220 replies to this topic

[doctordog]

was reading a little on copper. some sources mentioned that low copper is also linked to high ferritin (mine exceeded the normal range), so i guess that"s one more clue. on the one hand it"s a relief discovering a (potential) deficiency, but i feel so frustrated by the fact that it"s impossible to tell which of my symptoms at this point are psychological, which are biological, and which are the fallouts of med use.

*sigh*

i"m trying to pursue all three, but it"s tough finding an AD that doesn"t just make the fogginess etc. worse

[doctordog]

some sources mentioned that low copper is also linked to high ferritin (mine exceeded the normal range), so i guess that"s one more clue.

sorry i meant iron was high, not ferritin

[Lufega]

One thing I learned this past year is never to assume anything. By this I mean, just because you have a symptom that "might" be caused by a deficiency of something, doesn't mean you're actually deficient. I realized many different mechanisms can cause the same symptomatology so there isn't just one way to reach something.

With this, I started having a vast number of lab and imaging tests done. From the little you've told me, it seems you think you have low copper. It could be due to supplementing antagonists but also, your iron levels are high. Iron antagonizes copper absorption. Before you start using copper, I suggest you look into your iron status further. Have you been evaluated for hemochromatosis? What is your doctor saying about all this? Normalizing iron levels could solve your mineral imbalance. Do you supplement with iron? Eat a lot of red meat or other iron rich foods? Lactoferrin and IP6 come to mind as iron chelators (which are very good I must say) but further exploration by your Doctor is what I suggest you focus on.

Have you written about yourself in another post that I can read?

[Lufega]

I added Arginine late september because I found it alleviated tremors. But, I also noticed an increased incidence of fatigue and depression and my dysautonomia symptoms were worse. I realize I could have inadvertently re-activated Epstein barr infection/mono. This fatigue feels a lot like my initial Infectious mononucleosis at age 15. I was also eating a lot of dark chocolate, which is high in arginine. I might check the antibody titer and monotest to confirm...

Luckily, I have a kilo of Lysine handy

It looks like Lysine can benefit me in multiple ways:

1. Inhibit replication of EBV and possibly improve dysautonomia.
2. Lowers lipoprotein a, which lab tests showed was high. (per linus pauling theory)
3. Reduce chronic stress

Edited by Lufega, 06 November 2009 - 05:15 PM.

[Lufega]

I forgot another one:

4. Increase elastin and collagen production.

[doctordog]

One thing I learned this past year is never to assume anything. By this I mean, just because you have a symptom that "might" be caused by a deficiency of something, doesn't mean you're actually deficient. I realized many different mechanisms can cause the same symptomatology so there isn't just one way to reach something.

With this, I started having a vast number of lab and imaging tests done. From the little you've told me, it seems you think you have low copper. It could be due to supplementing antagonists but also, your iron levels are high. Iron antagonizes copper absorption. Before you start using copper, I suggest you look into your iron status further. Have you been evaluated for hemochromatosis? What is your doctor saying about all this? Normalizing iron levels could solve your mineral imbalance. Do you supplement with iron? Eat a lot of red meat or other iron rich foods? Lactoferrin and IP6 come to mind as iron chelators (which are very good I must say) but further exploration by your Doctor is what I suggest you focus on.

Have you written about yourself in another post that I can read?

hey sorry, didn't mean to hijack your thread. i've written about some of my problems as they crop up, but never with one big post summarizing my story; like i say, there's probably too many confounding factors to see much of a throughline at this point.

my GP didn't really want to run tests anymore because he thought i was a hypochondriac, so i left him. i ended up seeing another GP (i was having really bad nerve pain in my feet and hands which was getting worse by the day) who just prescribed me an AD and led me out the door. i looked back through my test results and found my B12 levels had dropped to about 200pmol/l, and heavy supplementation of methylb12 instantly resolved the problem.

so that's an example of why treatment for me is difficult - as soon as doctors discover i have an anxiety disorder, they pretty much refuse to run tests. even the integrative GP i saw was kinda like ... well, if things get really bad, we'll retest in a couple of months, but just stick to AD's for now. so part of the problem is i simply cannot find a responsive doctor. i am taking care of the psychiatric/psychological side (weekly CBT, AD trials), but they don't wanna take care of the other side of things. i could PM you some details/a short history if you had any suggestions of what avenues i could explore, but strictly on the condition that you had the time - i honestly don't want to burden you further, because it looks like you're dealing with a lot yourself.

