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ESME - Dr M Pall's MCS theory confirmed.
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Daisymay
Senior Member
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- 754
More Evidence of the Organic Nature of Multiple Chemical Sensitivity
Margaret Williams 6th July 2010
Attention is drawn to a recent paper which serves to confirm that multiple chemical sensitivity (MCS), a well-documented component of myalgic encephalomyelitis (ME), is not a somatoform disorder or any other kind of psychiatric disorder as asserted by certain psychiatrists, most notably those of the Wessely School.
The paper (Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes; De Luca C et al: Toxicol. Appl. Pharmacol 2010; doi:10.1016/j.taap.2010.04.017) supports the work of Professor Emeritus of Biochemistry and Basic Medical Sciences at Washington State University, Martin Pall, who proposed that MCS is caused by toxic chemical exposure leading to toxic brain injury.
This recent work was conducted by a research group based in Rome and was supported by grants from the Italian Ministry for Health, the Italian Ministry for University and Research, the Swedish Medical Society and the Swedish Research Council.
The authors note that the number of subjects affected by MCS has been growing steadily (reaching up to 15% of the US population) and that patients report recurring multi-organ symptoms affecting the nervous, cardiovascular, gastrointestinal, respiratory, musculo-skeletal, skin and ocular systems and that, following the primary triggering event, such symptoms occur after subsequent exposure to virtually negligible concentrations of everyday odours such as perfume, new paint, household cleaning chemicals, newsprint, new carpets etc.
These researchers sought to prove their working hypothesis about the inherited and/or acquired dysfunction of the chemical defence system as a molecular basis for MCS, focusing on genetic and metabolic markers of the chemical defence and immune systems exerted through cytokine dysregulation.
GST (glutathione S-transferase) belongs to a family of conjugating enzymes that play a key role in cellular processes of inflammation and the authors note that the GST isozyme polymorphisms have been implicated in other environment-related pathologies such as systemic lupus erythematosus as well as in MCS. Both reduced and oxidised forms of glutathione were severely depleted in MCS subjects compared with healthy controls. In addition, the authors found highly elevated levels of pro-inflammatory IFNgamma, IL-8 and MCP-1 (macrophage chemotactic protein) in the plasma of MCS patients compared with healthy controls, as well as higher than normal levels of IL-10, PDGF (platelet derived growth factor) and VEGF (vascular endothelial growth factor).
The authors note that high levels of IFNgamma suggest the prevalence of activated Th1 lymphocytes, whereas up-regulated IL-10 may represent the persistent effort of regulatory T cells to counteract Th1 activation, noting that differentiation of T helper cells in the direction of Th1 and regulatory T cells is characteristic of an autoimmune response and that these findings in MCS patients provide a promising link between impairment of immune and chemical defensive systems in such patients.
Based on the results obtained, the authors suggest that the serious and multiple dysfunctions of the chemical defence system found in MCS patients may not depend on genetic defects but on non-genetic modifications of metabolising/antioxidant enzyme expression and/or activity. They conclude that MCS is characterised by a number of biochemical and immunological disturbances and that these metabolic and immunological parameters should be taken into consideration in both the biological and clinical/laboratory diagnosis of MCS.
Margaret Williams 6th July 2010
Attention is drawn to a recent paper which serves to confirm that multiple chemical sensitivity (MCS), a well-documented component of myalgic encephalomyelitis (ME), is not a somatoform disorder or any other kind of psychiatric disorder as asserted by certain psychiatrists, most notably those of the Wessely School.
The paper (Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes; De Luca C et al: Toxicol. Appl. Pharmacol 2010; doi:10.1016/j.taap.2010.04.017) supports the work of Professor Emeritus of Biochemistry and Basic Medical Sciences at Washington State University, Martin Pall, who proposed that MCS is caused by toxic chemical exposure leading to toxic brain injury.
This recent work was conducted by a research group based in Rome and was supported by grants from the Italian Ministry for Health, the Italian Ministry for University and Research, the Swedish Medical Society and the Swedish Research Council.
