Benfotiamine Reduces Accelerated Aging

We know that too much sugar is bad for you. It causes diabetes, weight gain, and rots your teeth.

But the invisible harm that sugar causes goes beyond that.

A process known as glycation occurs when glucose in your bloodstream binds to proteins, fats, and nucleic acids in cells and tissues.

This causes the formation of advanced glycation end-products or AGEs.

Excessive glycation accelerates aging processes and contributes to many forms of chronic disease, from arterial blockage to dementia.^1-4

A specialized form of vitamin B1 called benfotiamine offers anti-glycation activity that may slow certain aging processes and maintain youthful tissue function.

The Danger of Glycation

Glucose is the main sugar that circulates in the blood. Cells break it down and use it as an energy source.

But glucose has a dark side.

It can combine with other compounds like proteins and fats, and even nucleic acids.* This process is known as glycation.

The result is toxic compounds being formed called advanced glycation end-products (AGEs).³

AGEs damage cellular structures, particularly the body’s proteins, and alter their function. The buildup of damaged proteins wreaks havoc on tissues throughout the body.

For example, blood vessels normally dilate or constrict to control blood flow. But with damaged proteins in their walls, blood vessels become stiff and unresponsive, hastening the onset of cardiovascular disease.³

AGEs also bind to cell receptors that activate chronic inflammation.³ This inflammation is a major cause of accelerated aging and age-related disease.⁵

The higher glucose levels are, the more glycation occurs.

This is an important reason why diabetes is so dangerous. When glucose levels are chronically high, more toxic glycation end-products are created.

But glycation occurs in all aging adults, not just diabetics, affecting every tissue in the body.

Glycation contributes to:

• Dementia,
• Heart and blood vessel disease,
• Kidney failure,
• Macular degeneration and vision loss,
• Nerve dysfunction,
• Osteoarthritis,
• Cancer,
• Aging, wrinkled skin,
• And more.^2-4,6-14

In elderly subjects, higher levels of AGEs detected on blood tests are associated with poor physical function.^15,16

Glycation slowly destroys the body from the inside out.

High Glucose Harms the Brain

The brain is constantly taking up glucose from the blood to use for energy.

The link between glucose metabolism and brain disease is so strong that many doctors and researchers have taken to calling Alzheimer’s disease “type III diabetes.”^17,18

There are a variety of ways that excess glucose harms brain function.^19-22

In the short term, hyperglycemia (high blood glucose) has a significant impact on mood and cognitive performance.

In patients with type II diabetes, one study found that information processing, memory, and attention were all impaired when blood glucose levels were high.²³

These individuals also tended to have a more depressed and anxious mood and reduced energy and arousal.²³

In the long term, glycation contributes to chronic loss of brain function and, eventually, dementia.^19-22

Research shows that people with diabetes have, on average, double the risk of developing dementia than non-diabetic individuals.²⁴

Among diabetics, those with poor blood glucose control have a 40% greater risk of dementia than those with better glucose control.²⁵ Even patients with prediabetes were found to be 18% more likely to develop dementia than people with normal glucose levels.

How Benfotiamine Helps

There are ways to prevent glycation damage.

Cutting back on sugar can help. But even if you cut out all simple sugars in the diet, the liver will produce a minimum level of blood glucose to ensure your survival via a process known as gluconeogenesis.

Glycation still occurs, though at a slower rate.

But there is more you can do.

Thiamine, or vitamin B1, is a nutrient required for various processes in the body. However, thiamine is not easily absorbed into the body. Researchers have found that a special form of thiamine can help prevent glycation.^26,27

Benfotiamine is a fat-soluble form of thiamine that is significantly more bioavailable (absorbable).^26,27

Taken orally, benfotiamine is rapidly absorbed and reaches much higher levels in the blood and in cells. Research shows that a single dose of benfotiamine leads to a five-times greater level in the blood than an equivalent dose of thiamine.^26,27

Benfotiamine blocks several tissue-damaging mechanisms, one of them being the advanced glycation end-products (AGEs) formation pathway.^26,27 It is also able to limit effects of AGEs by reducing inflammation and harmful AGE-triggered changes.²⁷

Through these actions, benfotiamine provides powerful protection against the aging process and development of disease.

Combating Sugar-Related Disease

Benfotiamine has been explored for the treatment or prevention of age- and diabetes-related disorders.

Given the excessive glycation that occurs with high blood glucose levels in diabetic patients, and benfotiamine’s ability to combat this damage, it is no surprise that it has been studied as a treatment for complications of diabetes.^28-31

For example, benfotiamine has been shown to help treat and manage neuropathy, a painful nerve disease common in diabetics.^29,30,32-34

It has also shown benefits for management of cognitive decline in non-diabetic subjects, ranging from mild cognitive impairment to moderate Alzheimer’s disease.

