Authia Cream

Functions

As co-enzymes, the B vitamins are essential components in most major metabolic reactions. They play an important role in energy production, including the metabolism of lipids, carbohydrates, and proteins. B vitamins are also important for blood cells, hormones, and nervous system function. As water-soluble substances, B vitamins are not generally stored in the body in any appreciable amounts (with the exception of vitamin B-12). Therefore, the body needs an adequate supply of B vitamins on a daily basis.

Thiamine (Vitamin B-1) is an essential coenzyme in energy production. Thiamine is converted quickly into thiamine pyrophosphate, which is required for glycolytic and Krebs cycle reactions. Thiamine also appears to be related to nerve impulse transmission.

Defenses against oxidative stress largely employ key endogenous antioxidant enzymes, many of which require redox-sensitive thiol groups in their active sites. Impaired oxidative metabolism and energy failure, due to loss of reducing equivalents, eventually leads to selective region-specific neuronal loss and diminished thiamine-dependent enzymes. The key enzyme involved here is transketolase (EC 2.2.1.1) (TK), which is a thiamine diphosphate-dependent enzyme that couples the non-oxidative branch of the pentose phosphate pathway (PPP) with the glycolytic pathway. The sugar phosphates generated by PPP are used for intermediary biosynthesis, nucleic acid synthesis and NADPH for reductive biosynthesis (Schenk, Duggleby et al. 1998).

Since thiamine is critical for transketolase function, thiamine deficiency diminishes thiamine dependent enzymes, disrupts mitochondrial function and leads to diminished energy metabolism and the production of NADPH. Gibson and Zhang (Gibson and Zhang 2002) found that interactions involving oxidative stress, together with abnormal thiamine homeostasis, promoted neurodegeneration in a number of chronic neurological diseases.

Both TTFD and vitamin B1 activate the transketolase enzyme and thiamine is important in glucose metabolism as it drives the flux of metabolites through the hexose mono-phosphate shunt. Further, Authia can be used in cases of sulfur depletion, TTFD is expected to act as a sulfate donor during its metabolism. It is suggested that TTFD acts as a metal-chelating agent as well.

Nerve cells are particularly sensitive to thiamine deficiency and our data on transketolase in ASD may be important to understanding the disease in light of B1 deficiency or insufficiency, which could affect neuronal function and potentially brain development or contribute to the development of the ASD phenotype. Loss of these brain cells has been noted during ischemia, hypoxia, excitotoxicity, G-protein dysfunction, viral infection, heavy metal toxicity and deficiency of both thiamine and magnesium (Kern 2002). In that regard, the significance of dysautonomia in ASD can be illustrated by Beriberi, the nutritional disease from thiamine deficiency, which is considered the prototypic model for early stages of dysautonomia (Inoouye 1965). However, this must be distinguished from frank thiamine deficiency (Platt 1967). Kern and Jones (Kern and Jones 2006) noted that loss of Purkinje cells in the cerebellum is a consistent finding in autopsy studies of autistic patients. This is also a consistent finding in Wernicke Korsakoff syndrome (Butterworth 1993), a pathological finding also reported to occur in children (Vasconcelos, Silva et al. 1999). Simon discussed evidence that brain damage in infantile autism may involve the same complex of brainstem nuclei that are damaged by alcohol abuse, thiamine deficiency, and asphyxia (Simon 1990). The most metabolically active structures in the brain make them vulnerable to many injurious factors. The high metabolic rate in brainstem nuclei supports a control function for multiplexing of neural pathways. If this control is lost it may result in the defects of awareness and responsiveness seen in autistic children (Simon 1990). Authia Cream is an easy form for these childen to supplement vitamin B1.

Structure and Mechanism of Action

Thiamine (vitamine B1) disulfide (TTFD) and methyl vitamin B12 is a pink liposomal cream for topical application. Transdermal application (TD) is a more efficient way of administering these vitamins and they are solely responsible for any therapeutic benefit from the cream. The use of TTFD has been shown to result in clinical improvement in 8 of 10 autistic children in a pilot study (See PDR).

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Indications

Authia may be a useful dietary adjunct for individuals who wish to supplement their diet with this essential B vitamin derivative.

Formula

Each milliliter Contains:
Thiamine (TTFD) ... 50 mg
Vitamin B12 .... 1000 mcg

Suggested Use

Adults and Children take 1/4 teaspoon (apx. 1ml) topically daily or as directed by physician.

Side Effects

Occasional localized rash at the site of application has been reported. No contraindications are known other than a rare sensitivity to excipients in the cream (Paraben Free)(See PDR Reference). Adverse reactions may include a "skunk-like odor" due to abnormal metabolism of the patient, which can gradually dissapear as clinical improvemnt occurs and can often be modified by taking 10mg of Biotin daily. (See Physcian's Desk Reference)

How Supplied

Thiamine (vitamine B1) disulfide and methyl vitamin B12 is is supplied in a 2 0z. plastic tube hat does not require refrigeration and apperas as a pink liposomal cream for topical application designed for transdermal delivery (TD) of the two vitamins. It has a mild thiol odor due to its sulfur content. It is also available as enteric coated tablets. Covered by U.S. patent Number 6,585,996.