[Lufega]

I have no problem helping you out, as much as my abilities will allow. Everyday I learn more and more that I don't know squat. I found a way to circumvent through the hypochondriac/anxious crazed patient label...I simply omit that part when asked. Anxiety, depression? No..never! I'm as happy as I can be bla bla bla...

Patients with emotional problems are more likely to sue than other patients, so Doctors try to be careful around them and avoid taking risks with them. It's terrible, I know. If you want, PM me.

[Lufega]

Monotest and HIV came back negative. Waiting on EBV IGM & IGG results. The monotest can be negative even if the patient has mono. It's interesting though, the CBC show low lymphocytes and high neutrophils. Hmmm...I think I have mono again, probably provoked by my dumbass self. Way to go! [pat in the back]

Edited by Lufega, 08 November 2009 - 03:07 AM.

[Lufega]

I'm starting to question whether trying to correct deficiency states is the right way to go. I feel like I'm always one step behind, trying to correct the damage inflicted on my system by viruses. When I used high dose benfotiamine with magnesium, my dysautonomia parameters improved until I ceased supplementing. Obviously, what's causing the damage is still there and that's what I really should be going after. I have a viral neuropathy manifesting as an autonomic neuropathy. I tested positive for HSV1, HSV2 and EBV. I've never had cold sored or viral warts. The HSV infection occurred at birth, and my folks tell me I was really sick my the first couple months after delivery. The herpes family loves to take residence in sensory neurons.

"Following active infection herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system."

However, I do not have paresthesias or numbness anywhere in my body. It seems my affect is at the level of the acetylcholine receptors. Mestinon improves this temporarily but this requires dosing every 3 hours and taking weeks off to avoid tolerance.

I'm going to have some tests to figure out where exactly the problem is. Next, I have to figure out if the attack is autoimmune in nature as a result of the infection, or due directly to viral residency at the receptor levels. I'm getting tired of using so many supplements.

Back in 2006, I was only using curcumin and drinking green tea instead of water. This had an inhibitory action against elastase and the results were evident. After this time, I stopped green tea and curcumin in favor of trying other supplements, none of which had any elastase inhibitory actions. Check out my profile picture from 2006 (elastase inhibition) and compare it to this one from 2009 (no elastase inhibition)

Edited by Lufega, 08 November 2009 - 06:59 PM.

[rwac]

Back in 2006, I was only using curcumin and drinking green tea instead of water. This had an inhibitory action against elastase and the results were evident. After this time, I stopped green tea and curcumin in favor of trying other supplements, none of which had any elastase inhibitory actions. Check out my profile picture from 2006 (elastase inhibition) and compare it to this one from 2009 (no elastase inhibition)

The angle is different for one thing. Also, the old picture is much, much smaller, so it's hard to tell ...

I'm seriously considering drinking white tea for it's elastase and collagenase inhibition.

[Lufega]

Anti-viral properties of green tea:

Antiviral properties of prodelphinidin B-2 3'-O-gallate from green tea leaf.

Cheng HY, Lin CC, Lin TC.

Graduate Institute of Pharmaceutical Science, College of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of China.