In one randomized controlled trial published in 2020, scientists from Columbia University and Weill Cornell Medicine treated patients with cognitive deficits ranging from mild cognitive impairment to mild Alzheimer’s dementia with either 300 mg of benfotiamine twice daily for one year, or placebo.³⁵

Over the year, decline in cognitive function (measured by the Clinical Dementia Rating Scale) was 77% less in the group receiving benfotiamine. This means that it slowed the clinical progression of the condition.

Benfotiamine also prevented AGEs from increasing. This means it interrupted toxic glycation reactions, suggesting it slowed an important contributor to biochemical aging.³⁵

In an earlier pilot trial in five patients with mild to moderate Alzheimer’s, 300 mg of benfotiamine daily for 18 months led to a cognitive improvement, not just a slowing of deterioration. The average increase on the Mini-Mental State Exam, the most common tool for assessing the severity of dementia, averaged 3.2 points.³⁶

Considering that a change as low as 1 point on this exam is considered “meaningful,” this 3.2 point improvement is remarkable.³⁷

Benfotiamine’s ability to prevent glycation, along with its anti-inflammatory and antioxidant properties, has great promise in slowing the aging process and reducing risk for many other diseases as well.²⁷

Life Extension® suggests taking 250-1,000 mg of benfotiamine daily to protect the body’s tissues against glycation. Those with worsening glycemic control should consider the higher dose range.

Summary

Blood glucose, both in diabetics and non-diabetics, can combine with other compounds in a process known as glycation.

This results in toxic end-products that cause significant damage to cells and tissues.

Glycation has been shown to be a major driver of aging, chronic disease, and complications of diabetes.

Scientists have found that a highly bioavailable form of vitamin B1 called benfotiamine effectively reduces buildup of glycated compounds in the body.

Benfotiamine intake has shown benefits in treating diabetic neuropathy, mild cognitive impairment, and Alzheimer’s disease in human trials.

Research also suggests that benfotiamine may be beneficial in slowing the aging process and lowering risk for many other age-related chronic diseases.

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.

