if your mag is down, you might want to consider looking at a few other nutrients. such as ones that are more likely to be low in athletes, as well as ones that are likely to be low in ms patients.
I have lots of info on how to work with magnesium and other nutrients if you are interested. I am self taught re health but with a background in science.. I have successfully diagnosed and treated athletic nutrient depletion before, in the 'real world' away from TIMS. there is no guesswork involved it's just tests, results, management, retest, etc. easy as pie as long as you can get the doc on board to run your tests and give you a copy of the results.
take control of your own health.
pursue optimal self care, with or without a diagnosis.
Welcome to THISISMS, LLL3885. You seem to be handling the situation appropriately. You have described your symptoms well; you are aware of family medical history; you are assembling your medical team. Does this sound like MS? There is always the possibility that it is; but since there is no definitive test for MS, it is not easy to diagnose. As you probably know, there is a wide assortment of possible MS symptoms – it is possible for two people with MS to have completely different sets of symptoms.Livelaughlove3885 wrote:Hi all, been having some weird problems over the past year. I saw an eye doc and he said I have to see this other eye specialist because I have a blepharospasm. I didn't tell him about the other stuff, I'll save that for when I see the specialist. I had the pulsating lower righteyelid all day long for 2 months straight. Then that stopped and the right side area of my mouth and chin started pulsating. Before that I had PVCs that came out of nowhere for 2 months all day long, about 4-10 per minute. I have been getting pulsations in other parts of my body but only right side. With my face, when the eyelid was spazzing if I touched my forehead it would really get out of control. My dad, his sister, and her daughter have MS. So does this sound like beginning stages of MS or just idiopathic hemifacial spasm/body spasms for no apparent reason? I am an actively fit 35 yr old female with no past medical history. I don't remember my dad and aunt having these problems when they had their initial MS flare ups and with them it never affected their vision which is what I am experiencing. With them it made them paralyzed whenever they had flares. Any advice?
Our best to you. Please stay in touch – inform us of your diagnosis; ask us any questions; read lots of information here.
I am more used to reading research than this kind of thing, but because of that, as I watch it the relevant studies pop into my head - so the research is definitely out there.
NEXIUM aahhhh I still have samples given to me by my doc, I took it for a day or two but soon read enough about it to turn me right off. always happens. it was as simple as, 'nope I need my stomach acid in order to get my nutrients, thank you very much! what my problem is, is a malfunctioning LES'. so I went after that instead. so much more logical
interesting re the rigidity comment - sounds like another indicator of a poss systemic mag issue.
love the sound of your phone app! some easy action items to follow up on.
I love this resource for its suggestions and info on specifically healthy, nutrient-dense food choices. have u seen it? you just look at mgs per serving and aim for 400mgs each day.
magnesium http://www.whfoods.com/genpage.php?tnam ... #foodchart
for mag rich foods, I have some or all of spinach, chard, hummous (sesame seeds), sunflower seeds, cashews and almonds going in on an almost daily basis, and am working on increasing brown rice and more variety with legumes. tonight's dinner will be enchiladas, and although we don't usually include them I had black beans soaking overnight and will throw them in the pressure cooker while i'm making tea this am, so that a little more bean-dip magnesium will be in the picture than would have been otherwise. oh! I have a great multi-green spinach-feta pie recipe on here somewhere if you want it.
here's the vit d3 page by the way: http://www.whfoods.com/genpage.php?tnam ... #foodchart
I only eat salmon weekly, but eggs go in almost daily, as well as a tiny bit of milk. this is defs one to supplement, with caution and *definitely* with a high mag diet.
curious, how does the app say you're doing for zinc and iron? and what are your main food sources of these, does it indicate that at all? I mention it bc you said grains make you sluggish and tired. you hae to have some pretty good nutrient stockpiles in place not to feel it when eating grains. I remember that feeling well :S not so fun!
just seeing your post re your daughter.. may I ask what her zinc level was? it's another case where deficiency states and associated illnesses are found over much of the so-called normal range.
take control of your own health.
pursue optimal self care, with or without a diagnosis.
