This Is MS Multiple Sclerosis Knowledge & Support Community

Well we have a poorer immune system anyway don't we? Regardless of drugs.

I've never had any DMD but was diagnosed with melanoma...

You can give B17 whatever name you want but the main thing to understand is once the doctor sends you home to die there is still hope. I choose to eat 6 apricot seeds a day as a precaution. I have been doing this for over a year and haven't been killed but have extremely good health. My mother and sister stop listening to the doctor when he wanted to cut on them and started eating apricot seeds along with a vegan diet and are still healthy. People all over the world eat apricot seeds and have excellent heath. Why is the FDA telling us this is bad for us when evidence shows it is good for us?

As to whether the copaxone is a immune suppressor the article I posted says it is. I am sure you can find articles to say what you want but it is my understanding that all of the MS drugs work by suppressing the immune system so the immune system will not attach itself. That is why you have fewer symptoms when you take the drugs. The question each of us must ask is the temporary relief worth what we might be doing to our immune system. There are people who have very serious side effects to taking copaxone and one person tell us it destroyed his liver. These people are telling us about the side effects of copaxone. Do you think they are lying to us? These side effects are the bodies way of telling you it does not like what you are doing to it. This does not happen over night. Once you get to a certain point where you have destroyed you immune system it is too late. The study done by the NHS in England show people doing the drugs did worse than those who didn't do the drugs. These doctors who are giving you drug are a leading cause of death in our country and most of it is due to the drugs the prescribe. There is no magic pill out there but you can have good health if you get the information and apply it.



http://www.askapatient.com/viewrating.a ... e=COPAXONE

The fact that you have MS does not mean you have poorer immune system. Your immune system is doing exactly what it is suppose to do. When you get toxins in the cells of your body the immune system will attack the cells. The key to healing is keeping the toxins out of the body and eating the vitamins and minerals the body needs to repair itself. Each of us must identify the toxins and stop putting them in our bodies. According to Dr. Lorraine Day the melanoma comes from not getting enough vitamins and minerals from the food we eat.

I guess that some guys (like want2bike) need to be more consistent.
You say not to put poisons into your body, but then say you eat apricot seeds.
Apricots seeds contain arsenic, and that is a poison for sure.
You plug the Roger McDougall story, which has been linked to a firm making supplements.
You quote a URL in the dentistry thread, which links straight to Mercola. OK, so we all know that Hank Mercola sells supplements, but the big unknown is where he gets them from. He sure does not make them. So where is the quality control, and what goes into the body with a Mercola supplement.
Try to get all your ducks in a row.

You do not seem to believe the information I have posted. Would you care to explain why Doctors are a leading cause of death in my country? Seems like going to the doctor would increase your chance of dying. Is JAMA telling us a lie? Am I missing something here? I will continue to support my immune system with healthy things and let others do the drugs. Yes I will continue to take the 6 apricot seeds until the government takes it away. It is important to know there is another way once the drugs stop working. Hopefully it will not be too late.



http://www.healingdaily.com/Doctors-Are ... the-US.htm

I previously posted some information on why patients with MS would have an increased risk of developing certain types of cancer, such as breast cancer and lymphoma, on this thread. http://www.thisisms.com/forum/general-d ... 22806.html

One reason would be due to the elevated levels of homocysteine found in patients with MS (studies posted on above mentioned thread). Homocysteine is linked to breast cancer because it directly damages DNA and also because it interferes with nitric oxide, which regulates vascular endothelial growth factor. In the following study the researchers stated that plasma homocysteine (Hcy) is a well known independent risk factor for coronary heart disease, and is also a risk factor for cancer. In addition, the researchers found that homocysteine increased in parallel with the growth of tumor cells. The study concluded, “Conceivably, Hcy may be used as a more accurate tumor marker for monitoring cancer patients during treatment, and hyperhomocysteinemia as a risk factor for carcinogenesis.”




Hyperhomocysteinemia is a risk factor for cancer and a new potential tumor marker.
Wu, L.L., J.T. Wu. 2002. Clin Chim Acta 322(1-2):21-8.

