Supplements Diet for Amyotrophic Lateral Sclerosis
ALS Diet Pages
Maximize Liver Function; Safely Chelate Out Heavy Metals; Naturally Squelch Excess Nitric Oxide [+Antioxidants in General]; Support Mitochondrial Energy + Re-establish Beneficial Flora in Gut
"Vitamin B2 decreased the plasma elevated NO levels in accordance with a reduction in expression of inducible NO synthase..." Inhibitory mechanisms of highly purified vitamin B2 on the productions of proinflammatory cytokine and NO in endotoxin-induced shock in mice. Life Sci. 2005 Nov 26;78(2):134-9.
"...neuroprotective property of magnesium might be mediated in part through the inhibition of nitric oxide production shortly after oxygen-glucose deprivation." Neuroprotective effects of magnesium on metabolic disturbances in fetal hippocampal slices after oxygen-glucose deprivation: Mediation by nitric oxide system. Journal of the Society for Gynecologic Investigation. Vol. 9, Issue 2, March-April 2002, Pages 86-92.
"Wogonin (wogonin is a flavonoid derived from the root of the scutellaria baicalensis herb) inhibited inflammatory activation of cultured brain microglia in vitro and provided neuroprotection in microglia..." Flavonoid wogonin from medicinal herb is neuroprotective by inhibiting inflammatory activation of microglia. Heasuk Lee et al. The FASEB Journal Vol 17, October 2003 Pg. 1943-44.
"Phosphatidylserine and Phosphatidylcholine liposomes can inhibit the microglial production of both NO and O(2)(-), and thus presumably prevent a subsequent formation of ONOO(-). Therefore, PS/PC liposomes appear to have both neuroprotective and anti-oxidative properties through the inhibition of microglial activation." Phospholipids modulate superoxide and nitric oxide production by lipopolysaccharide and phorbol 12-myristate-13-acetate-activated microglia. Hashioka S et al., Neurochem Int. 2007 Feb;50(3):499-506. Epub 2006 Nov 28
"Phosphatidylcholine and Glyceryl-phosphorylcholine may help build nerve cell membranes, facilitate electrical transmission in the brain, hold membrane proteins in place, and produce the neurotransmitter acetylcholine" ~ Because Phosphatidylserine competes with glutamate, it may protect us from glutamate toxicity." Soy Lecithin: From Sludge to Profit Kaayla T. Daniel , PhD, CCN
"KBV (Bee Venom) has anti-inflammatory properties that inhibit iNOS" Effect of honey bee venom on microglial cells nitric oxide and tumor necrosis factor-alpha production stimulated by LPS.
Hans S et al. J Ethnopharmacol. 2006 Nov 15; [Epub ahead of print]
"...significant suppressive effects of ginsenosides on proinflammatory responses of microglia implicate their therapeutic potential in neurodegenerative diseases accompanied by microglial activation." Differential effects of ginsenosides on NO and TNF-alpha production by LPS-activated N9 microglia. Wu CF et al. Int Immunopharmacol. 2007 Mar;7(3):313-20. Epub 2006 Dec 1.
"...pro-glutathione agents (like alpha-lipoic acid LA) can spare cellular glutathione and protect cells from glutamate insult ." Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Kobayashi MS et al. Free Radic Res. 2000 Feb;32(2):115-24
"SAMe is required in numerous transmethylation reactions involving...phospholipids, and amines with other neurotransmitters. The synthesis of SAMe is intimately linked with folate and vitamin B12....deficiencies of both these vitamins have been found to reduce CNS SAMe concentrations. Both folate and vitamin B12 deficiency may cause similar neurological and psychiatric disturbances, including depression, dementia, myelopathy and peripheral neuropathy." Bottiglieri T, et al. The clinical potential of ademetionine (S-adenosylmethionine) in neurological disorders. Metabolic Disease Center, Baylor Research Institute, Dallas, TX.
Ultra-high doses of methyl-B12 may be of clinical use for patients with peripheral neuropathies. Ultra-high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy.Watanabe T. et al. J Neurol Sci 1994 Apr;122(2):140-3
In 1941 Ca-AEP [amino ethyl phosphoric acid ] was discovered by biochemist Erwin Chargaff as a vital component in the structure of cell membranes: A cell sealer and protector; electrolyte and nutrient carrier, to maintain a cell's electrical charge. Studied for 30 years, mostly in Germany, Ca-AEP therapy has shown promising benefits to sufferers of neurological diseases like multiple sclerosis and amyotrophic lateral sclerosis. In high doses Ca-AEP temporarily "coats" nerves and aids in the transmission of messages.
Evidence to date shows that creatine supplementation has a good safety profile and is well tolerated by ALS patients. Creatine also offer hope for the treatment of diseases characterized by weakness and muscle atrophy. Creatine offers potential benefits for diseases involving mitochondrial dysfunction. Recent data also support the hypothesis that creatine may have a neuroprotective effect. Ellis AC, Rosenfeld J. The role of creatine in the management of amyotrophic lateral sclerosis and other neurodegenerative disorders. CNS Drugs. 2004;18(14):967-80.
Glutamate induces cell death by upsetting the cellular redox homeostasis, termed oxidative glutamate toxicity... Our results suggest that curcumin has a neuroprotective effect against oxidative glutamate toxicity by inhibiting MAP kinase signaling and influencing cell-cycle regulation. Suh HW et al. Curcumin attenuates glutamate-induced HT22 cell death by suppressing MAP kinase signaling. Mol Cell Biochem 2006 Nov 25
"The results of the study show that there is an interaction between curcumin and both cadmium and lead, with the possible formation of a complex between the metal and this ligand. These results imply that curcumin could be used therapeutically to chelate these toxic metals, thus potentially reducing their neurotoxicity and tissue damage." Daniel S., et al. Through metal binding, curcumin protects against lead- and cadmium-induced lipid peroxidation in rat brain homogenates and against lead-induced tissue damage in rat brain. J Inorg Biochem 2004 Feb;98(2):266-75
Mutations to the copper, zinc superoxide dismutase (SOD) gene are responsible for 2-3% of amyotrophic lateral sclerosis (ALS) cases. These mutations result in the protein having a reduced affinity for zinc. Zinc amplifies mSOD1-mediated toxicity in a transgenic mouse model of amyotrophic lateral sclerosis, Supplementing zinc with even 18 mg/kg/day resulted in a more rapid death of some mice; adding copper helped reverse the "death by zinc". Ermilova IP et al. Protection by dietary zinc in ALS mutant G93A SOD transgenic mice. Neurosci Lett. 2005 Apr 29;379(1):42-6. Epub 2005 Jan 13
Consult with your personalized regenerative medicine practitioner to discern the best possible supplemental program for you. It can prove to be an expensive proposition ($500 or more per month) and so you want to get the most benefit from the right supplements. Your practitioner will likely know the best brands of supplements to take, as all are not created equal. In addition, your practitioner will likely have you on certain intravenous and other therapies that may require certain supplements to be added or unnecessary.
ALS Diet Pages
|| Amyotrophic Lateral Sclerosis
Please click the PDF icon to the left to read or download the entire 36 page Amyotrophic Lateral Sclerosis Diet by Dr. David Steenblock