Lessions Gone What Next?

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a review: zinc, intestinal permeability (leaky gut) and cand

Postby jimmylegs » Tue Nov 22, 2011 10:15 am

yes as previously discussed elsewhere, if you have a set of dietary/nutritional problems that are common in ms and can also allow a candida overgrowth to occur, it can definitely exacerbate the underlying problem via a positive feedback loop. personally i used to be both zinc deficient and had candida issues., both confirmed via lab testing. once i corrected poor nutritional status the conditions for potential candida overgrowth did not exist, no more zinc deficiency, and no more positive candida results.

A critical physiological role of zinc in the structure and function of biomembranes
"Of the large number of recognized zinc metalloenzymes, the activities of only a few are significantly decreased in severely zinc deficient animals. On the other hand, physiological pathology is manifested rapidly after dietary zinc deprivation. This shows that zinc exerts physiological and biochemical roles other than as a component of the known zinc metalloenzymes. The research results reviewed here suggest that zinc plays an important role in the maintenance of membrane structure and function."

Zinc Deficiency Induces Membrane Barrier Damage and Increases Neutrophil Transmigration in Caco-2 Cells
"Zinc may contribute to the host defense by maintaining the membrane barrier. In this study, we questioned whether zinc deficiency affects the membrane function and junctional structure of intestinal epithelial cells, causing increased neutrophil migration. We used the Caco-2 cell line grown in control (C), zinc-deficient, or zinc-replete medium until differentiation. Zinc deprivation induced a decrease of transepithelial electrical resistance and alterations to tight and adherens junctions, with delocalization of zonula occludens (ZO-1), occludin, β-catenin, and E-cadherin. Disorganization of F-actin and β-tubulin was also found in zinc deficiency. These changes were associated with a loss of the amounts of ZO-1, occluding, and β-tubulin. In addition, zinc deficiency caused a dephosphorylation of occludin and hyperphosphorylation of β-catenin and ZO-1. Disruption of membrane barrier integrity led to increased migration of neutrophils. In addition, zinc deficiency induced an increase in the secretion of interleukin-8, epithelial neutrophil activating peptide-78, and growth-regulated oncogene-α, alterations that were not found when culture medium was replete with zinc. These results provide new information on the critical role played by dietary zinc in the maintenance of membrane barrier integrity and in controlling inflammatory cell infiltration."

Zinc deficiency and immune function
http://www.annualreviews.org/doi/abs/10 ... 190.002215
"Zn deficiency in adult animals can result in abnormal immune function. Zn-deficient animals can show an increased susceptibility to a number of pathogens including Candida albicans, Francisella tularensis, Trypanosoma cruzi, and Trypanosoma"

The Dynamic Link between the Integrity of the Immune System and Zinc Status
"The results of more than three decades of work indicate that zinc deficiency rapidly diminishes antibody- and cell-mediated responses in both humans and animals. The moderate deficiencies in zinc noted in sickle cell anemia, renal disease, chronic gastrointestinal disorders and acrodermatitis enteropathica; subjects with human immunodeficiency virus; children with diarrhea; and elderly persons can greatly alter host defense systems, leading to increases in opportunistic infections and mortality rates. Conversely, short periods of zinc supplementation substantially improve immune defense in individuals with these diseases. Mouse models demonstrate that 30 d of suboptimal intake of zinc can lead to 30-80% losses in defense capacity. Collectively, the data clearly demonstrate that immune integrity is tightly linked to zinc status. Lymphopenia and thymic atrophy, which were the early hallmarks of zinc deficiency, are now known to be due to high losses of precursor T and B cells in the bone marrow. This ultimately leads to lymphopenia or a failure to replenish the lymphocytic system. Glucocorticoid-mediated apoptosis induced by zinc deficiency causes down-regulation of lymphopoiesis. Indeed, zinc itself can modulate death processes in precursor lymphocytes. Finally, there is substantial evidence that zinc supplementation may well reduce the impact of many of the aforementioned diseases by preventing the dismantling of the immune system. The latter represents an important area for research."

and, it's certainly well known although not universally communicated to patients by their docs, that antibiotics wipe out healthy microflora and a probiotic supplement is key. in australia at least, probiotics are commonly advertised on tv as a followup to any prescribed course of abx.
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
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Re: Lessions Gone What Next?