“Plasma homocysteine (Hcy), a well-known independent risk factor for coronary heart disease, is also a risk factor for cancer. Results from our studies indicate that Hcy could be used as a tumor marker. We found elevated circulating total homocysteine (tHcy) in cancer patients even though they were not treated with anti-folate drugs. In serial specimens from cancer patients undergoing treatment, the change of tHcy coincided with the concentration of tumor markers. The rapid proliferation of tumor cells contributed to the much higher concentrations of circulating tHcy. Both concentrations of tHcy and tumor marker would increase in parallel during the growth of tumor cell, but only the Hcy concentration would decline in response to tumor cell death…Conceivably, tHcy may be used as a more accurate tumor marker for monitoring cancer patients during treatment, and hyperhomocysteinemia as a risk factor for carcinogenesis."


There would be numerous other reasons as well. For instance, the elevated levels of "prolactin" found in MS patients (studies posted on above mentioned thread). Research has shown that more than 95 percent of breast cancers express the receptor for prolactin (Reynolds, 1997). In the following study the researchers stated
that prolactin can promote cell proliferation and survival, increase cell motility, and support tumor vascularization. In addition, the researchers stated that a recent study of 235 cases reported a “significant positive association” between prolactin levels and breast cancer risk.

Prolactin and breast cancer risk.
Tworoger, S.S., S.E. Hankinson. 2006. Cancer Lett. 243(2):160-9. Epub 2006 Mar 10.

“Prolactin, a hormone involved in normal breast development and lactation, has been hypothesized to be important in the etiology of breast cancer… Experimental evidence indicates that prolactin can promote cell proliferation and survival, increase cell motility, and support tumor vascularization. Animal data suggest that prolactin can increase tumor growth rates and the number of metastases, as well as induce both estrogen receptor +(ER) and ER--tumors in a transgenic mouse model in which ER+ tumors are very rare. Epidemiologic data for premenopausal women are sparse; however a recent study with 235 cases reported a significant positive association between plasma prolactin levels and breast cancer risk. Studies in postmenopausal women have reported a positive association as well, and in the largest study (n=851 cases) the association was strongest for ER+ tumors. Overall, the available data support the hypothesis that prolactin increases risk of breast cancer…"

Following is some information from my book that is a little more specific for breast cancer and homocysteine.

The following study on homocysteine and metastatic breast cancer found that women with metastatic disease had significantly higher homocysteine concentrations.

Raised plasma homocysteine levels in women with metastatic breast cancer.
Makris, A., H. Cladd, R.J. Burcombe, J.M. Smith, M. Makris. 2001. Proc Am Soc Clin Oncol. 20: Abstract 179.

“…Women with metastatic disease had significantly higher plasma homocysteine concentrations compared to controls…We conclude that hyperhomocysteinaemia is common in women with metastatic breast cancer…”


In our next study the researchers found that elevated homocysteine (Hcy) levels were significantly linked to an increased risk of breast cancer and that the increased cancer risk was observed in both premenopausal and post-menopausal women. In addition, the researchers felt the link was so strong that homocysteine could be considered a metabolic risk factor for breast cancer.


Plasma homocysteine as a metabolic risk factor for breast cancer: findings from a case-control study in Taiwan.
Chou, Y.C., M.S. Lee, M.H. Wu, H.L. Shih, T. Yang, C.P. Yu, J.C. Yu, C.A. Sun. 2007. Breast Cancer Res Tr. 101(2):199-205.

“…Elevated plasma Hcy levels were significantly linked to increased risk of breast cancer… Moreover, a similar pattern of enhanced breast cancer risk at higher plasma Hcy levels was observed in both pre-menopausal and post-menopausal women. The current study results seem to suggest a possibility that the plasma Hcy levels could be a metabolic risk factor for breast cancer…”