The authors note that the number of subjects affected by MCS has been growing steadily (reaching up to 15% of the US population) and that patients report recurring multi-organ symptoms affecting the nervous, cardiovascular, gastrointestinal, respiratory, musculo-skeletal, skin and ocular systems and that, following the primary triggering event, such symptoms occur after subsequent exposure to virtually negligible concentrations of everyday odours such as perfume, new paint, household cleaning chemicals, newsprint, new carpets etc.
These researchers sought to prove their working hypothesis about the inherited and/or acquired dysfunction of the chemical defence system as a molecular basis for MCS, focusing on genetic and metabolic markers of the chemical defence and immune systems exerted through cytokine dysregulation.
GST (glutathione S-transferase) belongs to a family of conjugating enzymes that play a key role in cellular processes of inflammation and the authors note that the GST isozyme polymorphisms have been implicated in other environment-related pathologies such as systemic lupus erythematosus as well as in MCS. Both reduced and oxidised forms of glutathione were severely depleted in MCS subjects compared with healthy controls. In addition, the authors found highly elevated levels of pro-inflammatory IFNgamma, IL-8 and MCP-1 (macrophage chemotactic protein) in the plasma of MCS patients compared with healthy controls, as well as higher than normal levels of IL-10, PDGF (platelet derived growth factor) and VEGF (vascular endothelial growth factor).
The authors note that high levels of IFNgamma suggest the prevalence of activated Th1 lymphocytes, whereas up-regulated IL-10 may represent the persistent effort of regulatory T cells to counteract Th1 activation, noting that differentiation of T helper cells in the direction of Th1 and regulatory T cells is characteristic of an autoimmune response and that these findings in MCS patients provide a promising link between impairment of immune and chemical defensive systems in such patients.
Based on the results obtained, the authors suggest that the serious and multiple dysfunctions of the chemical defence system found in MCS patients may not depend on genetic defects but on non-genetic modifications of metabolising/antioxidant enzyme expression and/or activity. They conclude that MCS is characterised by a number of biochemical and immunological disturbances and that these metabolic and immunological parameters should be taken into consideration in both the biological and clinical/laboratory diagnosis of MCS.
SOC
Senior Member
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- 7,849
My daughter and I have used Dr Pall's Protocol. My MCS-like symptoms, that is, most of the sensitivities that prevented me from leaving the house, cleared up. My brain fog was lessened also. I didn't see any improvement in fatigue, though.
When my daughter was mostly in remission, she had a couple of bad relapses that seemed to improve when she took the supplements suggested by Dr Pall. Since she went out of remission (likely a VZV booster reactivated HHV-6), she's never been able to get back into remission, even with the Pall Protocol, but her symptoms were less severe when she was taking it.
We also have some experience with Valcyte and the Pall Protocol, but anyone who wants to know about that will have to PM me, because I'm pretty sure my Valcyte-prescribing doc would not entirely approve of our experiments, so I'm not "going public" on that one.
I am not suggesting a direct cause-effect here because there is no where enough data to show that. There are other explanations for our experiences. In addition, what worked for us may not work for others. I'm just trying to share our experiences for whatever worth it might be to others.
When my daughter was mostly in remission, she had a couple of bad relapses that seemed to improve when she took the supplements suggested by Dr Pall. Since she went out of remission (likely a VZV booster reactivated HHV-6), she's never been able to get back into remission, even with the Pall Protocol, but her symptoms were less severe when she was taking it.
We also have some experience with Valcyte and the Pall Protocol, but anyone who wants to know about that will have to PM me, because I'm pretty sure my Valcyte-prescribing doc would not entirely approve of our experiments, so I'm not "going public" on that one.