Prodelphinidin B-2 3-O-gallate, a proanthocyanidin gallate isolated from green tea leaf, was investigated for its anti-herpes simplex virus type 2 properties in vitro. Prodelphinidin B-2 3'-O-gallate exhibited antiviral activity with IC50 of 5.0 +/-1.0 microM and 1.6 +/-0.3 pM for XTT and plaque reduction (PRA) assays, respectively. Cytotoxicity assay had shown that prodelphinidin B-2 3'-O-gallate possessed cytotoxic effect toward Vero cell at concentration higher than its IC50. The 50% cytotoxic concentration for cell growth (CC50) was 33.3 +/- 3.7 microM. Thus, the selectivity index (SI) (ratio of IC50 to CC50) for XTT assay and PRA was 6.7 and 20.8, respectively. Prodelphinidin B-2 3'-O-gallate significantly reduced viral infectivity at concentrations 10 microM or more. Result of time-of-addition studies suggested that prodelphinidin B-2 3'-O-gallate affected the late stage of HSV-2 infection. In addition, it was also shown to inhibit the virus from attaching and penetrating into the cell. Thus, prodelphinidin B-2 3'-O-gallate was concluded to possess antiviral activity with mechanism of inhibiting viral attachment and penetration, and disturbing the late stage of viral infection.

Epigallocatechin gallate inactivates clinical isolates of herpes simplex virus.

Isaacs CE, Wen GY, Xu W, Jia JH, Rohan L, Corbo C, Di Maggio V, Jenkins EC Jr, Hillier S.

Department of Developmental Biochemistry, Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA. chisi@rcn.com

In the absence of a fully effective herpes simplex virus (HSV) vaccine, topical microbicides represent an important strategy for preventing HSV transmission. (-)-Epigallocatechin gallate (EGCG) (molecular weight, 458.4) is the primary catechin in green tea. The present study shows that EGCG has greater anti-HSV activity than other green tea catechins and inactivates multiple clinical isolates of HSV type 1 (HSV-1) and HSV-2. EGCG reduced HSV-2 titers by >or=1,000-fold in 10 to 20 min and reduced HSV-1 titers by the same amount in 30 to 40 min. The anti-HSV activity of EGCG is due to a direct effect on the virion, and incubating Vero and CV1 cells with EGCG for 48 h prior to infection with HSV-1 and HSV-2, respectively, does not reduce HSV production. Electron microscopic (EM) studies showed that purified virions exposed to EGCG were damaged, and EM immunogold labeling of the envelope glycoproteins gB and gD was significantly reduced following EGCG treatment while capsid protein labeling was unchanged. When purified HSV-1 envelope glycoproteins gB and gD were incubated with EGCG and then examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, lower-molecular-weight gB and gD bands decreased and new higher-molecular-weight bands appeared, indicating the EGCG-dependent production of macromolecular complexes. gB and gD are essential for HSV infectivity, and these results suggest that EGCG could inactivate HSV virions by binding to gB, gD, or another envelope glycoprotein. EGCG is stable in the pH range found in the vagina and appears to be a promising candidate for use in a microbicide to reduce HSV transmission.

[Lufega]

Back in 2006, I was only using curcumin and drinking green tea instead of water. This had an inhibitory action against elastase and the results were evident. After this time, I stopped green tea and curcumin in favor of trying other supplements, none of which had any elastase inhibitory actions. Check out my profile picture from 2006 (elastase inhibition) and compare it to this one from 2009 (no elastase inhibition)

The angle is different for one thing. Also, the old picture is much, much smaller, so it's hard to tell ...

I'm seriously considering drinking white tea for it's elastase and collagenase inhibition.

I started after reading Matts post last week. I add 1 teaspoon trehalose to the mix. This gives me a headache. White tea alone doesn't. Does this mean trehalose is inducing autophagy? I'm also going to order green tea again. I buy from these guys http://www.miroku-usa.com/

Good point on the pics. It's just something I've noticed. Lately, I don't like the way I look in pictures. I look old and busted. I have more wrinkles and my skin is sagging in all places. Remember, having an alpha 1 antitrypsin deficiency means Elastase is running wild in my body...