You are very wise to focus on diet – I agree with you that it is critical.Livelaughlove3885 wrote:Let me tell you about my family hx, it's pretty bad, I'm the only one with no diagnosed problems. My sister = hashimoto thyroiditis, autoimmune gastritis/intrinsic factor, lupus. My brother = alopecia areata and dyshidrosis. My dad, his sister, her daughter = MS. 2 maternal cousins with crohns, one maternal aunt UC. One cousin wheat allergy, negative celiac on maternal side. My mom, hodgkin's lymphoma. Her sister and their aunt, non-hodgkin's lymphoma. My mom also has diabetes but she has controlled it with exercise and diet so she has not had to take any meds for 7 years... so go mom!!! I think that's about it. I think the odds are that I have more likely of a chance to develop autoimmune disorder over the general population, and I really believe that if i didn't eat so healthy and exercise than i would be in really bad shape. I think diet is def a key factor in triggering inflammation that can affect the body, bring it down, and more likely to react to it's own self. I keep telling my family they should also try my diet, it is very anti-inflammatory. I don't know, just my theory, but you guys seem to also know a lot about diet, so that makes me feel good. I guess my thing is that I see what my family has gone through (being misdiagnosed for years and told it's just stress when it wasn't)
With your family history and preponderance of autoimmune diseases, you may be interested in the following essay, "The Common Thread," written by Dr. Noel Rose several years ago. Although I may not agree with his ideas 100%, it is a good starting point:
The Common Thread
Noel R. Rose, M.D., Ph.D.
Chairman Emeritus, AARDA National Scientific Advisory Board; Professor of Pathology and of Molecular Microbiology and Immunology; Director, Center for Autoimmune Disease Research, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, MD
What happened about 40 years ago? Well, a number of key discoveries were made--some of them in my own laboratory--which turned that doctrine of self, non-self distinction on its head. We found that there are a number of instances in which the immune response is directed to something in the body of the host itself. It seemed implausible, even contradictory; but, in fact, that was exactly what we found: there are some circumstances where the immune response attacks the body of the host itself. The host may be an animal or it may be a human patient. That is what we call autoimmunity. Autoimmunity is nothing more than the immune response directed to the body of the patient himself or herself.
Let me define a second term for you, autoimmune disease. These two terms do not mean exactly the same thing, and the difference may be important to us as we talk about some of these issues a little later this afternoon. Autoimmune disease is a disorder that occurs because of autoimmunity--a disease that is caused by an immune response to the body of the patient himself or herself.
Now, in defining autoimmune disease that way, I imply that there is autoimmunity without autoimmune disease. In fact, we now know that autoimmunity is not at all uncommon and that it exists in all of us. Every one of us has some degree of autoimmunity naturally, and it does not seem to do us any harm. It is, in fact, only a minority of cases where autoimmunity actually produces damage in the body, producing disease. So there are really two basic questions that I, as an investigator, and my colleagues in this field need to unravel.
First question is: How does autoimmunity arise? What causes the body to produce an immune response to itself? What are the circumstances, what are the mechanisms, what are the triggers for the phenomenon that we call autoimmunity? That's one question. That's a very basic question that involves biology, chemistry, even biophysics. It requires a deep understanding of the immune system. We need to know a lot more about how the body produces immunity reactions. We know a great deal, but there are still enormous voids in our understanding. We must know that in order to understand how the body normally distinguishes self from non-self.
The second question is: What are the factors in the autoimmune response that sometimes cause disease? These are the two critical questions that are the topics of basic research. Sometimes the feeling is expressed that basic research is scientists fooling around in the laboratory doing things that are unimportant. Well, there is nothing that is unimportant about these questions. They are absolutely critical. We must understand that if we are ever going to develop effective treatments or, more important, cures for preventing autoimmune disease, we must understand them. Just as we would never have been able to control infectious diseases until we found the bacteria or viruses that cause diseases, so we cannot deal effectively with autoimmune disease until we understand its cause.
Now, let's get to the question Mrs. Ladd [executive director of http://www.AARDA.org] put to us: Why are autoimmune diseases related? And here I have to give you a little bit of insider information about how medicine is organized in this country.
When medicine grew up in the middle ages, physicians had to divide diseases into various kinds and various categories. The only way they could classify diseases was anatomically, that is, where does the disease occur? Physicians later divided themselves into doctors who were interested in diseases of the lungs, and other doctors who were interested in diseases of the skin, and other doctors were interested in disease of the intestinal tract or the reproductive tract or the urinary tract. Most medicine is still organized on the basis of the anatomy of the disease, on where the disease occurs. You go to a heart specialist (a cardiologist) if you have heart disease, to a neurologist if you have nervous system disease, to a dermatologist if you have a skin disease, and on and on. The medical community organized itself that way because that's all the doctors knew. They didn't know what caused disease, but they knew where it occurred. But starting with Louis Pasteur about a hundred years ago, a change occurred. For the very first time we began to understand why disease occurs--not where it occurs, but why it occurs. And when we speak of why disease occurs, we speak of something else, and that is what we call etiology.