Postby fee002 » Tue Nov 22, 2011 10:37 am


Yes vits and zinc are very important, but so IS a possible CAUSE for that deficiency
Last edited by fee002 on Tue Nov 22, 2011 1:06 pm, edited 1 time in total.
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Re: Lessions Gone What Next?

Postby jimmylegs » Tue Nov 22, 2011 11:25 am

please abide by the rules of the forum, fee002. thank you. [update: thanks for self-editing your comment]
Personal attacks, which can consist of slightly veiled innuendo or sarcastic comments aimed at the poster as opposed to the content of the post, are not tolerated at This is MS. We of course reserve the right to ban or suspend any member who violates this rule.

some routes to zinc inadequacy:

-excess gluten (gluten-free diets also help elevate serum zinc in both celiac patients and healthy controls.. will post study once i track it down).

-excess phytate
Phytate and zinc bioavailability
"This review discusses evidence from human studies on the effects of dietary phytate on zinc bioavailability. In vitro and animal experiments have implicated calcium as a potentiating factor because it reacts with phytate, and zinc binds to the precipitate. Magnesium also reacts similarly to calcium, but most studies have not considered this factor. Protein provides amino acids, some of which are able to desorb zinc from the precipitate and improve bioavailability. Some predictive ratios, derived from animal studies, have been directly applied to human studies. The studies reviewed included those on: zinc status of groups, apparent absorption of zinc in normal subjects and ileostomists, true absorption using a stable isotope, plasma tolerance, and the accumulation in the body of a radioisotope. It was concluded that detrimental effects of phytate could be demonstrated on zinc bioavailability, but that the studies had not been designed specifically to demonstrate whether the interactions found in animal studies also apply to humans. It is suggested that more targeted research is required before predictive ratios are used for humans."

more reasons for poor zinc status, from the NIH
http://ods.od.nih.gov/factsheets/Zinc-H ... fessional/
-gastrointestinal surgery
-digestive disorders
-malabsorption syndrome
-chronic liver disease
-chronic renal disease
-sickle cell disease
-other chronic illnesses
-chronic diarrhea
-vegetarians (no meat, high phytate diet - this is what happened to me)
-pregnant and lactating women
-older infants who are exclusively breastfed
-people with sickle cell disease

the following info does not reference any research - if you're interested, micko, i can track down supporting research
Zinc Deficiency
Zinc metabolism is closely related to Candida because 1) the zinc/copper balance is critical, and 2) zinc is required for many essential enzyme systems, including production of digestive enzymes and synthesis of all body proteins.
Deficiency of zinc is common for several reasons:
• Use of superphosphate fertilizers and hybrid crops have contributed to widespread zinc deficiency in all foods.
• Processing and refining further depletes foods of their zinc content. For example, zinc loss occurs in the conversion of whole wheat to white flour, in the conversion of sugar cane to white sugar, and in spraying of frozen and canned vegetables with EDTA to retain color.
• Foods, relatively low in zinc, such as chicken and fish are being increasingly substituted for higher-zinc foods such as beef and red meats. Soy protein, commonly substituted for beef, is low in zinc.
• Stress of any type results in zinc depletion.
• Zinc deficiency is accentuated if copper exposure is high, because of a copper-zinc antagonism. Copper exposure is higher today for several reasons:
– Birth control pills raise tissue copper levels by raising estrogen levels.
– Copper is absorbed from the Copper-7 intrauterine device.
– Water remaining in copper pipes, and consumption of high-copper foods such as soy, avocado, and chocolate are sources of copper.
– Stress causes copper levels to increase, by causing a zinc deficiency.
odd sx? no dx? check w/ dietitian
DRI=MINIMUM eg bit.ly/1vgQclQ
99% don't meet these. meds/lifestyle can affect levels
status can be low in ms & other cond'ns
'but my results are normal'. typical panels don't test all
deficits occur in 'normal' range
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Re: Lessions Gone What Next?