Edited by Lufega, 08 November 2009 - 07:42 PM.

[rwac]

Also, have you put on some weight since 2006 ?
It looks like more body fat is causing your cheeks to sag just a bit.

I lost about 10 lb this year, and I think I look much better now.

[graatch]

The only way Mn is toxic is when you breathe it in, working in metallurgy and such. Also, if you have liver failure and your biliary system doesn't work. I really can't find any references linking diet to any problems, under normal circumstances. Mn is a heavily misunderstood mineral.

Have you determined what sort of concentration is achieved in toxicity states, in animals or humans? That some degree of accumulation occurs over time with regular exposure/intake is clear.

Edited by graatch, 09 November 2009 - 01:47 AM.

[Lufega]

The only way Mn is toxic is when you breathe it in, working in metallurgy and such. Also, if you have liver failure and your biliary system doesn't work. I really can't find any references linking diet to any problems, under normal circumstances. Mn is a heavily misunderstood mineral.

Have you determined what sort of concentration is achieved in toxicity states, in animals or humans? That some degree of accumulation occurs over time with regular exposure/intake is clear.

From what I read, the key to reaching toxic levels is caused by an imbalance between absorption and excretion. The quantity of Mn that is consumed as a single acute dose, or multiple chronic doses, has to be very high. The body is well designed to prevent toxicity. First, it's absorbed slowly. I think only 40% (+/-) is taken up by the intestines. Second, the body rapidly eliminates it via the bile, to prevent acute toxicity. So it's very difficult to concentrate it unless you are ingesting very high doses, which would overcome the speed of excretion. Mn will become toxic at any dose in the setting of liver failure. The same way magnesium and potassium are toxic in kidney failure. In a normal diet, the body excretes 4 mg Mn per day. I assume this will be higher if intake increases. The RDA is set at 2 mg and veg. diets that consume as much as 20 mg daily showed no adverse effects long term.

In the case of aspirated Mn, the acute dose is higher and this overcomes the capability of the body to excrete it. Thus, it accumulates specifically in the areas of the body and brain where it is normally used; dopaminergic neurons, kidneys, liver, etc. This is why you read that in toxicity cases, there's higher affinity for Mn in these areas. Basically, this is where the Mn is normally used in the body. Mn is also more bioavailable dissolved in water so it overcomes both of the protective mechanisms I mentioned above: Too much is absorbed too fast and not eliminated or used by metabolic processess quickly enough. The other scenario where Mn is toxic is in infant formulas containing soy. Soy makes it more bioavailable so you have, 1. increased absorption and 2. decreased excretion. In neonates/infacts, the liver/biliary systems is not fully developed/function, so Mn accumulates.

It's hard to determine at what concentration Mn is toxic because toxicity is reached via deposits, not increased serum levels of free floating Mn. So, this cannot be measured in live persons, at least to my knowledge. Maybe by liver biopsy? I had one done this year but failed to have Mn measured.

There's one or two studies indicating Mn toxicity via some unmentioned herbal supplements with chronic use over many, many years but these don't even have abstracts available so I don't know the full details.

[Lufega]

Astragalus seems like an interesting plant. I was looking for things that could up regulate tyrosine hydroxylase. This study made me take a closer look:

The Effects of Astragalus Membranaceus on Repeated Restraint Stress-induced Biochemical and Behavioral Responses.
Park HJ, Kim HY, Yoon KH, Kim KS, Shim I.

Department of Integrative Medicine, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.

