Carnosine supreme.qxd

Carnosine
Carnosine is a dipepeptide composed of Alanine and Histidine which occurs naturally in
meats and accumulates preferentially in muscle, brain, eyes and nervous tissue.
THIS INFORMATION IS PROVIDED FOR THE USE OF PHYSICIANS AND OTHER LICENSED HEALTH Benefits proven in studies with a dose of CARE PRACTITIONERS ONLY. THIS INFORMATION IS INTENDED FOR PHYSICIANS AND OTHER LICENSED HEALTH CARE PROVIDERS TO USE AS A BASIS FOR DETERMINING WHETHER OR NOT TO RECOMMEND THESE PRODUCTS TO THEIR PATIENTS. THIS MEDICAL AND SCIENTIFIC INFORMA- TION IS NOT FOR USE BY CONSUMERS. THE DIETARY SUPPLEMENT PRODUCTS OFFERED BY DESIGNS FOR HEALTH ARE NOT INTENDED FOR USE BY CONSUMERS AS A MEANS TO CURE, TREAT, PREVENT, DIAGNOSE, OR MITIGATE ANY DISEASE OR OTHER MEDICAL CONDITION.
a. Reduces glycosylation1, has antioxidant
a. “Carnosine has been shown to react with low-molecular-weight aldehydes
and ketones and has been proposed as a naturally occurring anti-glycating
toxicity, reduces diabetes complications8 agent. It is suggested here that carnosine can also react with (“carnosinylate”)
b. Protective effects on brain or heart,
proteins bearing carbonyl groups…. Accumulation of protein carbonyl groups especially during injuries such as stroke is associated with cellular ageing resulting from the effects of reactive oxygen or ischemic perfusion.4 Possibly helpful species, reducing sugars, and other reactive aldehydes and ketones.”1 “Carnosine and related dipeptides have been shown to prevent peroxidation
c. Speeds up wound healing by stimulating
of model membrane systems leading to the suggestion that they represent water-soluble counterparts to lipid-soluble antioxidants such as alpha-toco- d. Protective on eyesight, specifically cataract
pherol in protecting cell membranes from oxidative damage.”2
e. Proposed as anti-aging factor with tissue
b. “pronounced anti-ischemic effects of carnosine in the brain and heart
rejuvenative effects as evidenced by in vitro are due to the combination of antioxidant and membrane-protecting activity, proton buffering capacity, formation of complexes with transition metals,
and regulation of macrophage function. In experimental cerebral ischemia,carnosine decreases mortality and is beneficial for neurological conditions of f. Protective effect on the brain aging,
the animals. In cardiac ischemia, carnosine protects cardiomyocytes from dam- against amyloid plaque (Alzheimer's)7 and age and improves contractility of the heart. The data indicate that carnosine
potentially helpful with autistic disorder can be used as an anti-ischemic drug.”4
g. Protective on stomach lining in conditions
c. “Thus, the enhancement by carnosine of wound healing may be
ascribed to stimulation of early effusion by histamine and of collagen
biosynthesis by beta-alanine. The wound-healing effects of carnosine were
further demonstrated by the observation that carnosine significantly increased granulation suppressed by cortisone, mitomycin C, 5-fluorouracil, and bleomycin.”6 d., e. “It is proposed that the anti-ageing and rejuvenating effects of carnosine are more readily explainable by its ability to react
with protein carbonyls than its well-documented antioxidant activity.”2
“Carnosine is an endogenous free-radical scavenger. The latest research has indicated that apart from the function of protecting cells
from oxidation-induced stress damage, carnosine appears to be able to extend the lifespan of cultured cells, rejuvenate senescent cells,
inhibit the toxic effects of amyloid peptide (A beta), malondialdehyde, and hypochlorite to cells, inhibit glycosylation of proteins and
protein-DNA and protein-protein cross-linking, and maintain cellular homeostasis. Also, carnosine seems to delay the impair-
ment of eyesight with aging, effectively preventing and treating senile cataract and other age-related diseases. Therefore,
carnosine may be applied to human beings as a drug against aging.”7
e. “Carnosine can delay senescence in cultured human fibroblasts and reverse the senescent phenotype, restoring a more
juvenile appearance. As better antioxidants/free-radical scavengers than carnosine do not demonstrate these antisenescent effects,
additional properties of carnosine must contribute to its antisenescent activity.”3
1. Hipkiss AR. Carnosine and protein carbonyl groups: a possible relationship. Biochemistry (Mosc). 2000 Jul;65(7):771-8.
