Unique form of Vitamin B6 Protects Against Complications Related To Diabetes and Aging



by Laurie Barclay, MD, introduction by William Faloon

Pyridoxamine Protects Against Kidney Damage

“There is experimental evidence that pyridoxamine supplementation can be helpful in preventing and delaying diabetic complications,” Prof. Jain says.

In studies of diabetic or obese rats, pyridoxamine protected against kidney damage, as well as against development of retinopathy and neuropathy in diabetic rats. Compounds found in the urine of these rats confirmed that pyridoxamine was acting as an AGE/ALE inhibitor.9

Rats made diabetic by administration of a drug known as streptozotocin tend to develop kidney disease, similar to nephropathy seen in diabetic patients. Interestingly, pyridoxamine limited AGE formation and development of nephropathy in streptozotocin-diabetic rats without affecting control of blood sugar.13

Lipids appear to be an important source of AGEs in the diabetic rat, based on findings that pyridoxamine lowers lipids. Blood levels of cholesterol and triglycerides increase in proportion to AGEs in skin collagen.13 In Zucker rats, pyridoxamine lowered levels of cholesterol and triglycerides, inhibited AGE formation, and protected against kidney and blood vessel damage.13

Zucker rats given pyridoxamine in their drinking water, but not the untreated controls, had lowering of high blood pressure and less thickening of blood vessel walls associated with atherosclerosis. Even more amazing was that markers of kidney damage decreased in the pyridoxamine-treated rats. Blood creatinine levels decreased, as did leakage of total protein and of a specialized protein known as albumin into the urine, nearly returning to levels seen in nonobese rats.13

Similarly, in streptozotocin-diabetic rats, pyridoxamine significantly blocked the increase in albumin found in the urine, and of blood levels of creatinine and lipids.14

Pyridoxamine was as effective as aminoguanidine in correcting these abnormalities reflecting diabetic complications.14 However, pyridoxamine, but not aminoguanidine, improves insulin secretion, glycemic control, and beta-cell regeneration in diabetic animals.12

“Therapeutic effects of pyridoxamine in complications of diabetes were investigated in animal models and in clinical trials,” Prof. Voziyan says. “The most substantial data are available on pyridoxamine’s effects in diabetic nephropathy. In several different animal models, pyridoxamine inhibited increase in albuminuria and serum creatinine; pyridoxamine also ameliorated characteristic pathologic lesions such as increase in glomerular volume and expansion of mesangial matrix.”

In other words, pyridoxamine corrected not only functional markers of diabetic kidney damage, such as albumin in the urine and creatinine in the blood, but also anatomical markers. The glomerulus acts as a filter to control which beneficial compounds are retained in the blood and which waste products are excreted into the urine passing through each nephron, or urine collection unit within the kidney.

Blood volume within the glomerulus, which is an intricate web of capillaries (small blood vessels) surrounding each nephron, is increased in diabetic nephropathy.15 Pyridoxamine appears to reduce this increase in glomerular volume.

Another pathological change in diabetic nephropathy is that material within the glomerulus known as mesangial matrix progressively expands, ultimately blocking glomerular capillaries and hence reducing filtration of blood through the nephrons. One key factor leading to expansion of the mesangial matrix is abnormal glycation of matrix proteins, which interferes with their degradation and turnover.16

Not surprisingly, therefore, by preventing AGE formation, pyridoxamine is uniquely poised to prevent expansion of the mesangial matrix, an important marker of diabetic nephropathy.7

In streptozotocin-induced diabetic rats, PLP (an active form of pyridoxamine) significantly reduced evidence of nephropathy, namely albumin in the urine, glomerular hypertrophy, mesangial expansion, and accumulation of AGEs. Pyridoxamine itself had similar effects, although PLP was more effective.17

Shedding further light on the mechanisms of action of pyridoxamine in protecting kidney function are studies in a rare genetic disorder that results in overproduction of oxalate, leading to kidney stone formation and end-stage renal disease early in life. In an experimental model of this disorder, pyridoxamine cut urinary oxalate excretion by half, compared with untreated animals, and significantly reduced kidney stone formation.18

Another kidney disease in which pyridoxamine may be therapeutic is chronic allograft nephropathy, which occurs when the immune system attacks a transplanted kidney. In an animal model of this condition, pyridoxamine improved kidney function and reduced structural damage by inhibiting AGE formation.19

Pyridoxamine Protects Against Nerve and Eye Damage

“In diabetic animal models, pyridoxamine demonstrated relevant therapeutic effects in the retinal vasculature and in the peripheral nerves,” Prof. Voziyan says.

