LONGECITY

It's been a while since I've followed this thread, but I think Lufega had a liver biopsy (or something similar) at some point, and that ruled out the copper deficiency. Serum tests aren't exactly the most accurate. But Lufega can update that with more info that I can.

Lufega: Did you ever get a diagnosis as to the cause of your dysautonomia and other symptoms? I recall you checking out Lyme, then you saw a neurologist, I think... but I lost track after that.

Edit: And I just went back several posts and read that you did get checked out recently, and possibly have Sjogren's... although didn't really get a final diagnosis as to the cause. Did you have high Sjogren antibodies?
Edited by nameless, 12 March 2010 - 09:02 PM.

I found the post about his liver biopsy. His liver stores were in normal range. I forget now how long ago that was done.

If he is still taking 1 gram of MSM then that is why he has a copper deficiency.

Supplementing cu when deficient - particularly if the deficienncy is long standing - can help the neuropathy, though it will probably take some time.

I moved past the copper issue once I had the liver biopsy. All these mineral deficiencies I'm having, I realized, had a common link. So I went after that. The picture is very clear now. I have a mononeuritis multiplex associated with an autonomic neuropathy. The likely cause is Sjogren's but I couldn't get tested while I was in Japan. However, I have tested some paremeters like ANA and CRP before but those turned out negative. There is a type of Sjogren's that is ANA negative though.

Anyways, Sjogren's is associated with EBV infection and it makes sense. EBV is transmitted via saliva and this is where the body goes after the infection. The result is an auto attack on your salivary and tear glands/duct, right where EBV hides. It seems very logical to me now. Sorry I didn't save the link to back this up, but the connection has been well established. Many of my symptoms can be explained by specific mineral deficiencies but I've been supplementing endlessly with little progress.

I posted a study earlier ( I think) that suggested eradicating EBV and herpes virus using valtrex for at least one year. I've also read studies that say melatonin and astragalus enhances the antiviral action of it. So, that's what going to do. Try to eradicate EBV once and for all.

Astragalus seems like a cure-all panacea. The more I read about it, the more impressed I am. It does so much and it's dirt cheap. Like I said before, Im also noticing some improvement.

Additionally, I've cut out all grains and Im restricting the amount of calories I eat per day, although I'm not actually following a CR diet. Im making bone broth at home and re-adding foods like blueberries, coconuts and aloe and drinking green tea each day.

Some bands that were positive on the IGenex test can also be because of EBV. So Im sending a sample to test the C3 peptide ( I think?) so this should tell me whether the problem is Lyme of EBV.

Im also going to see an ENT and a neurologist here to determine whether it's Sjogren's or some other problem like amyloidosis. Either way, I think the thing to do is go after EBV and regenerate the peripheral nervous system with astragalus.

I assumed they diagnosed Sjogren's by testing for raised antibodies. If you have it, I think you also get dry eyes/dry mouth, etc. I recall my doc testing for it a while ago, because it can sometimes raise thyroid antibodies (I think), but I didn't have the dry mouth problem and my antibodies for Sjogren's came back fine.

And for EBV, did you test positive for an active infection?

Seeing another neurologist and ENT is a good idea -- they can run some extra tests, although I wasn't fond of that muscle pin sticking/nerve test neurologists like to do.

For Lyme, I'm not sure if C3 is a great marker for it, exactly. I think a low level can indicate an infection, but it doesn't really tell you what is causing the infection. It's worth getting tested, and maybe CD57, but a low level will just tell you that your body is fighting something, but not necessarily tell you what -- or at least that is what I have been told.

I think a better test would be to get EBV and other viruses checked. If they all come back IGM negative, they are unlikely to impact the IGM portion of the Igenex test. Check for all co-infections, including rickettsia stuff. And do an antibiotic trial for Lyme -- if antibiotics don't provoke some sort of reaction, it may be something else going on.
Edited by nameless, 13 March 2010 - 07:41 PM.

I'll update my stack in a few days. For now, I've removed magnesium and quercetin. They are making aggravating hypotension at this moment.

I'll update my stack in a few days. For now, I've removed magnesium and quercetin. They are making aggravating hypotension at this moment.

Actually, that's kinda interesting. Magnesium may not be agreeing with me either. Let's see if I can drop it.

