New Information

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Re: New Information

Postby harry1 » Mon May 07, 2012 2:45 am

Hi Annesse

Very interesting thread from you and while i do not have MS i do however have CIDP (Chronic Inflammatory Demyelinating Polyneuropathy) or bassically MS in the peripheral system and not CNS as it's paralysed my feet 100% and weakened my fingers as well as double vision over some years now.

So then after reading this thread (hard do to double vision) i assume that taking either digestive enzymes with meals and/or proteolytic enzymes on an empty stomach would slowly resolve our autoimmune issues?

I also enjoyed your post on garlic and your thoughts about me just starting to drink on empty stomach upon waking an hot tea mixture of pungent garlic powder (1 tbsp) and cayenne powder (1 tsp) to clean up the gut (bad bacteria) and for better blood flow etc.

Thanks :-D
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Re: New Information

Postby jimmylegs » Mon May 07, 2012 7:02 am

@scott, hi, okay right away the zn and k are noticeably in the bottom of those ranges. you know how i feel about lab ranges right? one example, the range they use for serum zinc in the lab which serves the infectious disease clinic at st. paul's hospital is something like 9-15 umol/L. meanwhile the published normal range is 11.5-18.5 umol/L. and healthy controls are nowhere near the bottom end of the range. and as for RBC tests, it's hard to collect enough research when the tests are RBC. if you ever get serum tests done, there's a lot more comparable accessible science out there for those. all i can demonstrate from the science i was able to find is that illness occurs within your lab's range for RBC zinc: "RBC Zn concentration was 'normal' (my emphasis) in 9 of 10 patients ... RBC Zn in patients with subacute thyroiditis was 162 +/- 9 umol/L"
if they had measured levels in healthy controls, this would have been the study. but they didn't.
couldn't find anything useful wrt K. but again, if you ever get serum testing, lots of info for comparison.
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Re: New Information

Postby Annesse » Mon May 07, 2012 9:16 am

Hi harry~I have a section in my book on diseases that we don't talk about in-depth to show how to be able to tell if a disease originates with PEDD (Pancreatic Enzyme Deficiency Disease). Basically how do you know if you have a cold? You have the symptoms of a cold. How do you know if you have PEDD? The same way. What are the symptoms of PEDD? Common symptoms of PEDD are autonomic dysfunction, elevated tumor necrosis factor, low vitamin B12 etc.

Chronic Inflammatory Demyelinating Polyneuropathy, also known as Guillain-Barre Syndrome is a demyelinating disease of the peripheral nervous system.

According to the Center for Peripheral Neuropathy at the University of Chicago, "A clear link has been established between peripheral neuropathy and vitamin B12." http://peripheralneuropathycenter.uchic ... tion.shtml

Without B12, you would not be able to synthesize acetylcholine, one of the neurotransmitters for the autonomic nervous system, so this would lead to autonomic dysfunction. The study entitled "Autonomic dysfunction in Guillain-Barre syndrome," states, "These abnormalities probably reflect pathological alterations of the sympathetic and parasympathetic components of the autonomic nervous system of patients with Guillain-Barre syndrome." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC491201/

Here is a study on the autonomic dysfunction found in MS and Guillain-Barre. http://www.ncbi.nlm.nih.gov/pubmed/17503142

Another symptom of PEDD is elevated tumor necrosis factor. Proteases regulate tumor necrosis factor. In this next study entitled "Tumor necrosis factor-alpha and other cytokines in Guillain-Barre syndrome" it states, "The data suggest that TNF may be a critical factor in the pathogenesis of Guillain-Barre syndrome." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1073140/

I do think it is important to take herbs to kill pathogenic bacteria in the gut. You could also make some capsules with whole organic powdered garlic and a pinch of cayenne. We will be making some herbal capsules with whole organic herbs such as goldenseal root, echinacea, myrrh, garlic etc. to kill pathogenic bacteria and to support the healing process. We are a few months away on that. In the meantime, you could get some great antibacterial capsules from Mountain Rose Herbs. Drinking the garlic tea as you are, if you are tolerating it, is good also. I think the addition of a few more herbs in capsule form would help though.