In a study from Queen’s University of Belfast in Northern Ireland, diabetic rats given pyridoxamine for 29 weeks had dramatically reduced development of retinal damage, whereas those given other antioxidants, namely vitamin E and lipoic acid, did not. Pyridoxamine protected against a wide variety of pathological changes in the diabetic retina, including blockage of small blood vessels, altered gene and protein expression, and accumulation of immunologically active AGE/ALEs.20

A laboratory study from Case Western Reserve University in Ohio showed that pyridoxamine prevented AGE formation in the lens, further supporting its benefits in protecting against the visual loss accompanying aging and diabetes. The same study showed that pyridoxamine reduced oxidative stress and AGE formation in red blood cells and plasma proteins from diabetic rats.22

“Pyridoxamine supplementation has shown benefit in prevention of diabetic nephropathy and retinopathy in experimental diabetes using high-dose supplementation,” Prof. Thornalley says.

Human Studies With Pyridoxamine

Pyridoxamine has shown promise for treatment of diabetic nephropathy, not only in animal models of diabetes, but also in phase 2 clinical trials with diabetic patients.23

“Pyridoxamine efficacy was also investigated in patients with type 1 and type 2 diabetes and overt nephropathy,” Prof. Voziyan says. “In these clinical trials, pyridoxamine significantly reduced the rise in serum creatinine.”

Phase 2 clinical studies of pyridoxamine in patients with kidney disease from type 1 or 2 diabetes were conducted at several specialty centers and were led by a group from the prestigious Joslin Diabetes Center at Harvard Medical School.23 One trial used a dose of 50 mg pyridoxamine given twice daily, whereas the second trial used doses of 250 mg twice daily.

When results from both trials were combined, pyridoxamine significantly decreased AGE formation, as expected. Even more promising was a reduction in the change from baseline in blood levels of creatinine, suggesting a protective effect on kidney function compared with placebo. However, there were no differences compared with placebo in excretion of albumin into the urine.23

Because of its role in combating AGE formation as well as oxidative stress, pyridoxamine is a novel approach being studied clinically for its possible contribution in treatment of diabetic nephropathy and other forms of chronic kidney disease.24

Pyridoxamine May Complement Other Kidney-Protecting Compounds

One of the advantages of using pyridoxamine to support kidney function is that its multiple mechanisms of action are likely to allow it to safely enhance the effects of other therapies—including pharmaceuticals and nutritional supplements—that may protect the kidney from injury related to diabetes or other chronic conditions. Two renal-protective agents identified by Life Extension are CoQ1021 and silymarin.25

Pyridoxamine may be used in concert with prescription therapies used in the management of conditions associated with diabetes. “Both animal studies and clinical trials have shown that pyridoxamine therapy is effective even when used together with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, which are standard anti-hypertensive treatments in diabetes,” Prof. Voziyan says. “This shows that pyridoxamine therapy provides additional benefits compared to existing standard treatments.”

To minimize the formation of advanced glycation end products in your body, avoid foods cooked higher than 250 degrees, especially high-fat, grilled meats and caramelized sugars. Optimally control blood glucose levels. Supplementation with pyridoxamine, antioxidants and other anti-glycating compounds such as carnosine and benfotiamine would be expected to further assist in protecting against glycation-induced protein damage.

http://www.lef.org/magazine/mag2008/oct2008_Vitamin-B6-Protects-Against-Diabetes-Aging_02.htm

Vitaminele şi mineralele ajută la regenerarea nervilor periferici

Vitaminele şi mineralele ajută la regenerarea nervilor periferici. Se recomandă vitamina  B12 (din drojdie, orez, ouă, lapte, germeni de grâu şi spanac), magneziul (din grâu, ovăz, polen, sfeclă, orz, porumb, spanac sau cartofi), cuprul (din nuci, migdale, alune, ceapă, spanac, polen, mere şi struguri) şi cobaltul (din pere, nuci, cireşe şi caise). (Dr. neurolog Daniel Manolescu, clinica Doctor Acasă)

B12 + Co + Mg + Cu – s-au facut experiente pe sobolani carora le-a regenerat nervii periferici.

Cobaltul (Co) – in piersici, prune, varza, spanac, linte, mazare, alge, viscere, carne, oua, lapte. Este vasodilatator. Intra in compozitia vitaminei B12 si este activator al unor enzime. Co participa la buna functionare a globulelor rosii. Se gaseste in caise (0,032 mg/100 g), pere (0,018 mg), cirese (0,005 mg), snochine (0,02 mg), nuca (0,005 mg), visine (0,004 mg), salata salbatica etc. (Conf. dr. vlihaescu Grigore – Fructele in alimentatie, bioenergie si cosmetica).