Updated my stack on page 1

Hey Lufega, this may be a bit off-topic, but I've seen you endorse graviola more than once in the site. I was wondering if the atypical parkinsonism side effect is reversible among the Caribbean / Southern American people who have this fruit as a staple.

I've only read one reference on graviola dosage advising a 2-3 week rest interval, similar to adaptogen cycling. That was from Ray Sahelian's website.

Thanks!

Lufega, I'm assuming the Jarrow's NAG is N Acetyl Glucosamine. If this is correct, what are you taking NAG for?

Hey Lufega, this may be a bit off-topic, but I've seen you endorse graviola more than once in the site. I was wondering if the atypical parkinsonism side effect is reversible among the Caribbean / Southern American people who have this fruit as a staple.

I've only read one reference on graviola dosage advising a 2-3 week rest interval, similar to adaptogen cycling. That was from Ray Sahelian's website.

Thanks!

The atypical parkinsonism if caused by an agent found in the seed. Our grandmothers taught us to always remove the seeds before eating or processing the fruit. The leaves do not appear to cause this.

Lufega, I'm assuming the Jarrow's NAG is N Acetyl Glucosamine. If this is correct, what are you taking NAG for?

I take it because a study showed that oral NAG can increase hyaluronic production in the body. It should be in my thread somewhere. I'm hoping NAG can be a less expensive replacement for hyaluronic acid supplements. It's good for the joints, connective tissue and digestive tract!

I don't know if this is relevant, or if you still suspect Lyme, but I have read that NAG + Lyme may not be such a good idea:

http://digitalcommon...ons/AAI3380537/

This doesn't necessarily mean NAG + Lyme leads to problems, but it's something you may want to research more.

I don't know if this is relevant, or if you still suspect Lyme, but I have read that NAG + Lyme may not be such a good idea:

http://digitalcommon...ons/AAI3380537/

This doesn't necessarily mean NAG + Lyme leads to problems, but it's something you may want to research more.

I wonder if this is a case where NAG is used up by the Borellia burgdorferi and more needs to be supplemented, or, NAG feeds the Borellia burgdorferi and allows it to thrive.

removed Melatonin. I think it was exacerbating gynecomastia and I definitely felt a decrease in libido. Yonkers!

Also removed Rutin/Quercetin temporarily. Gave it to my friend to help with her asthma.
Edited by Lufega, 10 April 2010 - 05:00 AM.

Lufega,

http://www.iherb.com...sules/2383?at=0

Is Twinlab manganese gluconate alright? I'd buy the Carlson chelated version, but it's about $5 more expensive and it will be my first time trying Mn.

Don't mean to hijack the thread or anything.
Edited by TigerMask, 18 April 2010 - 06:11 AM.

I should of just put my above post in the 'Manganese' thread. I think I'm going to do that now. If you have any input, you can answer it here or there.



EDIT: Oops, looks like that thread was about manganese in food. I haven't found any other recent threads on manganese, so I'll just leave this question here. If anyone else (besides Lufega) has any input on my question, that would be fine too.

I'll be trialing the Mn for social anxiety and depression, if that helps.
Edited by TigerMask, 18 April 2010 - 08:52 AM.

I'd chip in the extra buck and go for Carlson. I like their quality.

I will probably do that. IHerb has it back in stock.

What's confusing to me is the difference between bisglycinate and glycinate chelate. I've done some research, and I all I can really come up with is that they are likely the same thing, interchangeable.

Removed Astragalus. In theory, if it increases immune function, it will upregulate the activity of neutrophils and thus increase elastase secretion. I started having breathing difficulty again and the fatigue I'm experiencing lately is debilitating.

Astragalus did help me get rid of much of my body fat but it did nothing for saggy skin. For that, I'm using a homemade elastase inhibiting toner. My immune system was revved up to the max. Any small cut or abrasion produce a big immune response and inflammation. Also, while everyone around me was coming down with something, I was solid.

Can't really judge if it did anything for the nervous system. First few weeks made me sleepy and it made me hypotense a few times. I also notice my skin looks a lot better but that could be due to other things.

Here's a good review of alpha1 antitrypsin deficiency

http://www.ncbi.nlm....p;part=alpha1-a
Edited by Lufega, 23 May 2010 - 01:18 AM.

High dose astragalus failed miserably, partly due to my own oversight. I feel like hell right now. I possible worsened my disease outcome and on top of that, I am also getting over metronidazole toxicity. The fatigue is overwhealming right now.