I don't recommend you take any enzymes. I believe they would be counterproductive. Enzymes are themselves proteins. Taking isolated bundles of proteins would just further deplete your own pancreatic enzymes. The German researchers that discovered the missing DNase1 enzyme in lupus are trying to engineer a fake DNase 1 that is safe for humans. These specific enzymes can be replaced through diet though. The healing portion of my book is one-third of the book though, and not really possible or practical to reprint it here.
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Re: New Information

Postby Scott1 » Mon May 07, 2012 8:35 pm

Hi Annesse,

I hope your book launch is going well and we are not pestering you too much.

If I look at the 3 way dialogue between you, me and Jimmylegs I am inclined to think a carpenter, a plumber and an electrician have all been asked how to build a house. The emphasis in the answers varies according the background.

The data I posted earlier is very old so not a reliable place to start but the point Jimmylegs makes about Zinc is worth exploring. My issue is how best to do that. I agree with the point you made about supplements but I'm still going to keep doing the things that are keeping me well. I know if I stop I go backwards.
If we make it a case of one step at a time, how would you approach the zinc issue? If your approach is right and you accepted the readings on my B levels and methionine as correct then I must have a blocked pathway somewhere. Should I address the intrinsic factor (or hydrochloric acid) before I address the Zinc? I read in one of Jimmylegs links that Zinc is abundant in the body so her interpretation that the reading is low suggests a step is blocked.
I'm still drawn to peroxynitrite from a viral involvement as the disrupting agent but let's leave that to one side at the moment.
On a separate matter, I note I'm starting to experience the same herxing type symptoms on the oleuropein that I had when I first introduced carrot juice. (a frog in the throat, dry cough, headache) but not as strongly as then. I feel well otherwise but I feel like something doesn't like me taking this.
When you used this did you notice anything?

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Re: New Information

Postby jimmylegs » Tue May 08, 2012 4:22 am

hi again scott, you're almost bang on, but i'm the concrete contractor layin the foundation :) similar to what i've said here several times in the past about the blind men describing the elephant.
personally i would approach the zinc issue by ensuring optimal dietary intake/combinations, and if necessary, taking zinc supplements to ensure the levels were up in the optimal range. anything that is required for the function of over 300 enzymes sounds like it would be pretty important. zinc is one of the thing i've come to view as a lowest common denominator. i did have issues with high folate myself. when i was zinc deficient and didn't know it yet, i was taking a particular daily b-complex and my folate jumped up to 2170 nmol/L. i had side effects (phantom itch). now that i'm not zinc deficient, i can take the same amount and no side effects. (therefore no trip to the lab, so i can't tell you any more current folate numbers unfortunately).
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Re: New Information

Postby Scott1 » Tue May 08, 2012 5:20 am

Hi Jimmylegs

Following up on the zinc line I learned a new word today -Disaccharidase.

I was born lactose intolerant and apparently had a lot of problems as a baby. I certainly don't discount the infectious trigger but there's a sign of a predisposition to malabsorption which fits the B12/Zinc angle. I think this implies an inborn error of metabolism and that probably would make us susceptible to environmental triggers. The combination probably starts a cascade.
The EBV as an environmental trigger makes sense to me and I have had success but assuming that but the symptoms of B12 deficiency are things I can recognise as well.
If it is an inbuilt defect then supplementation might alleviate symptoms but it can't solve a genetic predisposition hence we don't have a cure.
The common path seems the process of glycolysis. Lots of enzymes at work there. I know peroxynitrite can disrupt that and I can see that B12/Zinc deficiency can impact it as well.
Sounds like we need to "weed and feed". The question is how to do it best.

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Re: New Information

Postby jimmylegs » Tue May 08, 2012 5:59 pm

ah yes, the zinc and lactose intolerance aspect. how did your symptoms manifest when you were a baby?
you could try getting your serum zinc up to 18 umol per litre, and measure RBC again too so you can compare your previous results at least.
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Re: New Information

Postby jimmylegs » Tue May 08, 2012 6:00 pm

next stop, potassium. but i will pm you, or meet me on my regimen thread :)
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Re: New Information

Postby Scott1 » Tue May 08, 2012 9:06 pm

I'm afraid i'm like treebeard the Ent! I will have to think about all this for some time yet.
I also want to see how the Oleuropein goes for a bit longer yet before I start changing things around. Something is going on but I need more time.

Apparently as a baby I looked like I'd come out of a concentration camp with spindly limbs and a distended stomach. All I did was scream my head off. Fortunately my mother was a well trained nurse and the lactose intolerance was diagnosed.

We should Annesse a chance to reclaim this thread.