Este un element simpatico-reglator, folosit in afectimi spastice digestive, spasme si blocaje vasculare (arterite). Co intra in alcatuirea unoi fermenti si hormoni. Deficit: sensibilitate la pneumonie si orice infectie, anxirtate, palpitatii, pericol in functia muschiului cardiac, anemie (mai ales la cei care tin strict regim vegetarian de lunga durata).
Co e important in ficat.
Alimentatia obisnuita ofera 5-7 /ig Co. Excesul de Co produce fenomene toxice. Co este necesar in anemii, dureri: anghina, coronariK, arterite, sciatica, nevrite.

Magneziul (Mg) – (necesar 0,32 g); se afla in: smochine, lapte, oua, crustacee, soia, leguminoase, paine integrala, cacao, varza alba, praz, urzici, salata salbatica, hrean, patrunjel, grau, ovaz, orz, porumb, spanac, cartofi, sfecla, migdale (255 mg), alune (150 mg), nuci (132 mg), castane (40-83 mg), catina (30 mg), coacaze rosii (32 mg), coacaze negre (17-30 mg), polen, zmeura (24-30 mg), macese (30 mg), mure (26 mg), visine (22 mg), capsune (14 mg), cirese (15 mg), prune (13 mg), lamai (13 mg), grape fruit (12 mg), afine (10 mg), fragi si porumbi (11 mg), caise (10 mg), pere (10 mg), piersici (10 mg). Magneziul este un component de structura al fermentilor (sunt injur de 300), influentand procesele energetice in toate organele si tesuturile, care pentru o buna functionare au nevoie de energie (inima, sistemul nervos, muschii). Magneziul este cardioprotector, ajutand inima in caz de infarct miocardic, imbunatatind oxigenarea miocardului, limitand zona de lezare, avand rol important in activitatea celulelor musculare si in stimularea circulatiei sangvine. Simultan, magneziul manifesta o actiune de dilatare a vaselor si contribuie la reducerea presiunii arteriale. Reglementeaza contractia musculara. Este un reechilibrant nervos, prevenind efectele perverse ale stresului. Se asimileaza mai bine cand este asociat cu vitamina Bg (deci sa se consume cereale integrale sau 1-3 linguri/zi tarate de grau).
Ajuta in diabetul zaharat prevenind complicatiile vasculare, iar in combinatie cu zincul, cromul, seleniul, imbunatateste functia celulelor beta, ale tesutului pancreatic. in bolile organelor respiratorii, ajuta la dilatarea bronhiilor si la disparitia bronhospasmului. Magneziul influenteaza pozitiv aparatul de reproducere si inlatura simptomele negative din perioada menopauzei. La femeile gravide, magneziul previne insuficienta dezvoltare a fatului (impreuna cu acidul folie si pantotenic) sau pierderea sarcinii. Activeaza diferite enzime participand la metabolismul glucidelor, lipidelor, proteinelor, actioneaza asupra sistemului nervos (0,05-0,06 g/1000 ml – efect de deprimare; 0,1-0,2 g/ 1000 ml – efect de anestezie). Ajuta la utilizarea vitaminelor C, E, B. Pe cale digestiva, este purgativ. Favorizeaza eliminarea fierii din vezica biliara in intestin. Magneziul ajuta la fixarea Ca, in lupta contra cancerului, este necesar pentru oase si dinti.
Deficit: hiperiritabilitate neuromusculara, spasmofilie, tromboze, tulburari de ritm cardiac, mai ales la diabetici, convulsii, decalcificare prin pierderea secretiilor gastrice si intestinale (fistule, steatoree), in alcoolism, ciroza hepatica, hipofunctie paratiroidiana, tetanie mai grava decat la Ca, dureri de cap, ameteli, tremuraturi, furnicaturi sau amorteli ale membrelor, carcei, scaderea tensiunii arteriale, fragilitate a unghiilor, a parului si a dintilor, reactii alergice frecvente, senzatie de lipsa de aer, insomnie, scadere a rezis­tentei la infectii, agravare a reumatismului degenerativ, stari depresive sau isterice, teama, lipsa de apetit, oboseala, hipoglicemie, sindrom premenstrual. Consumul de carne multa si de alcool (chiar si in cantitati mici) poate duce la deficit de Mg.
Hipermagnezemia tulbura metabolismul Ca, producand scaderea excitabilitatii neuromusculare, pierderea reflexelor, somnolenta si chiar anestezie.