2. Quinn PJ, Boldyrev AA Carnosine: its properties, functions and potential therapeutic applications. Mol Aspects Med. 1992;13(5):379-444.
3. Hipkiss AR, Brownson . Reaction of carnosine with aged proteins: another protective process? Ann N Y Acad Sci. 2002 Apr;959:285-94.
4. Stvolinsky SL, Dobrota D. Anti-ischemic activity of carnosine. Biochemistry (Mosc). 2000 Jul;65(7):849-55.
5. Chez MG, Buchanan CP . Double-blind, placebo-controlled study of L-carnosine supplementation in children with autistic spectrum disorders. J Child Neurol 2002 Nov;17(11):833-7.
6. Nagai K, Suda T Action of carnosine and beta-alanine on wound healing. Surgery. 1986 Nov;100(5):815-21.
7. Wang AM, Ma C . Use of carnosine as a natural anti-senescence drug for human beings. Biochemistry (Mosc). 2000 Jul;65(7):869-71.
8.
Price DL, Rhett PM Chelating activity of advanced glycation end-product inhibitors.J Biol Chem. 2001 Dec 28;276(52):48967-72. Epub 2001 Oct 24.
9. Stuerenburg HJ. The roles of carnosine in aging of skeletal muscle and in neuromusculardiseases.Biochemistry (Mosc). 2000 Jul;65(7):862-5. Review.
Benfothiamine
Benfothiamine (S-benzoylthiamin-o-monophosphate) is a highly efficient fat soluble form of
Thiamin (vitamin B1) and occurs naturally in small amounts in crushed garlic, shallots and leeks.
THIS INFORMATION IS PROVIDED FOR THE USE OF PHYSICIANS AND OTHER LICENSED Benefits proven in studies with a dose of HEALTH CARE PRACTITIONERS ONLY. THIS INFORMATION IS INTENDED FOR PHYSICIANS AND OTHER LICENSED HEALTH CARE PROVIDERS TO USE AS A BASIS FOR DETERMINING Benfothiamine ranging from 50-3350 mg/per day: WHETHER OR NOT TO RECOMMEND THESE PRODUCTS TO THEIR PATIENTS. THIS MEDICAL AND SCIENTIFIC INFORMATION IS NOT FOR USE BY CONSUMERS. THE DIETARY SUPPLE- MENT PRODUCTS OFFERED BY DESIGNS FOR HEALTH ARE NOT INTENDED FOR USE BY a. Reduces glycation products caused by excessively
CONSUMERS AS A MEANS TO CURE, TREAT, PREVENT, DIAGNOSE, OR MITIGATE ANY DIS- high glucose/fructose levels, especially inside endothelial, retinal, kidney and nerve cells.1,3,6 a, b. “Three of the major biochemical pathways implicated in the
b. Prevents the formation of inflammatory signals
pathogenesis of hyperglycemia induced vascular damage (the caused by excessive glycation such as NF- hexosamine pathway, the advanced glycation end product (AGE) formation pathway and the diacylglycerol (DAG)-protein kinase C c. Prevents or reduces diabetic neuropathy and
(PKC) pathway) are activated by increased availability of the glycolyt- retinopathy by as much as 30%-50% as well as ic metabolites glyceraldehyde-3-phosphate and fructose-6-phosphate.