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Re: New Information

Postby Scott1 » Wed May 09, 2012 8:54 pm

Hi Annesse,

In the first post you made you talked about DNase 1. Were you planning to takes us through the ubiquitin-proteasome pathway?

I think this the common ground. The glucocorticoid receptor is a zinc finger transcription factor which is regulated by the ubiquitin-proteasome pathway.

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Re: New Information

Postby Scott1 » Wed May 09, 2012 9:05 pm

Worth a read

http://users.rcn.com/jkimball.ma.ultran ... idREs.html

http://pats.atsjournals.org/content/1/3/239.full

C:\Documents and Settings\rasjb001\Desktop\Proteasome - Wikipedia, the free encyclopedia.mht
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Re: New Information

Postby Annesse » Thu May 10, 2012 10:48 am

Hi All~ Sorry for being absent. We were trying very hard to get the 2nd edition out by this weekend, but we just couldn't do it. Hopefully, next week. So, I will need to stay focused on that for a little while longer.

Hi Scott1~ I think I will need to stay on track and reinforce the protein-B12-enzyme pathway. It is alot of information to absorb and I don't want to add too much additional information right now. We can come back to it though.

I thought this information on iron, B12 and myelin was interesting. It reinforces the connection iron and B12 have to myelin. The following abstract entitled, "Iron and the folate-vitamin B12 methylation pathway in multiple sclerosis" states, "Myelin is regenerated continually, but prerequisites for this process are iron and a functional folate-vitamin B12-methylation pathway. In relapsing-remitting MS subjects, serum iron concentration correlated significantly with age at diagnosis. In Caucasian female MS subjects, serum iron and ferritin concentrations were significantly lower than in matched controls." We have previously shown that protease are responsible for regulating iron in the body.

http://www.ncbi.nlm.nih.gov/pubmed/16729250
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Re: New Information

Postby Annesse » Fri May 11, 2012 9:21 am

Studies show that MS patients have significantly higher levels of homocysteine. Like iron or tumor necrosis factor, homocysteine performs a desirable function in the body, but only if it is properly regulated. Homocysteine is derived from the essential amino acid methionine and is used to build and maintain tissue. During normal conditions, excess homocysteine, with the help of vitamin B12, is converted back to methionine or broken down for ecretion. The problem arises when the conversion process fails due to a lack of B12.

The elevated levels of homocysteine found in MS patients will explain the lack of our last missing nutrient-magnesium. Here is some info from my book:

The Discovery - Homocysteine
AUTOIMMUNE: THE CAUSE AND THE CURE
The following study found “a statistically significant decrease” in intracellular magnesium (Mg) in patients with multiple sclerosis. Erythrocytes are red blood cells.
Magnesium Concentration in Plasma and Erythrocytes in MS
Stelmasiak, Z, J. Solski, B. Jakubowska. 1995. Acta Neurol Scan 92(1):109-11.
Abstract: There are few reports of Mg in MS and none dealing with Mg content in erythrocytes. Mg concentration was determined in serum and in erythrocytes with the help of a BIOTROL Magnesium Calmagite colorimetric method (average sensitivity: 0.194 A per mmol/I) and a Hitachi autoanalyzer in 24 MS patients (7 men and 17 women, age 29-60; 37 years on average with the duration of the disease: 3-19; 11 years on average, at clinical disability stages according to the Kurtzke scale: 1-7; 3.2 on average, in remission stage. A statistically significant decrease (p < 0.001) of Mg concentration in erythrocytes and no changes in plasma of MS patients were found. The results obtained suggest the presence of changes in membrane of erythrocytes which could be connected with their shorter life and with affection of their function.

Another study entitled “Magnesium concentration in brains from multiple sclerosis patients” also found MS patients had significantly lower Mg (Yasui, 1990). The study states that, “The average Mg content in the CNS tissues, as well as visceral organs except for spleen, of MS patients showed a significantly lower value than that seen in controls."

Homocysteine interferes with the metabolism of magnesium. In the following study conducted at the Health Science Center in Brooklyn, it was determined that homocysteine causes a depletion of intracellular free magnesium.
http://www.ncbi.nlm.nih.gov/pubmed/10553943

The study states, "These findings are compatible with the hypothesis that an increased serum HC (homocysteine)concentration causes abnormal metabolism of Mg2+ in cerebral VSMC (vascular smooth muscle cells), thus priming these cells for HC-induced atherogenesis, cerebral vasospasm and stroke."
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Re: New Information

Postby Annesse » Sun May 13, 2012 10:19 am

Research shows that migraines are more common in women with MS. Here is some information on a study that looked at nearly 117,000 U.S. women and found that women with a migraine diagnosis were 47% more likely to develop MS.

http://news.health.com/2010/02/16/migra ... osis-risk/ Following is some info from my book.