Postby euphoniaa » Tue Nov 22, 2011 6:34 pm

micko77 wrote:So I was officially diagnosed with RRMS about 3 years ago now. I had multiple MRI's in the beginning to find a lession on my spine just below the base of my skull. My symptom at the time was right leg numb followed by enitre right side of body numb. This eventually went away about 8 to 12 weeks later. My neurologist stated there is a possibility it would come back. Sure enough less than 2 months later my left side went numb. Back tot he MRI and found two more lessions. Out comes my offical diagnosis.

Since then i have changed jobs and moved back to PEI (Canada) and now no longer have drug coverage because of the official diagnosis of MS. I have had no relapses in over 2 years and have just learned from my new neurologist that I have NO lessions. All previous lessions are gone. I have now had 3 MRI and same result.

I am hopeful that my MS is in full remission but feel strange that i have no lessions. I took Copaxane for about 12 months then stoped when no longer covered with a drug plan. I am not sure where to go from here? Is it possible I was misdiagnosed? If so how to turn that diagnosis around? If I am in remission (I would be extremely grateful) is this a normal course for MS patients?

Any thoughts would be greatly appreciated.



Ummmmm, okaaaay...now back to your original questions, :smile: mainly this one, "I had lessions on my spine on two different occassions. All three have since dissappeared. So thats where my question comes in now what?"

Hi Mike, and welcome! I'm sorry I don't really have a great answer, but I'm intrigued by the question and wanted to make sure it doesn't get lost in the thread so I copied your whole posts. I know that MS lesions change, especially in the brain, and people go into remission, but I don't think I've read a story quite like yours before.

Let's summarize for new readers and hope for some more responses. I'm fascinated by your story!

*You got typical MS symptoms.
*MRIs showed definite spinal lesions (no brain lesions) and you got a definite MS dx.
*For one year you took one of the basic four MS meds, whose only hope is to slightly slow down
lesions and relapses, but not cure anything.
*Now you seem to be in complete remission with no relapses.
*Subsequent MRIs also show your old lesions are completely gone.

This is fabulous news! Amazing! Enjoy it! But that still leaves another of your questions, "If I am in remission (I would be extremely grateful) is this a normal course for MS patients?" No, this is not the slightest bit typical. Really cool, but atypical. Maybe your choice of meds was the perfect one for your type. Congratulations for the relief, but welcome to the confusing world of MS.

And your other questions:

"I am not sure where to go from here? Is it possible I was misdiagnosed? If so how to turn that diagnosis around?"

Yes, it's definitely possible you were misdiagnosed originally. Or not. Misdiagnosis is actually quite common. There are many, many MS mimics (say that phrase fast 5 times – hey, that could be a new MS test...) and lots of reasons for lesions (now say THAT fast 5 times) besides MS. :smile: And MS is basically just a collection of symptoms and signs with no real test. We're all unique.

It sounds like you've had plenty of experience with doctors, so you'll have to continue with them - they're the only ones who can really evaluate your situation and either find you another medical condition or "turn that diagnosis around." MS patients are often undiagnosed. I'm interested in how your most recent neuro explained your current situation?

I'd like to hear more of your story - it's so different than mine - and I do hope more people stop in with similar experiences. I have a brain that's jammed full of lesions that have only grown slightly over the years – they don't enhance, they don't disappear.

A lot of people do go into 'relative' remission for years, but spinal lesions are different, and with you, it seems that everything has disappeared. Of course, maybe that scenario is much more common than I think. But with me, I don't think I've had a single day in 38 years without at least a touch of weird symptoms, even though I'm not positive I've ever had an official, full-blown exacerbation. :smile:

Best of luck to you and hope you get more input for your questions.
Dx'd with MS & HNPP (hereditary peripheral neuropathy) 7/03 but must have had MS for 30 yrs before that. I've never taken meds for MS except 1 yr experiment on LDN. (I found diet, exercise, sleep, humor, music help me the most.)
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