One of the drugs used to treat breast cancer is Herceptin®. The National Cancer Institute states, “Herceptin targets cancer cells that “over-express,” or make too much of a protein called HER-2 or erbB2, which is found on the surface of some cancer cells. Herceptin attaches to the HER-2 positive cancer cells and slows or stops the growth of the cells. Herceptin is used only to treat breast cancers that are HER-2 positive. HER-2 positive cancers overexpress the HER-2 protein or have amplification (too many copies) of the HER-2 gene.” The HER proteins regulate cell growth and migration. These functions can be amplified in cancer cells. The study entitled “Persistent transactivation of EGFR and ErbB2/ HER2 by protease-activated receptor-1 promotes breast carcinoma cell invasion” states, “In this study, we report that proteolytic activation of PAR1 by thrombin induces persistent transactivation of EGFR and ErbB2/ HER2 in invasive breast cancer carcinoma” (Arora, 2008). So, thrombin induces “persistent transactivation of HER2”. Thrombin is a protein in the blood that plays an important role in the blood clotting process. Transactivation is an increased rate of gene expression. In the following study researchers found that homocysteine potentiates thrombin generation.


Relationships between homocysteine, factor VIIa, and thrombin generation in acute coronary syndromes.
Al-Obaidi, M.K., H. Philippou, P.J. Stubbs, A. Adami, R. Amersey, M.M. Noble, D.A. Lane. 2000. Circulation 101(4):372-7.

“It has been suggested by clinical, epidemiological, and experimental in vitro studies that homocysteine potentiates thrombin generation…Elevated plasma homocysteine is associated with and may cause elevated Factor VIIa and thrombin generation in patients presenting with ACS. These findings suggest an explanation for the prothrombotic effect of homocysteine in ACS."

There always seems to be a MS study that goes against what other studies have found over the years and I'm guessing this is yet another one of those studies.

First, the article refers to MS as an "auto immune disease". Oh really? I didn't realize that someone was finally able to prove that MS was indeed an auto immune disease!! After years and years of research, nobody has yet to proved the cause of the disease.

This study was done in one country, Taiwan. Perhaps there may have been other factors involved that influenced the results that were obtained.

I do know that MS patients who use the powerful immune system altering drugs can end up with some kind of cancer as a side effect of the drug. After all, one's immune system becomes compromised and that can lead to a host of problems.

Harry

I think what may be one thing that could define an autoimmune disease is the activation of dendritic cells.
Dendritic cells are the prime initiators and mediators of autoimmune disease, as the following study confirms.

Dendritic cells in autoimmune diseases.
Maddur, M.S., J. Vani, J.D. Dimitrovi, K.N. Balaji, S.Lacroix-Desmazes, S.V. Kaveri, J. Bayry. 2010. The Open Arthritis Journal, 3, 1-7 1 1876-5394/10 Bentham Open.



“Dendritic cells are the prime initiators and mediators of autoimmune diseases…Dendritic cells (DCs) are professional antigen presenting cells, which play a crucial role both in maintaining immune tolerance and in inducing adaptive immune responses…Therefore, DCs are the most sought after cells in inciting autoimmunity and its sustenance to autoimmune diseases…DCs act in concert with adaptive and other in­nate immune cells in moulding the autoimmune response...Individuals with autoimmune disease show a high number of aberrantly activated DCs either in circulation or in the autoimmune lesions secreting large amounts of proinflammatory cytokines that mediate inflammation…”



Dendritic cells are activated in every autoimmune disease. For instance, in the following study the researchers confirm that dendritic cells (DCs) play a “pivotal role” in the initiation and progression of systemic lupus erythematosus (SLE).



The role of dendritic cells in the pathogenesis of systemic lupus erythematosus.
Fransen J, Van der Vlag J, Ruben J, Adema GJ, Berden JH, Hilbrands LB. 2010. Arthritis Research & Therapy 12:207 doi: 10.1186/ar2966

“…DCs play a pivotal role in the initiation and progression of SLE…”





In the next study the researchers stated that emerging evidence indicates that dendritic cells also play a “critical role” in the initiation and progression of MS.

Targeting dendritic cells to treat multiple sclerosis.
Comabella, M., X. Montalban, C. Münz, J.D. Lünemann. 2010. Nat Rev Neurol. 6(9):499-507. doi: 10.1038/nrneurol.2010.112. Epub 2010 Aug 17.

“Multiple sclerosis (MS) is considered to be a predominantly T-cell-mediated disease, and emerging evidence indicates that dendritic cells have a critical role in the initiation and progression of this debilitating condition…"


Glatiramer acetate (Copaxone) and Tecfidera, two of the drugs used in the treatment of MS also work, in part, by inhibiting dendritic cells. The following study confirms the inhibition of dendritic cells by Copaxone.