References

Botez MI, Botez T, Ross-Chouinard A, Lalonde R. Thiamine and folate treatment of chronic epileptic patients: a controlled study with the Wechsler IQ scale. Epilepsy Res 1993;16:157-63.

Cumming RG, Mitchell P, Smith W. Diet and cataract: the Blue Mountains Eye Study. Ophthalmology 2000;10:450-6.

Levy WC, Soine LA, Huth MM, Fishbein DP. Thiamine deficiency in heart failure (letter). Am J Med 1992;93:705-6.

Schellenberger A. Sixty years of thiamin diphosphate biochemistry. Biochim Biophys Acta. 1998 Jun 29;1385(2):177-86.

Suzuki M, Itokawa Y. Effects of thiamine supplementation on exercise-induced fatigue. Metab Brain Dis. 1996 Mar;11(1):95-106. Levy S E, Hyman S L. Novel treatments for autistic spectrum disorders. Ment Retard Dev Disabil Res Rev. 2005;11(2):131-42.

James S J, Cutler P, Melnyk S, Jernigan S, Janak L, Gaylor D W, Neubrander J A. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism Am J Clin Nutr 2004;89(6):1611-1617.
Gibson G E Zhang H. Interactions of oxidative stress with thiamin homeostasis promote neurodegeneration. Neurochem Int 2002;40:493-504.
Lonsdale D, Shamberger R J, Audhya T. Treatment of autistic children with thiamine tetrahydrofurfuryl disulfide. Neuroendocrin Lett 2002;23:303-308.
Brin M.Defects of pyruvate and pentose metabolism in relationship to transketolase activity in rats and man and to the startle response in thiamine deficient rats. In:
Wolstenholme G E W, O’Connor M,(eds). Thiamine Deficiency. Boston: Little, Brown and Company, 1967:87-102.
Boni L, Kieckens L Hendricx A An evaluation of a modified erythrocyte transketolase assay for assessing thiamine nutritional adequacy. J Nutr Sci Vitaminol 1980;26:507-514.
Jeyasingham M D, Pratt O, Burns A, Shaw G K Thompson A, Marsh A. The activation of red blood cell transketolase in groups of patients especially at risk from thiamin deficiency. Psych Med 1987; 117:311-318.
Lonsdale D. A review of the biochemistry, metabolism and clinical benefits of thiamin(e) and its derivatives eCAM 2006;3:49-59.
Massod M F, McGuire S L, Werner W R. Analysis of blood transketolase activity. Am J Clin Pathol 1971;55:465-470
Manzardo A M, Penick E C. A theoretical argument for inherited thiamine insensitivity as one possible biological cause of familial alcoholism. Alcohol Clin Exp Res 2006;30(9):1545-50.
Mukherjee A B, Svoronos S, Ghazanfari A, Martin P R, Fisher A, Roecklein B, et al. Transketolase abnormality in cultured fibroblasts from familial chronic alcoholic men and their male offspring. J Clin Invest 1987;79(4):1039-43.
Chaudhuri S K, Halder K, Chowdhury S R, Bagchi K. Relationship between toxaemia of pregnancy and thiamine deficiency. J Obstet Gynaecol Br Commonw 1969;76(2):123-126.
Lonsdale D. Recurrent febrile lymphadenopathy treated with large doses of vitamin B1: report of two cases. Dev Pharmacol Ther 1980;1(4):254-2
Cooper J R, Itokawa Y, Pincus J H. Thiamine triphosphate deficiency in subacute necrotizing encephalomyelopathy. Science 1969;164:72-73.
Cooper J R, Pincus J H. The role of thiamine in nervous tissue. Neurochem Res 1979;4:223-239.
Bettendorff L, Kolb H A, Schoffeniels E. Thiamine triphosphate activates channels of large unit conductance in neuroblastoma cells. J Membr Biol 1993;136(3):281-288.
Bettendorff L, Hennuy B, De Cherek A, Wins P. Chloride permeability of rat brain vesicle correlates with thiamine triphosphate content. Brain Res 1994;652(1):157-160.
Barker J N, Jordan F, Hillman D E, Barlow O. Phrenic nerve thiamin and neuropathy in Sudden Death Infants. In: Sable H Z, Gubler C J, (eds). Thiamin: twenty years of progress. Ann NY Acad Sci 1982;378:449-452.
Blass J. Abnormalities in pyruvate dehydrogenase and neurologic function. Intern J Neurosci 1972;4:65-9
Scriver C R, Mackenzie S, Claw C L, Delvin E. Thiamine-responsive maple-syrup-urine disease. Lancet 1971; Feb 13;1(7694):310-12.
Lonsdale D. Three case reports to illustrate clinical applications in the use of erythrocyte transketolase eCAM 2007;4(2):247-50
Wells D G, Baylis E M, Holoway L, et al. Erythrocyte transketolase in megaloblastic anaemia. Lancet 1966;ii:543-548.
Inoouye K, Katsura E. Clinical signs and metabolism of beriberi patients. In: Shimazono N, Katsura E, (eds.). Beriberi and Thiamine. Tokyo: Igaku Shoin Ltd, 1965:29-63.
