Product Details

ACTIVE B1

 
"B" Active Forever
  • Slows cellular aging
  • Provides active and highly bioavailable forms of B1
  • Supports healthy cognitive, nerve and muscle function
  • Excellent choice for life extensionists

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Discussion

Active B1 contains Sulbutiamine, a fat soluble thiamine (vitamin B1) derivative and Benfotiamine, another form of thiamine with a superior ability to penetrate cell membranes and increase bioavailability over conventional thiamin supplements. Vitamin B1 is a factor in the maintenance of good health, and helps the body metabolize carbohydrates, fats and proteins. 

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Supplement Facts

Amount Per Serving Amount: 1 Vegi-Cap
50 mg Sulbutiamine (Thiamin Disulfide O,O-Diisobutyrate)*
50 mg Benfotiamine (S-Benzoylthiamine-O-Monophosphate) *
* Produced through pharmaceutical synthesis. Non-medicinal ingredients: microcrystalline cellulose. Capsule: hypromellose, gellan gum, potassium acetate, water.

AOR™ guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, corn, nuts, dairy, eggs, fish or shellfish.

Suggested Use:

Take 1 capsule daily with food, or as directed by a qualified health care practitioner. 

Cautions :

Consult a health care practitioner for use beyond 6 weeks.

Pregnancy/Breastfeeding :

Do not use

Source:

Pharmaceutical synthesis

Main Applications:

Thiamine Deficiency
Diabetic Complications
Anti-Aging

The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.

Active B1 contains Sulbutiamine, a fat soluble thiamin (vitamin B1) derivative and Benfotiamine, another form of thiamine with a superior ability to penetrate cell membranes and increase bioavailability over conventional thiamin supplements. Vitamin B1 is a factor in the maintenance of good health, and helps the body metabolize carbohydrates, fats and proteins.

Thiamine is Vitamin B1, which is primarily obtained from the outer shell and germ of grains such as wheat, rice and barley, along with other B vitamins. It is also present in some vegetables and meats. However, yeast is the richest nutritional source of thiamine. In the body, thiamine helps with energy production, cognitive function, muscle function, and to prevent cellular aging.

Early research stemmed from Japan where it was noted that navy soldiers did not develop beriberi (a neuropathy condition that can quickly lead to death) when fed whole grain rice over polished white rice. Thiamine is the form in which Vitamin B1 is transported to the tissues, but its biologically active forms include various forms of phosphorylated thiamine derivatives such as thiamine pyrophosphate / diphosphate.

Foods such as coffee, tea and wine and preserved foods containing sulfites can actually break down thiamine or inhibit its conversion, leading to a thiamine deficiency.  Folic acid deficiency can also inhibit its absorption, and acidic conditions can accelerate these processes. Therefore, thiamine deficiency can be caused by an overconsumption of such foods or by conditions that cause impaired nutrition, such as some gastrointestinal disorders.

Thiamine deficiency is the cause of conditions such as beriberi and Wernicke’s encephalopathy. The first is characterized by neuropathy, muscle weakness and eventually paralysis, while the latter presents itself in cognitive and mental deficits.

Many people are interested in taking this supplement in order to improve their energy levels, mood, memory function including their ability to focus on things, multi tasking capabilities and to fight against cognitive decline. It has also been used to reduce the symptoms of erectile dysfunction and to assist in weight loss efforts.

AOR was the first to introduce Benfotiamine to North America in 2001 and one of the first to introduce Sulbutiamine to the Canadian supplement market in 2011. Sulbutiamine and benfotiamine (which is dephosphorylated to form S-benzoylthiamine, which is the absorbable form of benfotiamine) are much better absorbed than thiamine as they are able to passively diffuse across membranes rather than depending on a transport mechanism. These molecules are then converted into thiamine phosphates, such as thiamine pyrophosphate, which is the active co-enzyme form of vitamin B1.