However, curcumin has always shown to be promising in treating everything. I always pushed it aside to try newer and fancier things. After reading this study though, I'm going to try using ~5 grams C3 curcumin dissolved in my coconut milk shake (oh god!) and see what happens.

Curcumin attenuates elastase- and cigarette smoke-induced pulmonary emphysema in mice.
Suzuki M, Betsuyaku T, Ito Y, Nagai K, Odajima N, Moriyama C, Nasuhara Y, Nishimura M.

First Department of Medicine, Hokkaido University School of Medicine, Sapporo 060-8638, Japan.

Abstract
Curcumin, a yellow pigment obtained from turmeric (Curcumina longa), is a dietary polyphenol that has been reported to possess anti-inflammatory and antioxidant properties. The effect of curcumin against the development of pulmonary emphysema in animal models is unknown. The aim of this study was to determine whether curcumin is able to attenuate the development of pulmonary emphysema in mice. Nine-week-old male C57BL/6J mice were treated with intratracheal porcine pancreatic elastase (PPE) or exposed to mainstream cigarette smoke (CS) (60 min/day for 10 consecutive days or 5 days/wk for 12 wk) to induce pulmonary inflammation and emphysema. Curcumin (100 mg/kg) or vehicle was administrated daily by oral gavage 1 h and 24 h before intratracheal PPE treatment and daily thereafter throughout a 21-day period in PPE-exposed mice and 1 h before each CS exposure in CS-exposed mice. As a result, curcumin treatment significantly inhibited PPE-induced increase of neutrophils in bronchoalveolar lavage fluid at 6 h and on day 1 after PPE administration, with an increase in antioxidant gene expression at 6 h and significantly attenuated PPE-induced air space enlargement on day 21. It was also found that curcumin treatment significantly inhibited CS-induced increase of neutrophils and macrophages in bronchoalveolar lavage fluid after 10 consecutive days of CS exposure and significantly attenuated CS-induced air space enlargement after 12 wk of CS exposure. In conclusion, oral curcumin administration attenuated PPE- and CS-induced pulmonary inflammation and emphysema in mice.

Astragalus did the opposite, possibly increasing neutrophil degranulation and serine proteases secretion since I started having emphysema symptoms once again. You live and learn.

Also, today I was supposed to get IV magnesium sulfate and thiamin, but I chickened out !
Edited by Lufega, 30 May 2010 - 12:21 AM.

I saw a geneticist a few weeks ago and she diagnosed me with Ehlers Danlos syndrome. This is one of the types of connective tissue disorders that I found as a differential diagnosis for myself. Interestingly enough, there is a type 9, that is associated with a copper transport problem.

At this same time, I started using zinc, since some types of EDS are found to be caused by low levels. What I found was, supplemental zinc worsened my skin laxity. So the skin all over my body sagged more.. Intuitively, I dropped the zinc and started using copper once again. All these changes are slowly reversing. The copper is helping wonderfully. I guess I was right all along,..it was the copper !

I also want to add that I found studies supporting my copper theory. Low copper can cause neuropathy because it is needed for myelin formation. Low copper was also found to cause emphysema and while the mechanism is unknown, I think it is because it is needed for the formation of alpha 1 antirypsin. I sent in my genetic test for AAT def a few week ago. Now I suspect that it will be negative for a heritable disorder. I think the cause is low copper. Copper is also needed for dopamine and norepinephrine formation so all this stuff is relevant. I've been without internet for three weeks now, so I'll post additional info. when I plug in again.

I also notice much less anxiety since starting copper once again. This truly is miraculous.

A novel therapeutic strategy for Ehlers-Danlos syndrome based on nutritional supplements.
Mantle D, Wilkins RM, Preedy V.

Pharma Nord (UK), Telford Court, Morpeth, Northumberland NE61 2DB, UK. pharma.nord4@btconnect.com