"Compared with the general population, people with lupus may be twice as likely to experience migraine headaches, commonly known as lupus headaches. The paper entitled “A study of headaches and migraine in Sjögren’s syndrome and other rheumatic disorders” reported that nearly half (46%) of Sjögren’s patients and 32% of patients with scleroderma suffer from migraines as well (Pal, 1989). It concluded that, “There was a significant association between occurrence of Raynaud’s phenomenon and migraine. Small vessel pathology may underlie both migraine and Raynaud’s phenomenon in these connective tissue disorders--as has been suggested in systemic lupus erythematosus.”

In Headache: The Journal of Head and Face Pain, author Cris S. Constantinescu M.D., Ph.D., states, “Migraine and Raynaud phenomenon often coexist and may reflect similar vascular reactions. Both have been associated with vascular endothelial cell dysfunction,” (Constantinescu, 2002).

The following study found that homocysteine levels were significantly higher in patients with migraine with aura (MA) than in healthy controls.

Homocysteine Plasma Levels in Patients With Migraine With Aura
Moschiano. F., D. D’Amico, S. Usai, L. Grazzi, M. Di Stefano, E. Ciusani, N. Erba, G. Bussone. 2008, Neurol Sci 29(Suppl. 1):S173-5.
Abstract: We investigated homocysteine plasma levels in 136 MA sufferers and in 117 sex-and age-matched controls. Mean homocysteine plasma levels - as well as the proportion of subjects with hyperhomocysteinaemia - were significantly higher in patients with MA than in healthy controls. Hyperhomocysteinaemia may be a link between MA and ischaemic stroke.

The next study, done in Japan, is notably and appropriately titled, “Homocysteine Induces Programmed Cell Death in Human Vascular Endothelial Cells.”

Homocysteine Induces Programmed Cell Death in Human Vascular Endothelial Cells Through Activation of the Unfolded Protein Response
Zhang, C, Y. Cai, M.T. Adachi, S. Oshiro, T. Aso, R.J. Kaufman, S. Kitajima. 2001. J Biol Chem 276(38):35867-74.
Severe hyperhomocysteinemia is associated with endothelial cell injury that may contribute to an increased incidence of thromboembolic disease. In this study, homocysteine induced programmed cell death in human umbilical vein endothelial cells as measured by TdT-mediated dUTP nick end labeling assay, DNA ladder formation, induction of caspase 3-like activity, and cleavage of procaspase 3. Homocysteine-induced cell death was specific to homocysteine, was not mediated by oxidative stress, and was mimicked by inducers of the unfolded protein response (UPR), a signal transduction pathway activated by the accumulation of unfolded proteins in the lumen of the endoplasmic reticulum. Dominant negative forms of the endoplasmic reticulum-resident protein kinases IRE1alpha and -beta, which function as signal transducers of the UPR, prevented the activation of glucose-regulated protein 78/immunoglobulin chain-binding protein and C/EBP homologous protein/growth arrest and DNA damage-inducible protein 153 in response to homocysteine. Furthermore, overexpression of the point mutants of IRE1 with defective RNase more effectively suppressed the cell death than the kinase-defective mutant. These results indicate that homocysteine induces apoptosis in human umbilical vein endothelial cells by activation of the UPR and is signaled through IRE1. The studies implicate that the UPR may cause endothelial cell injury associated with severe hyperhomocysteinemia.

The previous studies on Raynaud’s and migraines, in addition to the study from Japan, show the damage homocysteine can do to the vascular endothelial cells. Endothelial cells line the entire circulatory system, from the heart to the smallest capillary.
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Re: New Information

Postby Annesse » Mon May 14, 2012 2:51 pm

This study shows that MS patients have been found to have endothelial dysfunction. The researchers state, "We've discovered in the plasma of MS patients the elevation of endothelial microparticles, a marker of endothelial dysfunction."

http://www.ncbi.nlm.nih.gov/pubmed/11376181

http://www.sciencedaily.com/releases/20 ... 072009.htm
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