Research has shown that many people with diabetes have thiamine deficiencies, either due to a lack of thiamine consumption or due to an excessive intake of foods that cause thiamine breakdown or excretion. Thiamine is essential for proper carbohydrate metabolism since it is a cofactor for the enzymes that help to process these sugars. When thiamine is deficient, sugars are metabolized through alternate pathways that do not require thiamine. Unfortunately, these alternate pathways produce harmful metabolites that damage the blood vessel lining and the myelin sheaths and axons of nerves, which can lead to heart disease and neuropathies. One of these metabolites is appropriately called an AGE, or an advanced glycation end-product. Slowly, imperceptibly, AGE reactions create chemical handcuffs, which gum up your proteins, deactivate your enzymes, trigger unhealthy biochemical signaling in your cells, and damage your DNA, producing cellular “AGEing.”

Thiamine uptake is generally limited by the rate of active transporters that move nutrients across cellular membranes. The brain requires large amounts of thiamine in order to function properly, however very little thiamine actually reaches the brain because it cannot cross the blood brain barrier. Luckily, sulbutiamine and benfotiamine (which is dephosphorylated to form S-benzoylthiamine, which is the absorbable form of benfotiamine) are much better absorbed than thiamine as they are able to passively diffuse across membranes rather than depending on a transport mechanism. These molecules are then converted into thiamine phosphates, such as thiamine pyrophosphate, which is the active co-enzyme form of vitamin B1.

Normally, AGE products and AGEd proteins are cleared out by the kidneys at an adequate rate. However, when there is a thiamine deficiency, AGEs build up in the tissues, wreaking havoc on nearby tissues. Cell AGE receptors, RAGEs, activate inflammatory cascades which cause oxidative stress, thereby damaging their surrounding blood vessels and neurons.  Thiamine pyrophosphate prevents the formation of AGEs via two mechanisms. First, it opens up an important biochemical “safety valve” in the normal metabolism of blood sugar through an enzyme known as transketolase. Activating transketolase allows the body to shunt excess triosephosphates into a safe alternative metabolic pathway, preventing the logjam that leads to the buildup of triosephosphates and thus the formation of AGEs. Secondly, adequate thiamine pyrophosphate levels can also prevent the conversion of amadori products (rearranged glycated proteins) into AGEs. When there is less AGE formation, the body can clear out AGEs more effectively.

The key is to get adequate levels of thiamine into the cells via the highly bioavailable forms of sulbutiamine and benfotiamine. The facts are that muscles, nerves and blood vessels function better with their help. One study examining the effects of sulbutiamine supplementation on diabetic neuropathy found that 400mg/day for 6 weeks resulted in an improvement in peripheral nerve function.  Two other studies found that 200 mg/day of sulbutiamine improved asthenic symptoms such as fatigue related to microbial infections. Sulbutiamine has also been suggested to enhance working and episodic memory in an animal study, demonstrating its ability to cross the blood-brain barrier. Sulbutiamine is one of few thiamine derivatives that is able to cross the blood-brain barrier and actually increase thiamine phosphate levels in the brain due to its lipophilic structure.

Thiamin absorption from benfotiamine has been shown to be about five times greater than from conventional thiamin supplements. It is well established that using varied doses of benfotiamine for painful diabetic neuropathy have shown that symptoms of pain can be improved with benfotiamine supplementation.  Pyridoxal-5’-phosphate (the biologically active form of vitamin B6) has also been found to be an excellent AGE inhibitor. One study combined P-5-P with benfotiamine and found significant improvements in pain levels in 86% of patients, sensory nerve conduction and motor nerve conduction in 45% of patients, and even HbA1c (indicator of blood sugar) levels in 63% of patients.

In conclusion, it is essential to consume adequate vitamin B1 levels in order to maintain healthy cells and keep glycation at bay. Consuming sulbutiamine to help with brain vitamin B1 levels and benfotiamine to help with peripheral B1 levels is much more beneficial than consuming regular thiamin. Together, they will enhance sugar metabolism and prevent neurotoxicity from glycated proteins, thereby improving the function of the muscles, nerves and blood vessels in order to prevent or improve the complications that result from the complications of vitamin B1 deficiency and sugar overload.