Etiology means cause, why the disease occurs. If we are concerned with curing disease and possibly even preventing disease, the etiology is the most important information. Why have we been able to control so many infectious diseases? Because we now know the bacteria and the viruses and the parasites that cause these diseases, and we can develop antibiotics and other drugs that will specifically attack that organism. Discovering the etiology has allowed medicine to progress to its present state where we can successfully treat and even cure many diseases.
Within the lifetime of most of us, we have ways of effectively treating infectious disease. Until World War II, until antibiotics were introduced, we did not have methods that cured disease. We had treatments that alleviated the symptoms of disease, but we really didn't cure disease. With the introduction of antibiotics--penicillin, streptomycin, and other substances--we now have a way of treating. And that's why it is so important to understand etiology.
Here are a few other groups of diseases which are now defined by their etiology. Allergies are an example. If you have an allergy, it doesn't matter whether it's an allergy of the nose, that is, hay fever, whether it's in the lungs, asthma, or whether it's atopic dermatitis, a skin disease. You may go to an allergist because all of these diseases have the same etiology. They have different anatomies, but they have the same etiology. That's the way progress is being made by bringing together diseases with the same etiology.
Autoimmunity is an etiology: it is a cause of disease. Anatomically, autoimmune disease is very diverse; and that's why we see specialists in so many areas of medicine studying autoimmunity. They may be rheumatologists who are interested in joints; they may be dermatologists who are interested in skin; they may be cardiologists who are interested in the heart; they may be gastroenterologists who are interested in the gastrointestinal tract. But the common etiology for all of these disease--for Crohn's disease of the gut; for lupus of the skin; for rheumatoid arthritis of the joint--the common etiology that brings together all of these diseases is autoimmunity.
A major aim of the American Autoimmune Related Diseases Association is to help us to understand that all of these diseases, diverse as they are, in their anatomical location, in their clinical manifestation, are related because they have the same etiology; they are all caused by autoimmunity. In my opinion, the only way we're going to develop really effective treatments will be to treat the cause of the disease, not the symptoms. The symptoms are late; the symptoms are at the end of the train of events. We want to get on the train at the very beginning.
Now, what are some of the specifics of this relationship? Let me lay out some of the principles that we now understand about the etiology of autoimmune disease.
Unlike some diseases, autoimmune diseases do not generally have a simple, single cause. There are usually two major categories of factors that are involved in causing autoimmune diseases: genetics and environment. Virtually every autoimmune disease combines these two. Let me explain more of what I mean. First, genetics. Genetics is involved in the development of autoimmune disease, but autoimmune diseases are not typical genetic diseases. What is a typical genetic disease? Most of us have heard of sickle cell anemia, and that's a genetic disease. That's a disease in which the victims of the disease have a specific genetic mutation. If you inherit this mutation from one parent, you have sickle cell trait; and if you inherit it from both parents, you have sickle cell disease. We know what the gene is, and we even know a great deal of how that works; so we know the etiology of that disease.
That's not the way genetics works in autoimmune disease. In autoimmune disease, multiple genes are involved; we have genes that collectively increase the vulnerability or susceptibility to autoimmune disease. What is inherited is not a specific gene that causes a specific defect in metabolism; several genes increase vulnerability or susceptibility to autoimmune disease.
How do we know that there is a genetic basis of autoimmune disease? I can cite three kinds of evidence. The first is autoimmune diseases tend to occur in families. If there's one case of autoimmune disease in the family, there's likely to be another case.
However, it is not a particular autoimmune disease; it is generally a tendency to autoimmunity. One family member may have lupus, another family member may have Sjogren's disease, a third member of the family may have rheumatoid arthritis. That's one bit of evidence for genetic involvement, and we've known this for a number of years. If we ask patients when they come to us, "Is there other autoimmune disease in your family?"--and we actually have to mention them because people don't know these are all autoimmune diseases--they will usually say, "Yes, my aunt had thyroid trouble...my grandmother had that disease...my grandmother had Crohn's disease...."
But we call this soft data in science because families share genes and that's some indication of genetics; but families share other things.