References

1. Moldogazieva NT, Mokhosoev IM, Mel’nikova TI, et al. Oxidative Stress and Advanced Lipoxidation and Glycation End Products (ALEs and AGEs) in Aging and Age-Related Diseases. Oxidative medicine and cellular longevity. 2019;2019:3085756-.
2. Li J, Liu D, Sun L, et al. Advanced glycation end products and neurodegenerative diseases: mechanisms and perspective. J Neurol Sci. 2012 Jun 15;317(1-2):1-5.
3. Simm A. Protein glycation during aging and in cardiovascular disease J Proteomics. 2013 Oct 30;92:248-59.
4. Ward MS, Fortheringham AK, Cooper ME, et al. Targeting advanced glycation endproducts and mitochondrial dysfunction in cardiovascular disease. Curr Opin Pharmacol. 2013 Aug;13(4):654-61.
5. Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci. 2014 Jun;69 Suppl 1:S4-9.
6. Burd J, Lum S, Cahn F, et al. Simultaneous noninvasive clinical measurement of lens autofluorescence and rayleigh scattering using a fluorescence biomicroscope. J Diabetes Sci Technol. 2012 Nov 1;6(6):1251-9.
7. Hipkiss AR. Aging risk factors and Parkinson’s disease: contrasting roles of common dietary constituents. Neurobiol Aging. 2014 Jun;35(6):1469-72.
8. Kim CS, Park S, Kim J. The role of glycation in the pathogenesis of aging and its prevention through herbal products and physical exercise. J Exerc Nutrition Biochem. 2017 Sep 30;21(3):55-61.
9. Qu D, Venzon D, Murray M, et al. Noninvasive measurement of advanced glycation end-products in the facial skin: New data for skin aging studies. <em>J Cosmet Sci.</em> 2017 May/Jun;68(3):195-204.
10. Qu D, Venzon D, Murray M, et al. Noninvasive measurement of advanced glycation end-products in the facial skin: New data for skin aging studies. J Cosmet Sci. 2017 May/Jun;68(3):195-204.
11. Rabbani N, Thornalley PJ. Advanced glycation end products in the pathogenesis of chronic kidney disease. Kidney Int. 2018 Apr;93(4):803-13.
12. Tsuru M, Nagata K, Jimi A, et al. Effect of AGEs on human disc herniation: intervertebral disc hernia is also effected by AGEs. Kurume Med J. 2002;49(1-2):7-13.
13. Verzijl N, DeGroot J, Ben ZC, et al. Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: a possible mechanism through which age is a risk factor for osteoarthritis. Arthritis Rheum. 2002 Jan;46(1):114-23.
14. Danby FW. Nutrition and aging skin: sugar and glycation. Clin Dermatol. 2010 Jul-Aug;28(4):409-11.
15. Gkogkolou P, Bohm M. Advanced glycation end products: Key players in skin aging? Dermatoendocrinol. 2012 Jul 1;4(3):259-70.
16. Arnold P, Njemini R, Vantieghem S, et al. Reaction time in healthy elderly is associated with chronic low-grade inflammation and advanced glycation end product. Exp Gerontol. 2018 Jul 15;108:118-24.
17. Drenth H, Zuidema SU, Krijnen WP, et al. Advanced Glycation End Products Are Associated With Physical Activity and Physical Functioning in the Older Population. J Gerontol A Biol Sci Med Sci. 2018 Oct 8;73(11):1545-51.
18. Ahmed S, Mahmood Z, Zahid S. Linking insulin with Alzheimer’s disease: emergence as type III diabetes. Neurol Sci. 2015 Oct;36(10):1763-9.
19. Kandimalla R, Thirumala V, Reddy PH. Is Alzheimer’s disease a Type 3 Diabetes? A critical appraisal. Biochim Biophys Acta Mol Basis Dis. 2017 May;1863(5):1078-89.
20. Chou PS, Wu MN, Yang CC, et al. Effect of Advanced Glycation End Products on the Progression of Alzheimer’s Disease. J Alzheimers Dis. 2019;72(1):191-7.
21. Batkulwar K, Godbole R, Banarjee R, et al. Advanced Glycation End Products Modulate Amyloidogenic APP Processing and Tau Phosphorylation: A Mechanistic Link between Glycation and the Development of Alzheimer’s Disease. ACS Chem Neurosci. 2018 May 16;9(5):988-1000.
22. Kong Y, Wang F, Wang J, et al. Pathological Mechanisms Linking Diabetes Mellitus and Alzheimer’s Disease: the Receptor for Advanced Glycation End Products (RAGE). Front Aging Neurosci. 2020 2020-July-22;12(217):217.
23. Muriach M, Flores-Bellver M, Romero FJ, et al. Diabetes and the brain: oxidative stress, inflammation, and autophagy. Oxidative medicine and cellular longevity. 2014;2014:102158-.
24. Sommerfield AJ, Deary IJ, Frier BM. Acute hyperglycemia alters mood state and impairs cognitive performance in people with type 2 diabetes. Diabetes Care. 2004 Oct;27(10):2335-40.
25. Exalto LG, Whitmer RA, Kappele LJ, et al. An update on type 2 diabetes, vascular dementia and Alzheimer’s disease. Exp Gerontol. 2012 Nov;47(11):858-64.
26. Crane PK, Walker R, Hubbard RA, et al. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540-8.
27. Balakumar P, Rohilla A, Krishan P, et al. The multifaceted therapeutic potential of benfotiamine. Pharmacol Res. 2010 Jun;61(6):482-8.
28. Raj V, Ojha S, Howarth FC, et al. Therapeutic potential of benfotiamine and its molecular targets. Eur Rev Med Pharmacol Sci. 2018 May;22(10):3261-73.
29. 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.
30. Varkonyi T, Korei A, Putz Z, et al. Advances in the management of diabetic neuropathy. Minerva Med. 2017 Oct;108(5):419-37.
31. Ziegler D, Papanas N, Schnell O, et al. Current concepts in the management of diabetic polyneuropathy. J Diabetes Investig. 2020 Sep 12.
32. Chakrabarti R, Chen M, Liu W, et al. Preventive effects of benfotiamine in chronic diabetic complications. J Diabetes Investig. 2011 Apr 7;2(2):123-31.
33. 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.
34. Stracke H, Gaus W, Achenbach U, et al. Benfotiamine in diabetic polyneuropathy (BENDIP): results of a randomised, double blind, placebo-controlled clinical study. Exp Clin Endocrinol Diabetes. 2008 Nov;116(10):600-5.
35. 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.
36. Gibson GE, Luchsinger JA, Cirio R, et al. Benfotiamine and Cognitive Decline in Alzheimer’s Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial. J Alzheimers Dis. 2020 Oct 16;78(3):989-1010.
37. Pan X, Chen Z, Fei G, et al. Long-Term Cognitive Improvement After Benfotiamine Administration in Patients with Alzheimer’s Disease. Neurosci Bull. 2016 Dec;32(6):591-6.
38. Andrews JS, Desai U, Kirson NY, et al. Disease severity and minimal clinically important differences in clinical outcome assessments for Alzheimer’s disease clinical trials. Alzheimers Dement (N Y). 2019;5:354-63.
39. 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.