Immunocal

Product Information

Given the prominent relationship between GSH depletion and neurodegeneration, it is not surprising that many studies have been undertaken to determine the neuroprotective effects of bolstering GSH levels through various treatment paradigms. Such treatments include administration of the GSH precursor, N-acetylcysteine (NAC), and GSH-monoethylester (GSH-MEE), a cell permeable form of GSH, and induction of the transcription factor, nuclear factor erythroid 2-related factor-2 (Nrf2), which is involved in transcriptional regulation of γ-glutamyl-cysteine ligase, the rate-limiting enzyme necessary for GSH synthesis [ 19]. Studies with NAC are extensive and indicate that NAC treatment offers a number of benefits across numerous disease models. For example, NAC demonstrated a significant protective capacity in a rotenone (complex I inhibition) rat model of Parkinson's disease by decreasing ROS generation, sustaining normal GSH levels, and ultimately preventing dopaminergic cell death [ 20]. In the G93A mutant SOD1 mouse model of familial ALS, NAC delayed the onset of disease-associated motor deficits and significantly extended survival, possibly due to its ability to elevate GSH levels in these animals [ 21]. Lastly, SAMP8 senescence-accelerated mice, which display many of the pathological features of Alzheimer's disease, demonstrated an increased cognitive performance with NAC treatment as compared to vehicle-treated controls [ 22]. Another study utilizing GSH-MEE in an MPTP rat model of Parkinson's disease demonstrated that GSH-MEE supplementation is capable of raising GSH levels in the brain when centrally delivered, and this increase in GSH corresponded to partial preservation of striatal dopamine levels [ 23]. Studies such as this have led to recent clinical trials testing the safety and tolerability of intranasal delivery of GSH to patients with PD [ 24]. Finally, Nrf2 induction or overexpression has shown similar promise in animal models of Parkinson's, ALS, and Alzheimer's disease. In the MPTP mouse model of Parkinson's disease, overexpression of Nrf2 in astrocytes attenuated the development of a Parkinsonian phenotype [ 25]. Likewise, astrocytic overexpression of Nrf2 in a mouse model of ALS both delayed onset and increased survival, as did treatment with chemical Nrf2 inducers [ 26, 27]. Comparatively, lentiviral Nrf2 overexpression caused significant improvements in observed learning deficits in a mouse model of Alzheimer's disease, accompanied by decreased amyloid plaque burden [ 28]. Cumulatively, these data indicate that treatments aimed at increasing GSH levels in the brain may be a viable option for treatment and prevention of neurodegenerative disease. Droge W, Holm E. Role of cysteine and glutathione in HIV infection and other diseases associated with muscle wasting and immunological dysfunction. FASEB J: 11(13):1077-1089, 1997

IMMUNOCAL is a U.S. patented natural food protein concentrate in the FDA category of GRAS (generally recognized as safe) which assists the body in maintaining optimal concentrations of glutathione (GSH) by supplying the precursors required for intracellular glutathione synthesis. It is clinically proven to raise glutathione values (Lands et al, 1999). To determine if the protective action of Immunocal observed in CGNs was reproducible in other neuronal cell types bearing relevance to neurodegenerative disease, we examined the capacity of this supplement to protect NSC34 motor neuron-like cells from oxidative stress and excitotoxicity. NSC34 cells are a hybrid cell line consisting of spinal cord motor neurons fused with mouse neuroblastoma cells [ 64]. We first analyzed the ability of Immunocal to protect NSC34 cells from H 2O 2-induced oxidative stress. Immunocal pretreatment of NSC34 cells dose-dependently attenuated H 2O 2-induced cell death. We next examined the potential of Immunocal to ameliorate damage induced by excitotoxic insult in NSC34 cells, which were differentiated by prolonged serum withdrawal to induce the expression of NMDA receptors [ 47]. Excitotoxicity is known to play a prevalent role in the pathogenesis of multiple neurodegenerative diseases, including ALS, and is intimately linked with both oxidative and nitrosative stress [ 65]. Immunocal pretreatment of differentiated NSC34 motor neuron-like cells significantly reduced the injurious effects of glutamate excitotoxicity in a dose-dependent manner. A broad Spectrum of Vitamins and Minerals are supplied at the correct levels to help support strong development and growth. Bounous G. Immunoenhancing properties of undenatured milk serum protein isolate in HIV patients. Int. Diary Fed: Whey: 293-305, 1998 The human body and its individual cells are protected from the ravages of oxidation by ‘antioxidants’. While many are aware of vitamins A, C and E being anti-oxidants, the most important is a substance called glutathione.