I am not suggesting a direct cause-effect here because there is no where enough data to show that. There are other explanations for our experiences. In addition, what worked for us may not work for others. I'm just trying to share our experiences for whatever worth it might be to others.
caledonia
Senior Member
- Messages
- 4,610
I'm doing Rich Vank's methylation block protocol - the Folapro and some methylcobalamin. My MCS is greatly improved (at least 80%). I no longer have to take the neutralization drops prescribed by my environmental medicine doc. At one point, I was housebound and reacting to seemingly everything.
ixchelkali
Senior Member
- Messages
- 1,107
- Location
- Long Beach, CA
Still Relevant to XMRV Related Diseases
Dr Bell wrote about this in his book "Cellular Hypoxia and Neuro-Immune Fatigue" (available through the PR bookstore http://www.aboutmecfs.org/Store/Bookstore.aspx). In spite of the title it's quite readable and is basically a simplified explanation of Dr Martin Pall's book "Explaining 'Unexplained Illnesses': Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, and Gulf War Syndrome," also available through PR (http://www.aboutmecfs.org/Store/Bookstore.aspx). I consider it a major accomplishment to have waded through the technical parts of Dr Pall's book with brain fog.
Even with the discovery of XMRV, I think that this is a valuable model for the mechanisms of how our symptoms are produced. That is, the vicious cycle of cellular damage that leads to disease progression. It seems to me that this model works as an explanation regardless of whether the initial insult is from a retrovirus or from toxic exposure. Dr Pall's emphasis has been on MCS, but I think it can also explain why, or rather how, some people with XMRV get sick and others don't. It also explains the odd array of multi-organ, multi-system symptoms we suffer from, as well as the crushing fatigue. It's a great model for explaining the HOW and WHY of ME/CFS symptoms, regardless of etiology.
Many of the treatment protocols that various clinicians have developed to help their ME/CFS patients help to substantiate this paradigm, because they serve to interrupt the NO/ONO cycle and reduce oxidative stress.
I'm happy to learn that someone is finally doing the research to test Dr Pall's hypothesis en vivo. It's the sort of research I'd like to see the NIH doing, because it's the kind of "pure research" that isn't going to get sponsored by drug companies, and it has wide application for understanding disease mechanism in many diseases. For instance, I'd like to see it studied in relation to the post-chemo fatigue and neuropathy that plague many cancer patients.
Dr Bell wrote about this in his book "Cellular Hypoxia and Neuro-Immune Fatigue" (available through the PR bookstore http://www.aboutmecfs.org/Store/Bookstore.aspx). In spite of the title it's quite readable and is basically a simplified explanation of Dr Martin Pall's book "Explaining 'Unexplained Illnesses': Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, and Gulf War Syndrome," also available through PR (http://www.aboutmecfs.org/Store/Bookstore.aspx). I consider it a major accomplishment to have waded through the technical parts of Dr Pall's book with brain fog.
Even with the discovery of XMRV, I think that this is a valuable model for the mechanisms of how our symptoms are produced. That is, the vicious cycle of cellular damage that leads to disease progression. It seems to me that this model works as an explanation regardless of whether the initial insult is from a retrovirus or from toxic exposure. Dr Pall's emphasis has been on MCS, but I think it can also explain why, or rather how, some people with XMRV get sick and others don't. It also explains the odd array of multi-organ, multi-system symptoms we suffer from, as well as the crushing fatigue. It's a great model for explaining the HOW and WHY of ME/CFS symptoms, regardless of etiology.
Many of the treatment protocols that various clinicians have developed to help their ME/CFS patients help to substantiate this paradigm, because they serve to interrupt the NO/ONO cycle and reduce oxidative stress.
I'm happy to learn that someone is finally doing the research to test Dr Pall's hypothesis en vivo. It's the sort of research I'd like to see the NIH doing, because it's the kind of "pure research" that isn't going to get sponsored by drug companies, and it has wide application for understanding disease mechanism in many diseases. For instance, I'd like to see it studied in relation to the post-chemo fatigue and neuropathy that plague many cancer patients.
"The recent study conducted by the research group in Rome is significant in regard to the NO/ONOO- cycle theory because it shows that three elements of the cycle are elevated in MCS patients (De Luca et al, Toxicology and Applied Pharmacology, 2010, April 27 Epub ahead of print). Those elements are the inflammatory cytokines, nitric oxide, and oxidative stress. Each of these measurements provides important confirmation of the disease mechanism proposed by Pall. "
How are cytokines, nitric oxide and oxidative stress measured? I know Quest has a cytokine panel, but I didn't know that nitric oxide and oxidative stress could be measured.