Doctors View Points & Testimonials # 137:
Dr. Cheney
This is from an interview with Dr. Cheney, who first coined the phrase "Chronic Fatigue Syndrome." He found that the organism mentioned here for MS was wiped out in the people he was treating for Fibromyalgia - Chronic Fatigue Syndrome, in 6 months of taking HMS 90, even those who were taking only one pack a day. The ones taking 2 packs did do better with their other symptoms.
Here's to unravelling the puzzle of MS.
From a radio interview with Dr. Cheney:
"This is exciting stuff. We wanted to see not only if this product (Immunocal/ HMS 90) improved glutathione functionality, which it did, but we also wanted to see if it knocked out micro-organisms, like the PNS article said it would.
So we measured for IgM (visa?) the inverse dilutions of IgM for chlamydia pneumoniae. Chlamydia pneumoniae is an intracellular pathogen. It's a common cause of hospital-acquired pneumonia. It ubiquitously infects the population, but seems to activate under certain conditions. And if it activates, some of the clinical conditions of this organism are chronic sinusitis, pharyngitis, and laryngitis.
But it also gets into the central nervous system. In a study published by a neurologist out of Vanderbilt showed that chlyamdia pneumoniae may be a very important pathogen in multiple sclerosis.
Indeed, data they shared with me recently (and this is coming to publication soon) showed that 80 percent of the cerebral spinal fluid of MS patients is actively infected with this organism. Versus 15 percent of other neurological diseases that are not MS.
In a journal-published article on neurology, aggressive treatment for chlyamdia pneumoniae rapidly reversed an acute exacerbation of multiple sclerosis. So we measured IgM levels for this pathogen at Vanderbilt.
Most laboratory measurements of this organism are not very good, so this is a research grade assessment, and probably may not generalize to the run-of-the-mill types of tests that you might get in your local labs.
But IgM elevations of 1 to 1600 (?) dilutions is evident of significant active infection with this organism. Six months later, it just wiped it out. IgM just fell to normal levels. It didn't really matter whether you were taking one pack a day or two packs a day. Just wiped it out. Makes you wonder what this might do for MS. Think about that.”
Doctors View Points & Testimonials #: 138
J Neurosci Res. 2002 Nov 15;70(4):580-7
Nitric oxide synthase is present in the cerebrospinal fluid of patients with active multiple sclerosis and is associated with increases in cerebrospinal fluid protein nitrotyrosine and S-nitrosothiols and with changes in glutathione levels. Calabrese V, Scapagnini G, Ravagna A, Bella R, Foresti R, Bates TE, Giuffrida Stella AM, Pennisi G.
Biochemistry and Molecular Biology Section, Department of Chemistry, Faculty of Medicine, University of Catania, Catania, Italy.
Nitric oxide (NO) is hypothesized to play a role in the immunopathogenesis of multiple sclerosis (MS). Increased levels of NO metabolites have been found in patients with MS. Peroxynitrite, generated by the reaction of NO with superoxide at sites of inflammation, is a strong oxidant capable of damaging tissues and cells.
Inducible NO synthase (iNOS) is up-regulated in the CNS of animals with experimental allergic encephalomyelitis (EAE) and in patients with MS. In this study, Western blots of cerebrospinal fluid (CSF) from patients with MS demonstrated the presence of iNOS, which was absent in CSF from control subjects. There was also NOS activity present in both MS and control CSF.
Total NOS activity was increased (by 24%) in the CSF from MS patients compared with matched controls. The addition of 0.1 mM ITU (a specific iNOS inhibitor) to the samples did not change the activity of the control samples but decreased the NOS activity in the MS samples to almost control levels.
The addition of 1 mM L-NMMA (a nonisoform specific NOS inhibitor), completely inhibited NOS activity in CSF from control and MS subjects. Nitrotyrosine immunostaining of CSF proteins was detectable in controls but was greatly increased in MS samples. There were also significant increases in CSF nitrate + nitrite and oxidant-enhanced luminescence in MS samples compared with controls.
Additionally, a significant decrease in reduced glutathione and significant increases in oxidized glutathione and S-nitrosothiols were found in MS samples compared with controls. Parallel changes in NO metabolites were observed in the plasma of MS patients, compared with controls, and accompanied a significant increase of reduced glutathione.
These data strongly support a role for nitrosative stress in the pathogenesis of MS and indicate that therapeutic strategies focussed on decreasing production of NO by iNOS and/or scavenging peroxynitrite may be useful in alleviating the neurological impairments that occur during MS relapse. Copyright 2002 Wiley-Liss, Inc. Publication Types: C
• Clinical Trial
• Controlled Clinical Trial
PMID: 12404512 [PubMed - indexed for MEDLINE]
Doctors View Points & Testimonials # 139:
Neurodegenerative Diseases – Alzheimer’s and Parkinson’s
By Patricia
Alzheimer’s and Parkinson’s are neurodegenerative diseases in which cell damage and degeneration is seen in certain specific areas of the brain.