Platt B S. Thiamine deficiency in human beriberi and in Wernicke;s encephalopthay. In: Wolstenholme G E W, O’Connor M (eds.) Thiamine Deficiency. Boston: Little, Brown and Company, 1967;135-143
Butterworth R F. Pathophysiology of cerebellar dysfunction in the Wernicke-Korsakoff syndrome. Can J Neurol Sci 1993;20:S123-126.
Bettendorff L, Sluse F,Goessens G, Wins P, Grisar T. Thiamine deficiency-induced partial necrosis and mitochondrial uncoupling in neuroblastoma cells are rapidly reversed by addition of thiamine. J Neurochem 1995;65(5):2178-84.
Lonsdale D. Glutamine protects thiamin deficient animals. J Acv Med 1996;9(3):203-9.
Olkowski A A, Gooneratne S R, Christensen D A. The effects of thiamine and EDTA on biliary and urinary lead excretion in sheep. Toxicol Lett 1991;59(1-3):153-159.
Kim J S, Hamilton D L, Blakley B R, Rousseaux C G. The effects of thiamin on lead metabolism: whole body retention of lead-203. Toxicol Lett 1991;56(1-2):43-52.
Bettendorff, L., H. A. Kolb, et al. (1993). "Thiamine triphosphate activates an anion channel of large unit conductance in neuroblastoma cells." J Membr Biol 136(3): 281-8.
Bettendorff, L. and P. Wins (1994). "Mechanism of thiamine transport in neuroblastoma cells. Inhibition of a high affinity carrier by sodium channel activators and dependence of thiamine uptake on membrane potential and intracellular ATP." J Biol Chem 269(20): 14379-85.
Blass, J. (1972). "Abnormalities in pyruvate dehydrogenase and neurologic function." Intern J Neurosci 4: 65-69.
Boni, L., L. Kieckens, et al. (1980). "An evaluation of a modified erythrocyte transketolase assay for assessing thiamine nutritional adequacy." J Nutr Sci Vitaminol (Tokyo) 26(5): 507-14.
Brin, M. (1962). "Effects of thiamine deficiency and of oxythiamine on rat tissue transketolase." J Nutr 78: 179-83.
Brin, M. (1967). "The oxidation of C14-pyruvate and of C14-ribose in thiamine deficient intact rats." Isr J Med Sci 3(6): 792-9.
Geier, D. A., J. K. Kern, et al. (2008). "A Prospective Study of Transsulfuration Biomarkers in Autistic Disorders." Neurochem Res.
Gibson, G. E. and H. Zhang (2002). "Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration." Neurochem Int 40(6): 493-504.
Platt, B. S. (1967). Thiamine deficiency in human beriberi and in Wernicke's encephalopthay. Boston, Little, Brown and Company.
Schenk, G., R. G. Duggleby, et al. (1998). "Properties and functions of the thiamin diphosphate dependent enzyme transketolase." Int. J. Biochem. Cell Biol. 30: 1297-1318.
Vasconcelos, M. M., K. P. Silva, et al. (1999). "Early diagnosis of pediatric Wernicke's encephalopathy." Pediatr Neurol 20(4): 289-94.
Waring, R. H. and L. V. Klovzra (2000). "Sulphur metabolism in autism." J Nutr Env Med 10: 25-32.
Waring, R. H., J. M. Ngong, et al. (1997). "Biochemical parameters in autistic children." Dev Brain Dysfunction 10: 40-43.
Wells, D. G., E. M. Baylis, et al. (1968). "Erythrocyte-transketolase activity in megaloblastic anaemia." Lancet 2(7567): 543-5.
Lonsdale, D. 2002. Autism; thiamine tetrahydrofurfuryl disulfides; urinary arsenic; sulfur metabolism. Neuroendocrinol. Lett. 23:303–308
Mark E. Obrenovich, and Vincent M. Monnier Vitamin B1 Blocks Damage Caused by Hyperglycemia, Science. Aging Knowl. Environ., 12 March 2003 Vol. 2003, Issue 10, p. pe6
Obrenovich, Ludis A. Morales, Celia J. Cobb, Justin C. Shenk, Gina M. Méndez, Kathryn Fischbach, Mark A. Smith, Eldar K. Qasimov, George Perry, Gjumrakch AlievInsights into cerebrovascular complications and Alzheimer disease through the selective loss of GRK2 regulation Alzheimer Review Series Guest Editor: B. O. Popescu Journal of Cellular and Molecular Medicine Volume 13 Issue 5, Pages 853 - 865 Published Online: 6 Oct 2008

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These statements have not been evaluated by the Food and Drug Administration.
This product is not intended to diagnose, treat, cure, or prevent any disease.

We at Westlake labs take heavy metal contamination seriously and thus test our products routinely to assure quality. We offer a survey compared to big box store brands randomly obtained over the last year.