jun;1043:784-92.

16. Sheehan P. Peripheral arterial disease in people with diabetes: consensus statement recommends screening. Clinical Diabetes. 2004:22:179-80.

17. Li SY, Du M, Dolence EK, et al. Aging induces cardiac diastolic dysfunction, oxidative stress, accumulation of advanced glycation endproducts and protein modification. Aging Cell. 2005 Apr;4(2):57-64.

18. Sadekov RA, Danilov AB, Vein AM. Diabetic polyneuropathy treatment by milgamma-100 preparation. Zh Nevrol Psikhiatr Im SS Korsakova. 1998;98(9):30-2.

19. Kolomoiskaia MB, Degonskii AI, Grishina RA. The myocardial contractile function and central hemodynamics of patients with insulin-dependent diabetes mellitus during treatment. Probl Endokrinol (Mosk). 1989 Jul;35(4):12-5.

20. Wu S, Ren J. Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-alpha. Neurosci Lett. 2006 Feb 13;394(2):158-62.

21. Available at: http://www.diabetesselfmanagement.com/article.cfm?aid=558. Accessed October 23, 2006.

22. Stirban A, Negrean M, Stratmann B, et al. Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care. 2006 Sep;29(9):2064-71.

23. Marchetti V, Menghini R, Rizza S, et al. Benfotiamine counteracts glucose toxicity effects on endothelial progenitor cell differentiation via Akt/FoxO signaling. Diabetes. 2006 Aug;55(8):2231-7.

24. Gadau S, Emanueli C, Van LS, et al. Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhibition of apoptosis. Diabetologia. 2006 Feb;49(2):405-20.

25. Sanada H, Higashi Y, Goto C, Chayama K, Yoshizumi M, Sueda T. Vascular function in patients with lower extremity peripheral arterial disease: a comparison of functions in upper and lower extremities. Atherosclerosis. 2005 Jan;178(1):179-85.

26. Fadini GP, Miorin M, Facco M, et al. Circulating endothelial progenitor cells are reduced in peripheral vascular complications of type 2 diabetes mellitus. J Am Coll Cardiol. 2005 May 3;45(9):1449-57.

27. Ceylan-Isik AF, Wu S, Li Q, Li SY, Ren J. High-dose benfotiamine rescues cardiomyocyte contractile dysfunction in streptozotocin-induced diabetes mellitus. J Appl Physiol. 2006 Jan;100(1):150-6.

28. Lonsdale D. A review of the biochemistry, metabolism and clinical benefits of thiamin(e) and its derivatives. Evid Based Complement Alternat Med. 2006 Mar;3(1):49-59.