nephropathy and hyperfiltration.4,5,7 Benefits We have discovered that the lipid-soluble thiamine derivative benfoth-
iamine can inhibit these three pathways, as well as hyperglycemia-
d. Reduces myocardial dysfunction stemming from
associated NF-kappaB activation, by activating the pentose
damage to the nerves that control the heart phosphate pathway enzyme transketolase.”1 c. “benfothiamine, a lipid-soluble form of vitamin B1, can prevent
e. Benfothiamine has a higher bioavailability than
diabetic retinopathy and all three forms of metabolic damage by
Thiamine or TTP (Thiamin Pyrophosphate-the stimulating transketolase activity and thus diverting excess metabolites activated coenzyme form of Thiamine) due to the toward the pentose pathway.”6 “Benfotiamine strongly inhibited the
1. Achieves 5 times higher plasma levels due to development of microalbuminuria …and diabetes-induced hyper-
filtration. This was achieved without change in elevated plasma
2. Better uptake and retention inside the cells due to glucose concentration and glycated hemoglobin in the diabetic state.
High-dose thiamine and benfothiamine therapy is a potential novel 3. It has the ability of upregulating the protective strategy for the prevention of clinical diabetic nephropathy.”7
transketolase enzyme significantly more than plain thiamin. This enzyme diverts potentially damaging d. “Clinical improvement resulting from the use of the above complex
sugar metabolites on a safer metabolic pathway, the (benfothiamine) showed good correlation with a positive course of f. Enhances heavy metal detoxification9,10
echocardiographic values of myocardial contractility and pumping g. Useful in correcting genetic or alcohol induced
function. Elimination of myocardial insufficiency was accompanied by thiamin deficiency and polyneuropathy11,12 an increase in the stroke volume, ejection fraction, the rate of
circulatory shortening of myocardial fibers, left ventricular mass,
and a decrease in end diastolic and systolic volumes.”
f. Some studies have suggested that benfothiamine9 or thiamine10 can increase the effectiveness of chelators such as DMSA or
thiol compounds, specifically reducing liver and kidney toxic metal loads. Heavy metals are known to be a catalyst for non-enzymat-
ic glycation, so this is another mechanism by which benfothiamine reduces glycation.
References1. D, Neumaier M, Bergfeld R, Giardino I, Brownlee M. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Feb 18 [epub ahead of print]; doi:10.1038/nm834.
2. Loew D.Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50. Review.
3. Lin J, Alt A, Liersch J. Benfotiamin inhibits intracellular formation of advanced glycation endproducts in vivo. Diabetes. 2000 May;49(Suppl1):A143(P583).
4. Stracke H, Lindemann A, Federlin K. A Benfotiamin-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.
5. Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different Benfotiamin dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar; 49(3): 220-4.
6. Obrenovich ME, Monnier VM Vitamin B1 blocks damage caused by hyperglycemia. Sci Aging Knowledge Environ. 2003 Mar 12;2003(10):PE67. Babaei-Jadidi R, Karachalias N Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003 Aug;52(8):2110-208. Kolomoiskaia MB, Degonskii AI.The myocardial contractile function and central hemodynamics of patients with insulin-dependent diabetes mellitus during treatment]Probl Endokrinol 9. Yamamoto J, Kaneda Y. Excretion of intracorporeal cadmium with S-benzoylthiamin monophosphate. Bull Environ Contam Toxicol. 1995 May;54(5):745-5010. Tandon SK, Prasad S, Effect of thiamine on the cadmium-chelating capacity of thiol compounds, Hum Exp Toxicol 2000 Sep;19(9):523-811. Woelk H, Lehrl S.Benfotiamine in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol Alcohol. 1998 Nov-Dec;33(6):631-8.
12. A.B. Mukherjee, S. Svoronos, et all "Transketolase abnormality in ultured fibroblasts from familial chronic alcoholic men and their male offspring." The Journal of Clinical Investigation, TO CONTACT DESIGNS FOR HEALTH, PLEASE CALL US AT (800) 847-8302, OR VISIT US ON THE WEB AT WWW.DESIGNSFORHEALTH.COM.

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