Abstract
Ehlers-Danlos syndrome is a rare disorder, comprising a group of related inherited disorders of connective tissue, resulting from underlying abnormalities in the synthesis and metabolism of collagen. This proposal is specifically concerned with Ehlers-Danlos syndrome classic type (formerly Types I-III), which is characterized by joint hypermobility and susceptibility to injury/arthritis, skin and vascular problems (including easy bruising, bleeding, varicose veins and poor tissue healing), cardiac mitral valve prolapse, musculo-skeletal problems (myopathy, myalgia, spinal scoliosis, osteoporosis), and susceptibility to periodontitis. No treatment is currently available for this disorder. The novel aspect of this proposal is based on: (i) increasing scientific evidence that nutrition may be a major factor in the pathogenesis of many disorders once thought to result from defective genes alone; (ii) the recognition that many of the symptoms associated with Ehlers-Danlos syndrome are also characteristic of nutritional deficiencies; (iii) the synergistic action within the body of appropriate combinations of nutritional supplements in promoting normal tissue function. We therefore hypothesize that the symptoms associated with Ehlers-Danlos syndrome may be successfully alleviated using a specific (and potentially synergistic) combination of nutritional supplements, comprising calcium, carnitine, coenzyme Q(10), glucosamine, magnesium, methyl sulphonyl methane, pycnogenol, silica, vitamin C, and vitamin K, at dosages which have previously been demonstrated to be effective against the above symptoms in other disorders.

PMID: 15607555 [PubMed - indexed for MEDLINE]

I wish I could find the full paper, but I guess you've already tried most of those. I have some of the symptoms of Ehlers-Danlos too, or perhaps just very copper deficient.

The genetic test came in for alpha-1-antitrypsin. I have the PiMZ phenotype. I don't have the severe type so I should live a long and (healthy?) life.

* PiMM: 100% (normal)
* PiMS: 80% of normal serum level of A1AT
* PiSS: 60% of normal serum level of A1AT
* PiMZ: 60% of normal serum level of A1AT
* PiSZ: 40% of normal serum level of A1AT
* PiZZ: 10-15% (severe alpha 1-antitrypsin deficiency)

Interesting enough, I was also given a diagnosis of ehlers danlos earlier. I found at least one study of a patient with these two conditions. What are the odds ??

[Complete alpha-1-antitrypsin deficiency in a patient with Ehlers-Danlos syndrome]

[Article in French]

Achten G, Ledoux-Corbusier M, Schandevyl W, Buneaux JJ.
Abstract

Complete alpha-1-antitrypsin deficiency of the type PiOO associated with chronic obstructive lung disease, cutaneous hyperextensibility and hyperlaxity of joints were found in a nineteen-year-old Moroccan boy. On a nosological point of view, this patient could be included as a 8th form, in the Ehlers-Danlos syndrome which now groups seven clinical variants. A causal relationship between the biological deficiency and the clinical alterations (pulmonary, cutaneous and articular) could be assumed according to the biological and ultrastructural findings.

PMID: 1088061 [PubMed - indexed for MEDLINE]

Have you tried eating a source of collagen, like gelatin or jello ?

It seems to be helping my GI problems a bit, anyway.

Have you tried eating a source of collagen, like gelatin or jello ?

It seems to be helping my GI problems a bit, anyway.

I do use Gelatin actually. It makes my hair and nails grow very fast and strong. The only way I can judge if something is affecting my connective tissue is the laxity of my skin. I really can't measure what's happening inside my body. Gelatin doesn't do much for that but it makes my skin seem fuller.

Something in my current stack is not agreeing with me. I'm fat. I gained a bunch of weight suddenly and I'm also feeling very, very depressed. It's time for an overhaul again.

In the last month of two I've gained 20 pounds. I had no idea how this happened until now. At the same time, I added copper. Copper is supposed to help with skin laxity and other connective tissue problems. For this reason, it's helping a bit. I also noticed an increase in strength, muscle volume and muscle tone. One sign of copper deficiency is low muscle tone. Interestingly enough, low muscle tone is also seen in cerebellar degeneration (this is also one of the causes of essential tremor, which I have). Lack of copper causes cerebellar degeneration. Funny how these all fit together.

It seems those extra 20 lbs. are not all fat. My legs feel more toned and muscular than they've ever been in my life. I'm not working out at this time. Unfortunately, copper also seems to increase fat deposition in the body. So as of right now, I look like a fat cow. I stopped using copper a few ago and I alreadly notice a slimming difference. On the other hand, zinc appears to keep this fat depot at bay. There's a good reason to keep minerals and their antagonists in balance. By the way, copper was also making me feel severe depressed, unmotivated and my social anxiety was also back. This is because copper upregulates monoamine oxidase, which degrades catecholamines. This makes sense as MAO-inhibitors and used to treat depression and social anxiety. Bummer.