Multiple sclerosis: glatiramer acetate inhibits monocyte reactivity in vitro and in vivo.
Weber MS, Starck M, Wagenpfeil S, Meinl E, Hohlfeld R, Farina C. 2004. Brain 127(Pt 6):1370-8. Epub 2004 Apr 16.

“It is widely assumed that glatiramer acetate (GA), an approved agent for the immunomodulatory treatment of multiple sclerosis, acts primarily as an antigen for T lymphocytes. Recent studies, however, indicated that in vitro, GA directly inhibits dendritic cells, a rare but potent type of professional antigen-presenting cell (APC). To investigate whether these in vitro observations are relevant to the actions of GA in vivo, we studied the effects of GA on monocytes, the major type of circulating APC…These results demonstrate for the first time that GA inhibits monocyte reactivity in vitro and in vivo, significantly extending the current concept of the mechanism of action of GA.”

Also, here is a quote from the first study: "Individuals with autoimmune disease show a high number of aberrantly activated DCs either in circulation or in the autoimmune lesions secreting large amounts of proinflammatory cytokines that mediate inflammation…”

So, do MS patients show a high number of activated DCs either in circulation or in the autoimmune lesions secreting large amounts of proinflammatory cytokines that mediate inflammation? Dendritic cells release proinflammatory cytokines such as interferon-gamma (IFN-gamma), tumor necrosis factor (TNF), and interleukin-6 (IL-6).

In the following study the researchers concluded that patients with MS had high levels of IFN-gamma, TNF, and IL-6 secreting dendritic cells.

J Neuroimmunol. 1999 Sep 1;99(1):82-90.
Multiple sclerosis is associated with high levels of circulating dendritic cells secreting pro-inflammatory cytokines.
Huang YM, Xiao BG, Ozenci V, Kouwenhoven M, Teleshova N, Fredrikson S, Link H.

“Recent evidence emphasises a pivotal role for dendritic cells (DC) in the control of immunity by priming and tolerising T cells. DC capture and process antigens, express co-stimulatory molecules, migrate to lymphoid organs and secrete cytokines to initiate immune responses…Patients with MS had higher levels of IFN-gamma, TNF-alpha and IL-6 secreting DC than healthy subjects…”



Researchers in the following study found an increase of TNF production preceding clinical symptoms and concluded that IFN-gamma and TNF may trigger exacerbations at a very early stage.

Acta Neurol Scand. 1988 Oct;78(4):318-23.
Increased production of interferon gamma and tumor necrosis factor precedes clinical manifestation in multiple sclerosis: do cytokines trigger off exacerbations?
Beck J, et al.

.“…Before exacerbations, however, we found an increase of…TNF production preceding clinical symptoms by a maximum of 2 weeks. In benign cases, the increase disappeared rapidly, even before the appearance of symptoms…In chronic progressive patients, we frequently found intervening increases. It may be that IFN-gamma and TNF trigger off exacerbations at a very early stage and that these cytokines may also play a role in maintaining disease in chronic progressive and invalidating forms.”



In the following study published in the New England Journal of Medicine the researchers concluded that the level of TNF in cerebrospinal fluid correlated with the severity and progression of MS.


N Engl J Med. 1991 Aug 15;325(7):467-72.
Association between tumor necrosis factor-alpha and disease progression in patients with multiple sclerosis.
Sharief MK, Hentges R.

“Tumor necrosis factor-alpha (TNF-alpha), is a principal mediator of the inflammatory response…These data provide evidence…of TNF-alpha in multiple sclerosis and suggest that the level of TNF-alpha in cerebrospinal fluid correlates with the severity and progression of the disease…”



Researchers in our next study discovered TNF in MS "lesions" and concluded that the presence of TNF in MS lesions suggests a significant role for cytokines and the immune response in disease progression.

J Exp Med. 1989 Aug 1;170(2):607-12.
Tumor necrosis factor identified in multiple sclerosis brain.
Hofman FM, Hinton DR, Johnson K, Merrill JE.