Immune system modulators, which enhance the body’s immune response against cancer. Some of these agents affect specific parts of the immune system, whereas others affect the immune system in a more general way. Immunocal protects NSC34 cells from H 2O 2 and glutamate/glycine-induced excitotoxicity. (a) Cell survival was quantified with MTT cell viability assay for 5 independent experiments in undifferentiated NSC34 left untreated (control), treated with H 2O 2 (250 μM), or preincubated with Immunocal for 24h before H 2O 2 treatment for further 24h. Results are shown as mean±SEM, n = 5. ∗∗ indicates p< 0.01 compared to control, † indicates p< 0.05 compared to H 2O 2, and †† indicates p< 0.01 compared to H 2O 2. (b) Representative images showing morphological differences between undifferentiated (wildtype (WT)) and differentiated (DIFF) NSC34 cells, β-tubulin (green), and DAPI (blue). Scale bar, 10 μm. (c) Cell survival was quantified for 5 independent experiments with an MTT cell viability assay in differentiated NSC34 cells left untreated (control), treated with glutamate/glycine (1mM/100 μM), or preincubated with Immunocal for 24h before glutamate/glycine treatment for further 24h. ∗ indicates p< 0.05 compared to control, and † indicates p< 0.05 compared to glutamate/glycine. Con: control; ICAL: Immunocal; GG: glutamate/glycine. Agrimin Bimeda Boehringer Ingelheim CEVA Chanelle Elanco MSD Nettex Norbrook Zoetis All Manufacturers Current treatment tends to focus on gentle aerobic exercise, as well as drug and psychological therapies designed to manage pain. However, these have proven ineffective in most patients and have left behind an enormous unmet clinical need, said Andersson. “The widespread paradigm at the moment is that this is a disease that emanates from the brain, and I think our findings suggest that that’s not the case,” he said.

Brain cancer. There are two approved types of targeted antibodies for brain and nervous system cancers. Researchers are testing several others in clinical trials to find out if immunotherapy might work where other treatments have failed. This article is in PubMed so appears legitimate, but I see the original study was published in PLOS which has been associsted with many dubious 'scientific' reports in the past. The cast of authors is many and varied, except that most of them appear to be administrators, and it is not clear who actually did the study or what institution was running it. It seems to be Baylor University Childrens Dept, and is mainly centered in Jamaica, Funding is declared and valid This one seems to be better controlled than the other but is looking at the problem from the other way round (i.e. does better diabetic control raise GSH levels? Study found that short term closed loop control with IV insulin did not raise the GSH levels.

Dr Wulf Droge, “many studies of my laboratory at the German Cancer Research Centre support the conclusion that Immunocal is effective in maintaining a strong immune system…” IMMUNOCAL is a natural food supplement and as such is limited from stating medical claims per se. Statements have not been evaluated by the FDA. As such, this product is thus not intended to diagnose, cure, prevent or treat any disease. Vitamins A, D3, E, B1, B2, B6 and B12, Vitamin K3, Vitamin C, Niacin, Folic acid, Biotin, Calcium, Sodium, Phosphorus, Potassium, Sulphur, Selenium, Cobalt, Iodine, Manganese, Zinc and Iron The disulphide bond in cystine is pepsin and trypsin resistant but may be split by heat, low pH or mechanical stress releasing free cysteine. When subject to heat or shearing forces (inherent in most extraction processes), the fragile disulfide bonds within the peptides are broken and the bioavailablility of cysteine is greatly diminished. Please note there is a small excess for despatch to Highlands and Islands and Isle of Wightas governed by your postcode.

Immucol is awater soluble, fortified colostrum powder helping to get calves off to the best start in life. Bounous G, Kongshavn P. Influence of protein type in nutritionally adequate diets on the development of immunity. In Absorption and Utilization of Amino Acids Vol.II. Ed. M. Friedman. CRC Press, Inc., Fla. 2:219-32, 1989 Multiple myeloma. Several monoclonal antibodies are used to treat this blood cancer. Doctors may use them after a stem cell transplant to help keep cancer at bay. Andersson and his colleagues harvested blood from 44 people with fibromyalgia and injected purified antibodies from each of them into different mice. The mice rapidly became more sensitive to pressure and cold, and displayed reduced grip strength in their paws. Animals injected with antibodies from healthy people were unaffected. Another factor implicated in the pathogenesis of several neurodegenerative diseases is copper toxicity. GSH is known to play a significant role in mitigating copper toxicity by facilitating the transport of copper to proteins that can safely store this toxic metal in the intracellular environment [ 53]. Depletion of GSH disrupts this important process and sensitizes neuronal cells to copper toxicity through copper-associated ROS generation, even when exposed to only trace amounts of copper [ 17, 54, 55]. Thus, copper toxicity may be a process that is dependent on GSH depletion, and indeed, increased concentrations of copper and dysregulation of copper homeostasis are observed in several neurodegenerative diseases in which GSH status is reduced, including Alzheimer's disease and models of ALS [ 54, 56]. In our study, elevation of GSH levels in cultured primary neurons with Immunocal proved to be an effective way to ameliorate the toxic effects of copper treatment by attenuating copper-induced lipid peroxidation, resulting in reduced cell death.A critical requirement of the newborn calf. High levels of oils and fats replenish the calves' own reserves to aid absorption of nutrients in the gut while aiding survival, particularly during the colder periods of the year.