Cuprul (Cu) – (necesar 2 mg): nuci, (0,80 mg/100 g) alune (0,72 mg/100 g), piersici (0,50 mg), zmeura (0,21 mg), grau, sfecla, ceapa, spanac, afine (0,18 mg), mure (0,18 mg), capsune (0,17 mg), lamai (0,15 mg), portocale (0,15 mg), coacaze negre (0,14 mg), gutui (0,13 mg), cirese (0,10 mg), mere (0,10 mg), pere (0,10 mg), struguri, polen, morcov, patrunjel, pastarnac, telina, cartof, tomate, loboda, andive, cicoare, fasole, vinete, alune, castane, salata salbatica.
Cuprul este necesar in procesele de generare a energiei in celula. impreuna cu zincul intra in structura tesutului fermentului antioxidant si al unei proteine antioxidante a plasmei sangelui, care reprezinta un purtator al acestui metal. Cuprul poseda proprietati antiseptice (probabil pe baza actiunii antioxidante). Regleaza schimbul catecolaminelor, a serotoninei, a tirozinei, a melaninei, contribuie la cresterea activitatii insulinei si la o utilizare deplina a hidratilor de carbon. Participa la formarea structurii proteinelor din tesutul conjunctiv, colagen si elastina, acestea fiind componente structurale ale tesutului osos, cartilaginos, ale pielii, ale plamanilor, ale vaselor de sange.
Ajuta tiroida, e antiinfectios. Are rol in metabolismul glucidelor si in formarea clorofilei. Participa la formarea hemoglobinei si a globulelor rosii, inlesnind absorbtia Fe. Este constituent al unor metaloenzime si participa la sinteza fosfolipidelor. Influenteaza circulatia si transformarile fierului in organism. Este antiinflamator (in reumatisme inflamatorii, artroza). Cu vitamina C, este eficient la gripa.
Cuprul participa in transportul oxigenului alaturi de fier ca un constituent al unor proteine. Rolul cel mai important revine in hematopoieza, scade numarul celulelor rosii.
Deficit: formarea anevrismului aortei si al vaselor creierului, demineralizarea tesutului osos, anemie, lipsa poftei de mancare, intarzierea cresterii, acnee, osteoporoza etc.
Surse : viscere mai ales de vitel si oaie (inima, ficat, rinichi, splina) cereale, legume verzi, fructe uscate, nuci, struguri, moluste.

http://www.boli-medicina.com

Vitamina B afecteaza functiile renale ale diabeticilor

(Miercuri, 5 mai 2010)

Pacientii diagnosticati cu nefropatie diabetica, o afectiune renala cauzata de diabet, care au primit doze mari de vitamina B, au suferit o deteriorare rapida a functiilor renale, potrivit unui studiu publicat in Journal of the American Medical Association (JAMA). De asemenea, in randul diabeticilor a fost inregistrat si un procent mai mare de infarcte si atacuri cerebrale comparativ cu pacientii care au primit un placebo. Nefropatia diabetica afecteaza capilarele sangvine din interiorul rinichilor, care au un rol vital in filtrarea sangelui. In ciuda unor terapii eficiente in ceea ce priveste controlarea bolii, aproximativ 40% din circa 21 de milioane de americani suferind de diabet se imbolnavesc de nefropatie diabetica.

Mai multe studii au demonstrat o asociere neta intre concentratiile ridicate de homocisteina, un aminoacid sulfurat, si riscul de nefropatie diabetica, de retinopatie (leziuni ale retinei) si de maladii vasculare precum infarct miocardic si atacuri cerebrale.
Concentratii ridicate de vitamina B – vitamina B6, B12 si B9 – au fost asociate cu o reducere a concentratiei de homocisteina.

Medicii de la Institutul Robarts din Ontario au realizat un studiu pe 238 de pacienti, suferind de diabet 1 (infantil) si 2 (adult), pentru a determina daca un tratament cu vitamina B permite incetinirea evolutiei nefropatiei diabetice si daca impiedica producerea accidentelor vasculare. Acest test clinic a fost realizat in cinci centre medicale universitare din Canada, in perioada mai 2001 – iulie 2007. O parte dintre voluntari a primit un singur comprimat pe zi, continand 2,5 miligrame de vitamina B9, 25 de miligrame de vitamina B6 si 1 miligram de vitamina B12, iar al doilea grup a primit un placebo. Dupa o perioada de monitorizare medie de 31,9 luni, cercetatorii au constatat ca grupul tratat cu vitamina B prezenta o scadere a ratei de filtrare renala, functiile renale ale pacientilor din acest grup fiind mai putin eficiente comparativ cu cele ale pacientilor tratati cu placebo.

http://www.ziarulprahova.ro