“Frozen brain specimens from patients with multiple sclerosis (MS) and other neurologic diseases were analyzed using immunocytochemical techniques for the presence of TNF…TNF+ cells were demonstrated. At the lesion site in MS, TNF+ staining is associated with both astrocytes and macrophages…The presence of TNF in MS lesions suggests a significant role for cytokines and the immune response in disease progression.”


In the following study the researchers concluded their results point to TNF as a primary neurotoxic molecule in progressive forms of MS.

Mult Scler. 2013 Jul 25.
Tumor necrosis factor is elevated in progressive multiple sclerosis and causes excitotoxic neurodegeneration.
Rossi S, Motta C, Studer V, Barbieri F, Buttari F, Bergami A, Sancesario G, Bernardini S, De Angelis G, Martino G, Furlan R, Centonze D.

“The objective of this paper is to investigate the synaptic mechanism of inflammatory neurodegeneration in progressive forms of MS…Our results point to TNF as a primary neurotoxic molecule in progressive forms of MS.”


And of course, TNF is just one of the inflammatory cytokines being released by dendritic cells and causing damage. We would also expect to find these same cytokines being produced in other patients with autoimmune disease and research confirms this is the case.

Great information that helps explain the link between Cancer and MS. Whether MS is classified as a classic “auto-immune” disease or not the immune system plays a part. Disorders of the immune system have been shown to result in autoimmune diseases, inflammatory diseases and cancer.

The Immune system is broken in pwMS therefore to cure MS we need a new one, making the only logical treatment in MS a complete re-write of our immune system. Destroy the immune system completely with chemo and then build it back up, preferably with stem cells. Dr. Wahls underwent significant chemo (which she tends not to mention in her diet books) and numerous other individuals have traveled to Germany and Israel to do the same. Chemo puts a cytotoxic chemical into the body which destroys all cells. Fortunately only rapidly growing cells tend to be affected such as cancer, and immune cells. A study on this procedure has been completed in many countries with a greater than 70% success rate. Most patients live symptom free after. The mortality rate is 5% due to the invasive techniques and risk of infection.

Hi Kronk~I actually think the immune system is just doing what it is designed to do in autoimmune disease. It is reacting to foreign proteins. For instance, research shows that the dendritic cells in MS and other autoimmune diseases are activated due to the presence of neutrophil extracellular traps (NETs). As the following study confirms, NETs trigger the activation of dendritic cells (DC).

Neutrophils Activate Plasmacytoid Dendritic Cells by Releasing Self-DNA–Peptide Complexes in Systemic Lupus Erythematosus
Roberto Lande, et.al. 1Sci Transl Med 9 March 2011:
Vol. 3, Issue 73, p. 73ra19

"...Here, we identified in the sera of SLE patients immunogenic complexes...These complexes were produced by activated neutrophils in the form of web-like structures known as neutrophil extracellular traps (NETs) and efficiently triggered innate DC activation..."


These NETs are a result of unbroken down proteins and DNA entering the bloodstream. The immune system targets these "foreign" invaders by trapping them in the NETs. The body has enzymes called protease and DNase 1 that digest dietary proteins and also degrade the NETs. The lack of these enzymes is the real culprit, not the immune system. In the following study published in the Journal of Neuroimmunology the researchers concluded that patients with MS had higher levels than controls of neutrophil extracellular traps (NETs) in their blood. Remember, the NETs trigger the dendritic cells.

Neutrophils in multiple sclerosis are characterized by a primed phenotype.
Naegele M, Tillack K, Reinhardt S, Schippling S, Martin R, Sospedra M. 2012. J Neuroimmunol. 242(1-2):60-71. doi: 10.1016/j.jneuroim.2011.11.009. Epub 2011 Dec 9.


“…Here, we show that neutrophils in multiple sclerosis patients are more numerous and exhibit a primed state based on reduced apoptosis…as well as higher levels of neutrophil extracellular traps in serum…”

The following study confirms that DNase 1 is essential for the degradation of the NETs.