Astragalus Membranaceus (AM) is a useful Korean herb that has been clinically prescribed for stress-related illness. The objective of the present study was to examine the anti-stress effects of AM on repeated stress-induced alterations of anxiety, learning and memory in rats. Restraint stress was administered for 14 days (2h/day) and AM (400mg/kg) given by oral administration, in the AM group, for the same period. Starting on the eighth day, the rats were tested for spatial memory on the Morris water maze test (MW) and for anxiety on the elevated plus maze (EPM). Changes of expression on immunohistochemistry were studied for cholineacetyl transferase (ChAT) and tyrosine hydroxylase (TH) in the brain. The results showed that the rats treated with AM had significantly reduced stress-induced deficits on learning and memory on the spatial memory tasks. In addition, the ChAT immunoreactivities were increased. In the EPM, treatment with AM increased the time spent in the open arms (p<0.001) compared to the control group. In addition, AM treatment also normalized increases of TH expression in the LC (p<0.001). In conclusion, administration of AM improved spatial learning and memory and reduced stress-induced anxiety. Thus, the present results suggest that AM is able to recover behavioral and neurochemical impairments induced by stress

I've taken this before to boost the immune system. Ofcourse, I used doses way lower than used by this study. I also found that it can do a bunch of other things. It's antiviral ( EBV?), tones the body, decreases fatigue, etc. The different constituents have different roles. I know astragaloside IV is supposed to elongate telomeres, for example. These are others:

Constituents
Triperpenoid saponins (cycloastragenol, astragaloside I to VIII, and cyclocanthoside)
Cycloartane triterpene
Polysaccharide
Isoflavonoids
Amino acids

Based on this, it looks like the whole root is better but according to the above study, I need 36 grams a day! I wonder what they powder tastes like....According to Rosemountain herbs, it tastes sweet! and I can get 1 lb for 1 bucks.

This study is also appealing to me:

The role of astragaloside in regeneration of the peripheral nerve system
Chun-Yuan Cheng 1 2, Chun-Hsu Yao 3, Bai-Shuan Liu 3, Chien-Ju Liu 4, Guan-Wei Chen 2, Yueh-Sheng Chen 4 5 *

Abstract
The aim of this study was to evaluate peripheral nerve regeneration across a 15-mm gap in the sciatic nerve of the rat, using a silicone rubber nerve guide filled with different concentrations of astragaloside (0, 50, 100, and 200 M). Collagen was also filled in the chambers to prevent the astragaloside from leakage. At the end of 8 weeks, animals from the group treated with astragaloside, especially at the concentration of 50 M, had a higher rate of successful regeneration across the wide gap, a significantly larger number of myelinated axons, and a greater evoked action potential than the control group. However, the high-dose astragaloside (200 M) completely reversed this positive effect of growth-promoting capability and inhibited nerve regeneration. Thus, astragaloside plays a dual role in anastomosis, being salutary in aiding the growth of axons in peripheral nerve but also detrimental, terminating the nerve regenerative processes if improperly applied. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2006

[Lufega]

I went in for an electromyography and the results were abnormal. After years of guessing (correctly, mostly), I've been diagnosed with an axonal polyneuropathy. Acetylcholine production is normal and my receptors appear normal. There also is no problem with the myelinization. The problem is that I have less axons innervating muscle tissue, glands, etc., than normal. They are regressing, dying, whatever.

My Doctor did say, however, that if the cause is edentified, this process can be halted of possibly reversed. Additionally, because there are less nerves innervating muscle tissue, there is an muscular membrane hyperexcitable state. All this explains a lot. In polyneuropathy, there is a motor, sensory as well as an autonomic component. Most of my symptoms are autonomic in nature so my self-diagnosed dysautonomia was dead on.

Some of the causes she briefly mentioned were B12 deficiency and mercury poisoning. Interesting. Mercury? Regressing axons? This sounds very familiar doesn't it? Remember this video, that shows the effect of mercury on the nervous system? A cranial MRI showed no central neurodegeneration. My problem is exclusively peripheral.

I'm going to see a neurologist to identify the exact cause.

In the meanwhile, what supplements/substances induces neuronal/axonal growth??

[NDM]

the one that first comes to mind is ashwagandha; but also do a pubmed search for lithium and valproate - i remember reading some time ago some stuff about prefrontal neural regeneration as a result of taking these two.