Reduction of fat deposition by combined inhibition of monoamine oxidases and semicarbazide-sensitive amine oxidases in obese Zucker rats.
Carpéné C, Iffiú-Soltesz Z, Bour S, Prévot D, Valet P.

Institut National de la Santé et de la Recherche Médicale, INSERM U858 équipe 3, Université Paul Sabatier, IFR31, Centre Hospitalier Universitaire de Rangueil, BP 84225, 31432 Toulouse Cedex 4, France. carpene@toulouse.inserm.fr


Abstract
Semicarbazide-sensitive amine oxidase (SSAO) and monoamine oxidases (MAO) are highly expressed in adipocytes and generate hydrogen peroxide when activated. Consequently, high concentrations of MAO- or SSAO-substrates acutely stimulate glucose transport and inhibit lipolysis in isolated adipocytes in a hydrogen peroxide-dependent manner. Chronic treatments with MAO and SSAO substrates also increase in vitro adipogenesis and in vivo glucose utilization and fat deposition in diabetic rodents. To further investigate the interplay between amine oxidases, energy balance and fat deposition, prolonged MAO and/or SSAO blockade was performed in obese rats. Pargyline (P, MAO inhibitor), semicarbazide (S, SSAO inhibitor), alone or in combination (P+S), were daily i.p. administered for 3-5 weeks to obese Zucker rats at doses ranging from 20 to 300 micromol/kg. P+S treatments abolished MAO and SSAO activities in any tested tissue. P and S led to a 12-17% reduction of food intake when given in combination but were inactive when given separately. Despite a similar body weight gain reduction in P+S-treated and pair-fed rats, the mitigation of fat deposition was greater in rats receiving both inhibitors. Adipocytes from P+S-treated rats responded as control to insulin but exhibited impaired responses to tyramine, benzylamine or methylamine plus vanadate when considering glucose transport activation or lipolysis inhibition. Although our results did not directly demonstrate that amines are able to spontaneously produce in vivo the insulin-like effects described in vitro, we propose that P+S-induced reduction of fat deposition results from decreased food intake and from impaired MAO- and SSAO-dependent lipogenic and antilipolytic actions of endogenous or alimentary amines.

So, MAO increases production of new fat cells, decreases their breakdown and increases glucose transport into them. Ouch !

How much copper were you taking ?

How much copper were you taking ?

3 mg Copper Sebacate daily.

On the other hand, Manganese seems to counter all the effects of copper.

From here: http://www.ithyroid....ao_and_maoi.htm

Quite a few studies have been done on rats showing the effects of manganese on MAO. One study showed that prolonged exposure to low levels of manganese caused MAO to be decreased significantly. Another study showed that manganese given to rats at high levels showed significant reduction in both MAO-A and MAO-B. Another study showed that manganese in rat drinking water decreased dopamine beta-hydoxylase. A study showed manganese-exposed human workers in a ferro-alloy manufacturing plant had lower MAO-B activity. Since manganese is copper and iron antagonist, it appears that the effects of manganese on MAO are mediated by decreasing copper and iron levels.

This is true from personal experience. When I use manganese I have no social anxiety. Mn seems to act as a natural MAOi. Makes sense. I was also leaner and more outgoing when I used manganese.

The genetic test came in for alpha-1-antitrypsin. I have the PiMZ phenotype. I don't have the severe type so I should live a long and (healthy?) life.

* PiMM: 100% (normal)
* PiMS: 80% of normal serum level of A1AT
* PiSS: 60% of normal serum level of A1AT
* PiMZ: 60% of normal serum level of A1AT
* PiSZ: 40% of normal serum level of A1AT
* PiZZ: 10-15% (severe alpha 1-antitrypsin deficiency)

There was a big mistake. A relative gave me the results over the phone and I guess they didn't know how to read it. I finally got the hard copy of the test. I do not have the MZ genotype like I thought before. Instead, it's much worse. I have the PiSNull. This is bad. This means, I have one gene that produces bad antitrypsin protein, the "S". Another gene, the "null", produces NO AAT at all. Nothing, nada !

From the letter "Individuals with SNull or ZNull genotypes are more severely deficient and have risks for lung and liver diseases similar to Pi ZZ participants." So I have a rare form that is as bad or worse and the worst of the comon types, the PiZZ.

I'mma gonna die ! jeje

Last night I had to rush to the ER with profuse sweating and breathing difficulties. "IT HAS BEGUN !"