Proc Natl Acad Sci U S A. 2010 May 25;107(21):9813-8. doi: 10.1073/pnas.0909927107. Epub 2010 May 3.
Impairment of neutrophil extracellular trap degradation is associated with lupus nephritis.
Hakkim A, Fürnrohr BG, Amann K, Laube B, Abed UA, Brinkmann V, Herrmann M, Voll RE, Zychlinsky A.


"...Here we show that serum endonuclease DNase1 is essential for disassembly of NETs..."

So, if you could properly degrade the NETs and prevent them from continually forming you would not activate the dendritic cells.

Here is a picture of one of these NETs. Notice the last paragraph where it states lupus patients lack the enzyme DNase 1.

http://www.sciencedaily.com/releases/20 ... 161423.htm

The formation of these NETs in lupus, MS, and in other autoimmune diseases is not faulty behavior on the part of the immune system. It is their continual formation and the inability to degrade them, due to missing enzymes, that is the problem.

While several theories abound as to the cause of MS, nobody to date has been able to prove any one of them.

Some docs insist that MS is auto-immune while others ask the question if another unknown mechanism causes the problem and the immune system is simply re-acting to this underlying event.

We see some patients getting positive results from drugs like Copaxone, Avonex and Tysabri yet others receiving no benefit whatsoever. Autopsies on the brains of some deceased MS patients show no activity of the immune system at all where the serious lesions have appeared. You would think that if MS was indeed an auto-immune initiated disease, the benefits of these drugs would be far greater but they simply are not.

The only sure thing is that MS appears to be a very complex disease which has avoided a cause by researchers for decades. Despite thousands of studies involving the immune system and all the indicators that show up in these studies, we still don' have a cause and certainly not a cure.

I've been following all of this since the mid 60's and can't count the times I've read that a cure is just around that proverbial corner. It certainly is one big corner.

Harry

I think there are two different components to autoimmune disease. There is the immune system component and then there is the nutritional deficiency component, but they are linked by one common denominator-missing enzymes. These missing enzymes bind and transport vitamin B12. The inability to properly metabolize vitamin B12 would explain why patients with MS would have lesions with no immune involvement.

In the following study the researchers stated they suspected the vitamin B12 deficiency in MS may be due to problems with binding and/or transport. In addition, the researchers concluded that further studies of vitamin B12 metabolism, binding, and transport in MS are indicated, as they feel this may offer clues to the understanding of MS.

Multiple sclerosis associated with vitamin B12 deficiency.
Reynolds EH, Linnell JC, Faludy JE. 1991. Arch Neurol. 48(8):808-11.

“…A vitamin B12 binding and/or transport is suspected. The nature of the association of multiple sclerosis and vitamin B12 deficiency is unclear but is likely to be more than coincidental. Further studies of vitamin B12 metabolism, binding, and transport in multiple sclerosis are indicated, as these cases may offer a clue to the understanding of a still mysterious neurologic disorder.”





In the following study the researchers also found that MS patients have a decrease in the binding capacity of vitamin B12, thus inhibiting the transport of vitamin B12 into the cells, even with normal levels in their blood.


Vitamin B12 metabolism and massive-dose methyl vitamin B12 therapy in Japanese patients with multiple sclerosis.
Kira J, Tobimatsu S, Goto I. 1994. Intern Med. 33(2):82-6.


“Serum vitamin B12 levels and unsaturated vitamin B12 binding capacities were measured in 24 patients with multiple sclerosis (MS), 73 patients with other neurological disorders and 21 healthy subjects. There was no decrease in the vitamin B12 levels, however, a significant decrease in the unsaturated vitamin B12 binding capacities was observed in patients with MS when compared with other groups…”



In the following study the researchers concluded that vitamin B12 in the normal range was significantly associated with the severity of white-matter lesions, especially periventricular lesions.

Plasma vitamin B12 status and cerebral white-matter lesions.
De Lau LM, Smith AD, Refsum H, Johnston C, Breteler MM. 2009. J Neurol Neurosurg Psychiatry 80(2):149-57.


“…Poorer vitamin B12 status was significantly associated with greater severity of white-matter lesions, in particular periventricular white-matter lesions, in a concentration-related manner…These results indicate that vitamin B12 status in the normal range is associated with severity of white-matter lesions, especially periventricular lesions…”