[Lufega]

Reading into it some more, the type of polyneuropathy I have is called Distal Axonopathy. It seems to be exclusively caused by some kind of toxin. Interesting.

Distal axonopathy, or "dying-back neuropathy", is the result of some metabolic or toxic derangement of neurons. It is the most common response of neurones to metabolic or toxic disturbances, and as such may be caused by metabolic diseases such as diabetes, renal failure, deficiency syndromes such as malnutrition and alcoholism, or the effects of toxins or drugs such as chemotherapy. They can be further divided according to the type of axon affected: large-fiber, small-fiber, or both. The most distal portions of axons are usually the first to degenerate, and axonal atrophy advances slowly towards the nerve's cell body. If the cause is removed, regeneration is possible, though the prognosis depends on the duration and severity of the stimulus. Those with distal axonopathies usually present with sensorimotor disturbances that have a symmetrical "stocking and glove" distribution. Deep tendon reflexes and autonomic nervous system functions are also lost or diminished in affected areas.

Edited by Lufega, 06 December 2009 - 01:17 AM.

[VespeneGas]

Forgive me if this has been discussed and ruled out in another thread, but I can't help noticing that each of the following symptoms,

1. Connective tissue problems
2. Cardiovascular abnormalities
3. Depression, anger, emotional lability
4. Cognitive problems, fatigue
5. Poor recovery/results from exercise
6. Immune system dysregulation
7. High lipoprotein (a)
8. Tall, scrawny phenotype
9. Acne, other dermatological issues
10. Poor appetite

Can potentially directly be explained by clinically low estrogen, which you have. One possible explanation would be hyperprolactinemia (which I realize you don't suffer from now, but) which could cause:

1. Gynecomastia
2. Idiopathic parkinsons?
3. Tremors via dopamine suppression?

4. Low testosterone (which you do have) -->
a. abnormal distribution of body fat
b. low muscle mass
c. sexual dysfunction
d. poor recovery from exercise
e. emotional lability, depression, anger, anxiety
f. cognitive problems, fatigue
g. gynecomastia
h. poor appetite

And downstream of low estrogen it gets really good, with

1. Reduced cortisol/dysfunctional glucocorticoid metabolism (which you apparently don't have?) -->
a. Depression, anger, emotional lability, anxiety
b. Cognitive problems, fatigue
c. Poor recovery/results from exercise
d. Immune system dysregulation
e. low blood pressure
f. acne
g. poor sodium retention
h. urinary retention
i. Schamberg disease
j. poor appetite

2. Refractory magnesium deficiency --> Refractory potassium and thiamine deficiencies -->
a. Connective tissue problems
b. Cardiovascular abnormalities
c. Depression, anger, emotional lability, anxiety, poor stress tolerance
d. Cognitive problems, fatigue
e. neuropathies/tremors
f. hypersensitivity to noise, light
g. muscle weakness
h. hypercalcemia

Low estrogen could also explain your grandma's autoabortions, either through magnesium deficiency (preeclampsia) or through failure to suppress the TH1 response sufficiently for her immune system to tolerate the fetuses.

Did I miss anything?

[Lufega]

VG,

Thank you for taking the time. You pretty much covered all the grounds. I also considered my low estrogen levels as something I should correct. I was thinking of adding a soy extract to try and elevate it. Soy caught my interest because it increases production of hyaluronic acid and elastin while inhibiting elastase and downregulating the production of the same. I think all these are mediated by binding to estrogen receptors or something.

I asked my endocrinologist what he thought about the low E levels. He said that wasn't important. I reassured him that even males need healthy levels of E (just as women need a little T ) but he dismissed this idea. I can probably explain the low E in terms of the polyneuropathy, maybe due to decreased innervation to the adrenals. I also think that raising my estrogen levels to the normal range might alleviate many of the symptoms you listed above, especially the magnesium def. and connective tissue problems. Estrogen also increases salt and water retention, which I desperately need.