Balakumar et al. The multifaceted therapeutic potential of benfotiamine. Pharmacological Research. 2010; 61:482–488

Bizot JC, Herpin A, Pothion S, Pirot S, Trovero F, Ollat H. 2005. Chronic treatment with sulbutiamine improves memory in an object recognition task and reduces some amnesic effects of dizocilpine in a spatial delayed-non-match-to-sample task. Prog Neuropsychopharmacol Biol Psychiatry 29(6): 928-935.

Cameron NE, Gibson TM, Nangle MR, Cotter MA. 2005. Inhibitors of advanced glycation end product formation and neurovascular dysfunction in experimental diabetes. Ann NY Acad Sci 1043: 784-792.

Fujiwari M, Watanabe H. 1952. Allithiamine, a newly found compound of Vitamin B1. Proceedings of the Japan Academy 28(3): 156-158.

Greenwood J, Love ER, Pratt OE. 1982. Kinetics of thiamine transport across the blood brain barrier in the rat. Journal of Physiology 327:95-103.

Johnson BC. 1955. Water Soluble Vitamins Part III. Annual Review of Biochemistry 24: 419-464.

Kiew KK, Wan Mohamad WB, Ridzuan A, Mafauzy M. 2002. Effects of Sulbutiamine on diabetic polyneuropathy: and open randomized controlled study in type 2 diabetics. Malaysian Journal of Medical Sciences 9(1): 21-27.

Lockman PR, Mumper RJ, Allen DD. 2003. Evaluation of blood-brain barrier thiamine efflux using the in situ rat brain perfusion method. Journal of Neurochemistry 86(3): 627-634.
Lonsdale D. 2004. Thiamine tetrahydrofurfuryl disulfide: a little known therapeutic agent. Med Sci Monit 10(9): Epub.

Miyazawa T, Nakagawa K, Shimasaki S, Nagai R. Lipid glycation and protein glycation in diabetes and atherosclerosis. Amino Acids. 2010 Oct 19. [Epub ahead of print]
Mizuhira B, Uchida K, Totsu J, Shindo H. 1968. Studies on the absorption of S-benzoylthiamine O-monophosphate: (IV) Elecronmicroscopic autoradiography on the intestinal absorption of S-benzoyl-3H O-monophosphate in rat. Vitamins 38: 334-336.

Netzel M, Ziems M, Jung KH, Noll E, Borsch C, Bitsch I. 2000. Effect of high-dosed thiamine hydrochloride and S-benzoyl-thiamine-O-monophosphate on thiamine status after chronic ethanol administration. Biofactors 11: 111-113.

Nikoli? A, Kacar A, Lavrni? D, Basta I, Apostolski S.The effect of benfothiamine in the therapy of diabetic polyneuropathy. Srp Arh Celok Lek. 2009 Nov-Dec;137(11-12):594-600.

Page GL, Laight D, Cummings MH. Thiamine deficiency in diabetes mellitus and the impact of thiamine replacement on glucose metabolism and vascular disease. Int J Clin Pract. 2011 Jun;65(6):684-90.

Shah, SN. 2003 Adjuvant role of vitamin B analogue – (Sulbutiamine) with anti-infective treatment in infection associated asthenia. Journal of Association of Physicians of India, 51.

Sugimoto K, Yasujima M, Yagihashi S. Role of advanced glycation end products in diabetic neuropathy. Current Pharmaceutical Design. 2008;14(10):953-61.

Thornalley PJ. 2005. The potential role of thiamine (vitamin B1) in diabetic complications. Curr Diabetes Rev 1(3): 287-298.

Tiev KP, Cabane J, & Imbert JC. Traitement de l’asthénie en période postinfectieuse: etude randomisée en double aveugle de deux doses de sulbutiamine (400-600 mg/j) versus placebo. La Revue de Médicine Interne, 1999. 20:912-8.