So we need to look further. The second thing we do is to look at twins. We compare two kinds of twins. There are twins that are genetically identical, and there are twins that are non-genetically identical. If something is caused by an environmental factor, there should be no difference between identical twins and non-identical twins. If there's a difference, it suggests that genetics plays a role. These studies have been done for a number of autoimmune diseases, and the answer has always come up about the same. Genetic components represent something in the order of half of the risks. In other words, if you have a genetic predisposition to autoimmunity, you may have twice or five times as much chance of developing autoimmunity as someone else--not 100 times, but not zero. So genetics plays an important role.
One group of genetic factors is particularly important. One of the things that immunology has taught us through the years is obvious but needed some kind of physical basis, it is simply that every human being is different from every other human being (unless you have a genetically identical twin). Every person is a little different from everybody else; we know that for certain when we try to transplant tissues, like kidneys or hearts. In general you cannot accept a kidney or heart from someone else unless we dampen your immune response.
There clearly are significant physical differences between different people. And we call the substance that causes that difference histocompatibility complex. We call the genes that provide that difference "major histocompatibility complex genes". Everybody abbreviates that long tongue twister by just saying MHC; and every species has an MHC, a major histocompatibility gene. In a human we call it HLA.
HLA is the major group of genes that distinguishes one human being from another. It is important in transplantation, and we do HLA typing regularly. It's important to us in autoimmunity because susceptibility to autoimmunity is associated with the HLA type. It represents the most important single genetic trait in estimating susceptibility to autoimmune disease.
There are three kinds of information that tell us if autoimmune diseases are genetic. I've mentioned two. One is family clustering; the second is the association with HLA. What's the third?
The third is that autoimmune diseases occur in animals as well as in human beings. With animals we can do the breedings that are necessary.
We can infer the same must be true in humans. In animals the equivalent of HLA determines susceptibility. In animals this trait is actually predictive. In humans we aren't yet at that point because we don't have enough information from humans to say, "Because of your HLA factor you're going to develop an autoimmune disease." We can, however, say that you have a greater likelihood of this happening.
So we're getting to a point where we can almost predict who is more likely or less likely to develop autoimmune disease. Now this, again, is an example of how very basic research on a molecular level or on a genetic molecular level is beginning to pay off in human medicine.
I would like to conclude with the second half of the story. I've said that genetics accounts for about half of the risk that you develop an autoimmune disease.
The other half is the agent in the environment which triggers the process. Unfortunately, we do not know very many of the triggers. We know there are certain drugs that can induce lupus. We know there are certain environmental substances like silica that can induce scleroderma. We suspect that there are certain dietary substances, such as iodine, that can exacerbate thyroid disease. So we're beginning to define the other half of the story, the environmental half. It is going to be, I think, an equally fascinating chapter in the saga of autoimmune disease in the next decade.
So, in summary, that's what autoimmune diseases have in common. That's why we feel very strongly there should be a society like the American Autoimmune Related Diseases Association that brings together all of the research and all of the investigators and all of the physicians as well as all of the patients interested in autoimmune diseases. Let us begin to get to questions of etiology, to get at the root causes of these diseases, rather than being left at the superficial level, that is, treating the symptoms after the disease has had its destructive effects.
The multifaceted and widespread pathology of magnesium deficiency
http://www.sciencedirect.com/science/ar ... 7700911332
...The range of pathologies associated with Mg deficiency is staggering: hypertension (cardiovascular disease, kidney and liver damage, etc.), peroxynitrite damage (migraine, multiple sclerosis, glaucoma, Alzheimers disease, etc.), recurrent bacterial infection due to low levels of nitric oxide in the cavities (sinuses, vagina, middle ear, lungs, throat, etc.), fungal infections due to a depressed immune system, thiamine deactivation (low gastric acid, behavioral disorders, etc.), premenstrual syndrome, Ca deficiency (osteoporosis, hypertension, mood swings, etc.), tooth cavities, hearing loss, diabetes type II, cramps, muscle weakness, impotence (lack of NO), aggression (lack of NO), fibromas, K deficiency (arrhythmia, hypertension, some forms of cancer), Fe accumulation, etc. Finally, because there are so many variables involved in the Mg metabolism, evaluating the effect of Mg in many diseases has frustrated many researchers who have simply tried supplementation with Mg, without undertaking the task of ensuring its absorption and preventing excessive elimination, rendering the study of Mg deficiency much more difficult than for most other nutrients.
might be worthwhile to look at zinc too b/c it is also involved with fighting infection and is needed for the body to properly absorb/utilize magnesium.
serum tests of magnesium and zinc could be useful. be aware that they will come back normal, but that in order to be healthy your levels need to be very very high normal for both zinc and magnesium. being in the middle of the normal range is not even close to good enough, according to existing research on healthy controls.
take control of your own health.
pursue optimal self care, with or without a diagnosis.
if you're reacting strongly to grains you may want to check your zinc status. how much is in that multi? and what does your phone have to say about your daily zinc intake?
zinc is known to be on the low side in ms patients. it also helps you absorb other nutrients that tend to be trouble for ms patients, such as vit d3, magnesium, and vit b12.