In Parkinson’s disease nerve cells slowly degenerate in the part of the mid-brain (the substantia nigra layer of the basal ganglia) that controls movement, resulting in progressive loss of muscular coordination and balance.
In Alzheimer’s disease brain cells degenerate, brain mass shrinks and characteristic neurofibrillary tangles and neural plaques are seen post mortem.
Increasing lines of evidence suggest that mitochondrial damage plays a key role in Parkinson’s, Alzheimer’s and some other neurodegenerative diseases (1-5). This, in turn, increases the generation of reactive oxygen species and the onset of oxidative stress, leading to oxidative damage and programmed cell death.
At the same time, glutathione homeostasis is disturbed (6-9). In one study, glutathione levels were reduced by 40% in the substantia nigra in early stage Parkinson’s disease (7). These levels fall even much further in later stages, the magnitude of reduction in glutathione seeming to parallel the severity of the disease (9). The lowered glutathione values and increased oxidative stress are thought to be responsible for the loss of dopamine producing cells in the substantia nigra in Parkinson’s disease patients (7, 8).
The use of antioxidants, particularly glutathione, for the treatment of neurodegenerative diseases is an obvious consideration (6-9). In an in vitro study, glutathione was shown to protect human neural cells from apoptosis i.e. cell death, induced by dopamine (8). Sechi et al. showed that intravenous injection of glutathione was effective in reducing symptoms (42% decline in disability) in early Parkinson’s disease patients and possibly retarded the progression of the disease (9).
Other treatment options to increase brain concentrations of glutathione are better choices for long-term treatment. Banaclocha has reviewed the putative usefulness of N-acetyl cysteine for this purpose in the treatment of Parkinson’s, Alzheimer’s and other age-associated neurodegenerative diseases
(1). Immunocal is an even better choice than this drug, being entirely non-toxic and proven to raise intracellular glutathione (10).
References.
1. Banaclocha, MM. Therapeutic potential of N-acetylcysteine in age-related mitochondrial
neurodegenerative diseases. Med Hypotheses 56:472-477, 2001.
2. Schultz JB, Lindenau J, Seyfried J et al. Glutathione, oxidative stress and neurodegeneration. Eur J
Biochem 267:4904-4911, 2000.
3. Jenner P, Olanow CW Neurology 47:S1161-S170, 1996.
4. Kidd PM. Parkinson’s disease as a multifactorial oxidative neurodegeneration: implications for
integrative management. Altern Med Rev 5:501, 2000.
5. Lohr JB, Browning JA Free radical involvement in neuropsychiatric illnesses. Psychopharmacol Bull
31:159-165, 1995.
6. Reid M, Jahoor F. Glutathione in disease. Curr Opin Clin Nutr Metab Care 4:65-71, 2001.
7. Sian J, Dexter DT, Lees AJ, et al. Alterations in glutathione levels in Parkinson’s disease and other
neurodegenerative disorders affecting basal ganglia. Ann Neurol 348-355, 1994.
8. Gabby M, Tauber M.Porat S et al. Selective role of glutathione in protecting human neuronal cells from
dopamine-induced apoptosis. Neuropharmacology 35:571-578, 1996.
9. Sechi G, Deledda MG, Bua G et al. Reduced intravenous glutathione in the treatment of early
Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry 20: 1159-1170, 1996.
10. Lands L, Grey VL, and Smountas AA Effect of supplementation with a cysteine donor on muscular
performance. J Appl Physiol 87:1381-1385, 1999
Doctors View Points &
Professor Dr. Wulf Droge, Immunologist and former head of Cancer Research at the Heidelberg Cancer Institute, Heidelberg, Germany.
Professor Wulf Droge is now Medical Director of Immunotec Research in charge of research with Immunocal.
The human immune system is extremely dependent on adequate glutathione levels to perform properly, in the words of Wulf Droge et. al. : "Thiols And The Immune System: Effect of N-Acetyl cysteine on T Cell System in Human Subjects"; Methods in Enzymology, Vol. 251; 255-270,1995):
"Even a partial depletion of the intracellular glutathione pool has a dramatic consequence for the process of blast transformation and proliferation, and for the generation of cytotoxic T cells." ( T –cells are those cells which help the body defend against diseases.)