What's the best (non-pharma.) way to go about this? Should I ramp up soy consumption??

[rwac]

What's the best (non-pharma.) way to go about this? Should I ramp up soy consumption??

Soy is bad for you (thyroid, etc)

How about licorice ?
Have you tried DHEA ? I've heard that oral intake of DHEA ends up as E.

Edited by rwac, 23 December 2009 - 04:32 PM.

[Lufega]

What would be a good starting dose for DHEA?

[livingguy]

What would be a good starting dose for DHEA?

10mg per day.

[sentrysnipe]

Hello, Lufega. Are you still taking graviola?

[rwac]

Hi Lufega, Recently my doctor told me that tocotrienols are good for dysautonomia.

The catch is that tocopherols block this effect, so you need to get a supp without them.

[Lufega]

Hi Lufega, Recently my doctor told me that tocotrienols are good for dysautonomia.

The catch is that tocopherols block this effect, so you need to get a supp without them.

Thanks for the tip rwac. I think the diagnosis of dysautonomia is incomplete. Autonomic dysfunctions are part of a broader disease spectrum. I sometimes write in a dysautonomia forum but Im afraid most people there quit seeing doctors after receiving this diagnosis. There's little info there about THE CAUSES OF IT.

I just returned from my trip to Japan. I tried to have a Doctor check me out, but without insurance, no one would give me the time, even If I offered to pay cash. I did have a neurologist look at my EMG at the same hospital I was rotating. He suggested I have a mononeuritis multiplex, which is different from the distal axonopathy diagnosis I got in my country. Problem is, he also said the EMG I had done was of poor quality and technique. Sigh.

Lyme disease is one of the differentials for many types of neuropathies so that's probably the cause of your autonomic neuropathy. In my case, the differential differs by the type of neuropathy. The distal type is usually caused by some toxin while the multiplex is more commonly seen in vasculitis, amyloidosis, etc.

I learned a bit more about my problems but I still know nothing at all. I was hoping to finally get a diagnosis in Japan, but the language barrier and cultural formalities made it very difficult. However, one Doctor was very insistant that I had Sjogren's so I supposed I owe it to myself to search this through. Whatever it is I have though, it seems like will likely be incurable. I just have to prepare myself mentally for that.


edit: I also wanted to add that after living in Japan for 1 month and eating a strickly japanese diet (soy, tofu, miso, kelp, sashimi, rice, LOTS of seafood, broth based soups, noodles, 5-6 cups of green tea, japanese vegetables, exercise in the form of riding my bicycle everywhere), I feel and look better than I have in a long time.
I've heard about tocotrienols before but could produce any studies or mechanisms as to why they are helpful. Have you had any luck??

Edited by Lufega, 17 February 2010 - 09:37 AM.

[rwac]

I'm guess this is what they're going by.

Tocotrienols induce IKBKAP expression: a possible therapy for familial dysautonomia


Well I tried it on monday night, and I was feeling awesome on tuesday, right up until I took some tocopherols in a sports drink, at which point I started feeling lightheaded. Lets see how it works on the long run.

[Lufega]

I've been using astragalus whole root powder, 1 tablespoon a day. Some parameters are slowly improving. I've noticed a reduction in tremors and blood blood pooling on my feet. It also feels like my neuropathy symptoms as awhole, are slowly improving. Im going to work my way up to 3 spoonfuls per days. Muscle tone also improved.

[jazzcat]

I can't say I've read every post here but I'm wondering if you have treated your copper deficiency. In Nov '09 you had some test and the doc said something about possible cause might be B12 def or hg issues. A copper deficiency can cause the same symptoms as a B12 def. Both can be serious if left undiagnosed and untreated.

You had high B12 at the start of this thread and I think low CP besides CU def. You also have or had low estrogen.

I think the neuropathy could be explained by your copper def.

The real question is how could you have a copper deficiency. I think you were checked for CU overload.

A CU def can cause a magnesium def.