800IU of d3 is a good start but that pill formulation is basically relying on you getting a LOT more from diet and sunshine to meet your daily needs (some sources say 4000IU gets used daily). d3 is fat soluble too, so getting adequate healthy fat in diet is definitely important. also, adding d3 should boost calcium absorption.
weakness would definitely have a logical link to depleted calcium. I don't run across calcium much as pertains ms in particular, but it's absolutely wise to address depletion in any nutrient.
glad you are feeling better
I am not sure why this is getting glossed over:
if you add d3 and calcium to your regimen, do take note of the magnesium balance or lack thereof.As far as magnesium goes, according to my phone, i get around 25 % of the 100% I should be getting every day.
you mentioned you get 300mg of calcium per day and 25% of required magnesium which I'm guessing is about 100mg. is that 100mg of magnesium coming from the multi, or foods, or a combination of the two?
either way, it looks like your daily calcium magnesium balance is about 3:1. i'd be working to push the magnesium side of the equation up somewhat. let's say, you want to be at least 2:1, if not 1:1. so if you boost your calcium intake to 1000mg per day, it would be wise to boost the magnesium intake to at least 500mg (ie 5x what you get now if my intake assumptions are on track) to get that intake ratio closer to 2:1 calcium to magnesium.
if you boost your calcium intake to 1000mg per day without balancing mag intake, do keep in mind that the recent calcium emphasis has been killing people -women in particular, cardiac issues (read 'muscle spasm') in particular- according to 2011 research findings, and it's logically directly related to ignoring the magnesium side of the equation.. I would expect additional d3 to be a drain on magnesium supplies, and since calcium competes with magnesium, with added calcium but not magnesium i'd be quite surprised really, if your spasms clear up UNLESS the foods you choose to address the d3 and calcium problems also happen to correct the low magnesium intake.
dexilant, omg another ppi ppis are known magnesium depleters. and the interference with stomach acid makes nutrient absorption difficult. you know about the increased fracture risk in ppi users? poss links to magnesium there too.
Could Magnesium Depletion Play a Role on Fracture Risk in PPI Users? (2010)
http://archinte.jamanetwork.com/article ... eid=486933
no harm trying to boost your dad's magnesium and calcium intake (in a balanced way of course) but with dexilant in the picture it could be tough. your dad sounds like a likely candidate for topical application of magnesium, eg via Epsom salts (magnesium sulfate) baths or magnesium chloride flakes baths.
if a bath is not in the picture, you can just make a solution and apply it to the affected muscle areas.
http://wellnessmama.com/5804/how-to-mak ... esium-oil/
1/2 cup Magnesium Chloride Flakes
1/2 cup distilled water
a glass bowl or glass measuring cup
A glass spray bottle (plastic will work too)
just as an aside, re the meds for GERD that treat stomach ph, researchers are finally figuring out they need to target the known-to-be-poor function of the LES not the acid level in the stomach:
Advances in Gerd (Dec 2009)
"Over the last few years, due to the effectiveness of controlling the acid component of reflux, we have become aware that up to half of these reflux patients continue to have symptoms (most commonly, regurgitation and chronic cough) and will reflux even though there is minimal acid left in the stomach, due to the relaxation (ie, opening) of the sphincter. This reflux is considered nonacid reflux or weakly acidic reflux (ie, reflux of a pH greater than 4). It is very important at this point to stress that acid is not the cause of all reflux nor the only component of reflux that causes symptoms."
in other words, the drugs never addressed the fundamental problem, ie a poorly sealed LES.
at the end of the day, you need the stomach acid to get nutrients properly. GERD allows acid into the esophagus via excessive relaxation (and possibly also via spasm) of the LES. that definitely happened to me at one time, what an awful year :S glad it's behind me. anyway. I was given nexium samples but instead I focused on making sure my LES was working properly, and it was a successful approach.
recent chats about ppis and magnesium http://www.thisisms.com/forum/general-d ... 22349.html
take control of your own health.
pursue optimal self care, with or without a diagnosis.
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