Volvert ML, Seyen S, Piette M, Evrard B, Gangolf M, Plumier JC, Bettendorff L. 2008. Benfotiamine, a synthetic S-acyl thiamine derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble thiamine disulfide derivatives. BMC Pharmacology 8:10:10.

Winkler G, Pál B, Nagybéganyi E, Ory I, Porochnavec M, Kempler P. 1999. Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung 49(3): 220-224.

The multifaceted therapeutic potential of benfotiamine.

Pharmacological Research. 2010; 61:482–488

Pitchai Balakumar, Ankur Rohilla, Pawan Krishan, Ponnu Solairaj, Arunachalam Thangathirupathi.

Thiamine, known as vitamin B1, plays an essential role in energy metabolism. Benfotiamine (Sbenzoylthiamine 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 diabetesassociated 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 thatmayadditionally 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.

 

Adjuvant role of vitamin B analogue – (Sulbutiamine) with anti-infective treatment in infection associated asthenia.

Journal of Association of Physicians of India. 2003  51.

Shah, SN.

Aims of the study : Asthenic symptoms such as weakness accompany illness. This study investigates whether the centrally acting cholinergic agent, vitamin B analogue (sulbutiamine), is effective and acceptable in relieving these symptoms in infectious disease when combined with specific anti-infective treatment.

Methodology : In a prospective uncontrolled, non-randomised, commercial, observational study, 1772 patients with an infectious disease and asthenic symptoms, drawn from the practice of 350 randomly selected physicians throughout India, received vitamin B analogue (sulbutiamine) in addition to specific anti-infective treatment for 15 days. The primary outcome variable was complete resolution of asthenic symptoms with treatment.

Results : The number (%, 95% confidence interval) of patients with complete resolution of all asthenic symptoms was 916 (51.7, 49.4-54). In the remaining patients, severe asthenia was reduced but persisted in 11 (0.6, 0-26); and moderate asthenia in 94 (5.3, 0-17.6). The response was greater in patients with acute infection and symptoms more related to cerebral function. Side effects occurred in 10 (0.6%), patients and well being improved significantly.

Conclusions : Vitamin B analogue (sulbutiamine) may be a useful adjunct to specific anti-infective treatment.

 

Effects of Sulbutiamine on diabetic polyneuropathy: and open randomized controlled study in type 2 diabetics.

Malaysian Journal of Medical Sciences. 2002 9(1): 21-27.

Kiew KK, Wan Mohamad WB, Ridzuan A, Mafauzy M.

Thirty patients with diabetic polyneuropathy were recruited from the diabetic clinic in Hospital Universiti Sains Malaysia from 1996 to 1998. They were randomlyassigned either sulbutiamine (Arcalion®) (15 patients) or no treatment (controlgroup; 15 patients). Glycaemic control was assessed by blood glucose and HbA1. Severity of neuropathy was assessed by symptom and sign score, and electrophysiological parameters (nerve conduction velocity and compound muscle action potential) at entry to the study and after 6 weeks. There were improvements in the electrophysiological parameters in the treatment group when compared to the controls with significant improvement in the median nerve conduction velocity.

 

A Benfotiamine – vitamin B combination in treatment of diabetic polyneuropathy.

Exp Clin Endocrinol Diabetes. 1996 104: 311-316.

H. Stracke, A. Lindemann, K. Federlin.

In a double-blind, randomized, controlled study, the effectiveness of treatment with a combination of Benfotiamine (an Allithiamine, a lipid-soluble derivative of vitamin B1 with high bioavailability) plus vitamin B6/B12 on objective parameters of neuropathy was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement (p = 0.006) of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold. Long-term observation of 9 patients with verum over a period of 9 months support the results. Therapy-specific adverse effects were not seen. The results of this double-blind investigation, of the long-term observation and of the reports in the literature support the contention that the neurotropic benfotiamine – vitamin B combination represents a starting point in the treatment of diabetic polyneuropathy.

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