Immunocal

Product Information

Glutathione is a tripeptide made intracellularly from its constituent amino acids L-glutamate, L-cysteine and glycine. The sulfhydryl (thiol) group (SH) of cysteine serves as a proton donor and is responsible for the biological activity of glutathione. Provision of this amino acid is the rate-limiting factor in glutathione synthesis by the cells since cysteine is relatively rare in foodstuffs and furthermore, if released as the free amino acid, is toxic and spontaneously catabolized in the gastrointestinal tract and blood plasma. Locigno R, Castronovo V. Reduced glutathione System: Role in cancer development, prevention and treatment. International Journal of Oncology 19:221-236, 2001 New born calves are particularly prone to antioxidant deficiency. Symptoms may appear at any time from just after birth up to several weeks. Antioxidant levels in the diet of the mother can often be low and variable. Studies of vitamin E levels in silage confirm this. Transfer across the placenta is typically poor and many calves are born with critically low levels. This compromises the immune system, may result in heart failure and frequently render the calf too weak to be viable.

If you need guidance on how to bottle feed crias, please see our Feeding Guide for Crias. What makes Immucol Platinum so good?

Dr Jim McCallum, “… when I first heard about Immunocal I wasn’t very interested. When I finally read the clinical studies about Immunocal and realised how this product worked on optimising the immune system response, I felt strongly that this product was going to have a major impact on the health profession…having seen such dramatic health results of those people on it.”

Patients undergoing immunosuppressive therapy should discuss the use of this product with their health professional. Adverse Reactions Finally I am pleased to report all the cria have gone on to thrive and enjoy life on the farm without having any further issues.At least, that was how it was until 15 years ago an Italian doctor and researcher discovered a way to take a protein from cows milk and turn it into a ‘cysteine delivery system’ that has now been clinically proven to boost glutathione levels in the body. Kennedy R, Konok G, Bounous G et al.. The use of a whey protein concentrate in the treatment of patients with metastatic carcinoma: A phase 1-II clinical study. Anticancer Res. 15:2643-50,1995

Watanabe A, Higachi K, Yasumura S. et al. Nutritional modulation of glutathione level and cellular immunity in chronic hepatitis B and C. Hepatology. 24:597A, 1996 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. We gave no Plasma transfusions to any of these crias, and we do not use cow or goat colostrum through fear of infections like TB. Whilst I know there is no substitute for the dam’s colostrum, Immucol came a good second and our success with the 3rd cria was solely down to our 16 years of experience, dedication with no sleep and Immucol. Immunocal preserves CGN viability and protects from apoptosis after exposure to SNP. (a) Representative images of CGNs left untreated (control), treated with SNP (100 μM), or preincubated with Immunocal for 24h before SNP treatment for further 24h. Immunofluorescence shows β-tubulin (green) and DAPI (blue). Scale bar, 10 μm. (b) Quantification of apoptosis for 5 independent experiments performed as in (a). Results are shown as mean±SEM, n = 5. (c) MTT cell viability was measured as described in Materials and Methods. Results are shown as mean±SEM, n = 3. For (b) and (c), ∗∗∗ indicates p< 0.001 compared to control, and ††† indicates p< 0.001 compared to SNP. Con: control; ICAL: Immunocal.

Our Address

They could also have implications for patients suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and “long Covid”. “These different syndromes are symptomatically very similar, so I think it could be very relevant to both of these conditions,” said Dr David Andersson from the Institute of Psychiatry, Psychology and Neuroscience at King’s College London, who led the new study.

THE MANAGEMENT OF TYPE 1 DIABETES IN ADULTS: A CONSENSUS REPORT BY THE AMERICAN DIABETES ASSOCIATION AND THE EUROPEAN ASSOCIATION FOR THE STUDY OF DIABETES Gastrointestinal bloating and cramps if not sufficiently rehydrated. Transient urticarial-like rash in rare individuals undergoing severe detoxification reaction. Rash abates when product intake stopped or reduced. Overdosage

IMMUNOCAL

Des Quinn, the chair of Fibromyalgia Action UK, said: “The prospect of fibromyalgia being an autoimmune condition has been debated many times and this will add to that discussion. If these results can be replicated and expanded upon, then the prospect of a new treatment for people with fibromyalgia would be extraordinary. However, the results need further confirmation and investigation before the outcomes can be applied universally.” It is well known that aging is accompanied by a precipitous fall in glutathione levels. Lower glutathione levels are implicated in many diseases associated with aging, including cataracts, Alzheimer’s disease, Parkinson’s, atherosclerosis and others” Journal of Clinical Epidemiology 47: 1021-26 1994 Both the 2016 and 2019 Japan Diabetes Society (JDS) clinical practice guidelines include diagnostic criteria for fulminant type 1 DM, unlike other guidelines [ 65]. Patients with fulminant type 1 diabetes frequently develop ketosis or ketoacidosis within 1 week of the onset of hyperglycemia, require insulin therapy immediately, and are characterized as having lower A1C values relative to their glucose values. Patients with fulminant type 1 diabetes are expected to have casual blood glucose values 288 mg/dL or higher and A1C values <8.7%, fasting C-peptide values <0.3 ng/mL, and post-glucagon load or 2-hour postprandial C-peptide values <0.5 ng/mL. Affected individuals are expected to test negative for islet autoantibodies [ 66]. 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. 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.