Abstract: - Cysteine and glutathione in catabolic conditions and immunological dysfunction. Current Opinion in Clinical Nutrition & Metabolic Care. 2(3):227-233, May 1999. Droge, Wulf
The conspicuous increase in the plasma cysteine disulphide/thiol ratio in elderly persons and cancer patients indicates a shift of the plasma redox state.
The most important redox buffers in skeletal muscle tissue and blood plasma, i.e. glutathione and albumin, respectively, are significantly decreased in different models of cachexia.
Treatment with N-acetyl cysteine, i.e. a thiol-containing antioxidant, was found to increase the plasma albumin level and to ameliorate the loss of body cell mass in cancer patients and healthy individuals.
The treatment of HIV infection with N-acetyl cysteine, in contrast, serves mainly as a tool to ameliorate the physiological and immunological consequences of the virus-induced cysteine deficiency.
NOTE: Immunocal, a natural cysteine delivery system, developed and researched at McGill University Medical Research Center (often referred to by Doctorsin the USA as “The Harvard of the North” in Montreal, Canada, was found to increase glutathione and the plasma albumin levels in vitro, in animal and human studies.
Dr. Wulf Droge is now Medical Director of Immunotec Research’s Medical Advisory Board, in charge of research with Immunocal. Here is a list of his ACADEMIC CREDENTIALS:
1958 – 1964 Studied chemistry and biochemistry at the Universities of Hanover and Freiburg, Germany Masters degree in chemistry
1964 - 1967 PH.D. thesis at the Max-Planck-Institute of Immunology, Freiburg (topic of thesis, Bacterial Lipopolysaccharides)
1967 PH.D. in biochemistry, University of Freiburg postdoctoral DFG fellowship at the Max-Planck- Institute of Immunology, Freiburg
1968 Visiting fellow at the University of Minnesota, Minneapolis
1968-1971 Postdoctoral research fellow at Harvard University,Biological Laboratories, Cambridge, Mass. with professor Strominger
1971-72 Fellow at the Max-Planck-Institute in Munchan, Germany
1973-76 Scientific member at the Basel Institute for Immunology
1974 Habilitation at University of Freiburg
Since 1976 Professor, faculty of Biology at the University of Heidelburg and head of the Department of Immunochemistry
RESEARCH AREAS:
Redox regulation and signaling pathways in lymphocytes
Pathogenesis of HIV infection
Mechanism of disease related wasting and aging
Action of tumor necrosis factor
1977-1980- and 1983-1986- Acting Director of the Institute of Immunology and Genetics, Heidelburg, Germany
MEMBERSHIPS:
European Association for Cancer Research
American Association of Immunologists
British Society of Immunology
Gesellschaft fur Immunologie
Doctors View Points & Testimonials #: 136
GLUTATHIONE (GSH) DEFICIENCY AND THE PATHOGENESIS OF
MULTIPLE SCLEROSIS
Recent findings in tissue from multiple sclerosis victims corroborate the mechanisms documented in a growing body of research based evidence as to the steps leading to disease expression.
“Observed depletion of GSH, elevation of ceramide level and apoptosis in banked human brains from patients with neuroinflammatory diseases (e.g. x-adrenoleukodystrophy and multiple sclerosis) suggest that the intracellular level of GSH may play a crucial role in the regulation of cytokine-induced generation of ceramide leading to apoptosis of brain cells in these diseases.”
1 Cytokine, tumor necrosis factor-alpha (TNF-˜) or interleukin-1 beta (IL-1˜)-mediated activation of sphingomyelinases (SMases), leads to degradation of sphingomyelin to ceramide, a sphingolipid 1,2, and the universal lipid second messenger.
This potentiated a 2-fold increase in H2O2 generation, leading to lipid peroxidation and loss of activity of respiratory chain complex IV in the GSH depleted state compared to GSH-replete mitochondria 3.
“Mitochondria are a target of ceramide produced in the signaling of TNF.3”
Pretreatment of cells so as to increase intracellular GSH inhibited the TNF-˜-induced sphingomyelin hydrolysis and ceramide generation as well as cell death 4.
The literature implicates excessive or inappropriate generation of nitric oxide (NO) in Parkinson’s Disease, Alzheimer’s Disease, multiple sclerosis, stroke and amyotrophic lateral sclerosis 5.
“Human astrocytes released abundant NO upon stimulation with the pro-inflammatory cytokine (IL)-1˜, which was potentiated by interferon (IFN)-gamma and TNF-˜. IL-1 receptor antagonist protein markedly attenuated astrocyte NO production.6” “
It is now well documented that NO and its toxic metabolite, peroxynitrite (ONOO-–) can inhibit components of the mitochondrial respiratory chain...5
“...neurones, in contrast to astrocytes, appear particularly vulnerable to the action of these molecules.5” “...the susceptibility of different brain cells to NO and ONOO– exposure may be dependent on factors such as the intracellular GSH concentration...5”
“Evidence is now available to support this scenario for neurological disorders, such as multiple sclerosis.5”
Variable vulnerability to oxidative stress has been well documented in various neurological cell types. “Astrocytes maintain high intracellular concentrations of certain antioxidants, making these cells resistant to oxidative stress relative to oligodendrocytes and neurons.7”
In fact, astrocytes appear to play a central role in the antioxidant defense of the brain.7 One of the major antioxidants used by astrocytes is GSH and, “...astroglial cells prefer cystine from [instead of] cysteine for GSH synthesis...8”
Other conditions give insight into the effect of GSH on SMases and ceramide. “Cell culture studies of hypoxic PC12 cell death...suggest that GSH protects cells from hypoxic injury by direct inhibition of neutral SMases activity and ceramide formation...9”
This protection appears to be lost in MS patients as GSH is decreased in plaques10, and was absent in the CSF in MS.11 Protective mechanisms involving GSH appear to occur in MS, “...blood GSH was increased (p<0.01) [in MS] during exacerbation and remission as well. This rise in this thiol is likely to be a compensatory mechanism defending the cells from further oxidant injuries.12”
The relationship between cytokines and GSH has been demonstrated in cell cultures of TNF-resistant (TNFr) and TNF-sensative (TNFs) cell lines.
“The basic level of GSH was significantly higher in the TNFr cells than in TNFs cells. Treatment with 20 microM ceramide decreased cellular GSH in TNFs cells by 50% in contrast to an insignificant decrease in the TNFr cells.13”
Also, the effect of intracellular GSH on neutrophil and lymphoid apoptosis give further insight into the crucial regulator role played by this important thiol.
“Because apoptosis is a critical mechanism regulating PMN survival in vivo, manipulation of PMN intracellular thiols may represent a novel therapeutic target for the regulation of cellular function.14 Thiol compounds, such as L-cysteine and GSH, play crucial roles in the regulation of lymphocyte proliferation.15”
These data suggest that the inability to neutralize oxidative stress results in the apoptosis of lymphoid cells under L-cystine-and GSH-depleted conditions. The protective effects of rADF may be explained by...enhancing the L-cystine internalization and elevating the intracellular GSH content.15
Doctors View Points & Testimonials # 140:
I am an Oral and Maxillo Facial Surgeon and when I first heard about Immunocal I wasn't very interested.
When I finally read the clinical studies about Immunocal and realized how this product worked on optimizing the immune system response, I felt strongly that this product was going to have a major impact on the health profession and I wanted to be a part of it.
I feel more convinced today about the impact of Immunocal on the health of people after having seen such dramatic health results of those people on it."
Dr. Jim McCallum
Doctors View Points & Testimonials # 141
"Almost everyone I put on Immunocal tells me that they feel better as soon as they start taking the product. This is explained by the fact that Immunocal brings to all the cells in our body, the building blocks necessary to produce glutathione, a small protein that each cell needs to function properly.
In severe asthmatics taking Immunocal, the attacks become less frequent and less severe. The need for medication is decreased, they sleep better, they don't miss work or school as often, resulting in a better quality of life."
Dr. Jean Marcoux, Board Certified Allergist, Immunologist
Doctors View Points & Testimonials # 142:
"Immunocal is the future of the wellness movement - nothing else I know can impact the ability of every cell in the human body to defend itself from the common pathological mechanisms.
To raise glutathione levels is to reduce premature oxidation, to quench destructive free radicals and help detoxify the poisons inside each cell when it needs to. Only Immunocal is clinically proven to do that in a safe, effective and convenient way.
Doctors View Points & Testimonials #: 143
"Current research is uncovering the fact that the underlying culprit in most disease and aging processes is free radical damage and oxidative stress.
Therefore, the most reasonable way to combat these degenerative changes is to find a safe and effective way to raise anti-oxidant levels.
I have concluded that glutathione is the crucial anti-oxidant. I believe that Immunocal is the safe, effective, and natural way to raise glutathione levels.
Taking Immunocal everyday should be a vital component to anybody's proactive health plan."
Dr. Tom Iwama
Doctors View Points & Testimonials # 144:
" Immunocal works and it's safe. I believe it is the safest and most effective antioxidant available. Also, Immunocal is the best way that I know to support and maintain the immune system.
This is especially important at a time when medicine is beginning to recognize how many diseases are caused by a deficiency of the immune system. But that's not the whole story - just as important, are the people behind the product.
Everyone at Home Office is of the highest integrity. As a doctor, I appreciate the power and efficacy of Immunocal. As a person, I enjoy being associated with dedicated and delightful people."
Dr. Tom Kwyer