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Ya know Kim, my daughter hes really flimsy toe nails. Not so much her finger nails but I keep them short so I probbaly would not notice. But her toe nails peel and rip alot. I wonder if this does play in all this....interesting if someone could shed some light.

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My son has irregular toe nails also. They are very thin and tear easily. His finger nails are very short and the cuticles are very jagged.

 

Michele

 

Ya know Kim, my daughter hes really flimsy toe nails. Not so much her finger nails but I keep them short so I probbaly would not notice. But her toe nails peel and rip alot. I wonder if this does play in all this....interesting if someone could shed some light.
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My guy had THE WORST nails ever as an infant. His toenails wrere creey (warped, thin, and split in layers). He was quite bald, and had only fine duck fluff for the first two years of his life. Even when his hair was one inch in length, it stuck straight up as though it was charged electrically. Charming. Supplements have helped his nails dramatically, and he sprouted more hair just as his daddy started losing his. :blink:

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not to keep anyone in suspense, this whole thing just looks to be a problem with sulfur metabolism again.

 

strong thick hair and nails for both my kids

 

Cheri, I'm really glad that you posted that. My oldest son has never had any nail problems either. Just my youngest. I thought he was born with weird (short, jagged, thin nails, but I wasn't completley sure until Sunshine posted about her son. She had shared "first things noticed" about new baby and it was everything beautiful except those nails.

 

Sunshine, before I get off on a big tangent here, is your son is considered PANDAS?

 

I really like this site. Just easy practical info on sulfur stuff.

 

Found in

 

http://www.canarys-eye-view.org/metabolic_...lism/index.html

 

amino acids

methionine and cysteine, important for detoxification of the blood

taurine, which acts as a "dock" for sulfur [what does that mean?]

Sulfur-rich foods

A few sulfur compounds important to the human body:

chondroitin - a major component of cartilage; helps keep it resilient by absorbing water. Also accelerates bone mineralization & bone repair. (Biochemical basis of the pharmacologic action of chondroitin sulfates on the osteoarticular system. Bali JP, Cousse H, Neuzil E.)

heparin - a glycosaminoglycan blood anticoagulant produced by the liver

fibrinogen - a large plasma protein molecule, essential for blood clotting.

thiamine (vitamin B1): thiamin pyrophosphate participates as a coenzyme in the decarboxylation of both alpha-ketoglutarate and pyruvate, and in transketolase reactions. Important to skin

biotin - necessary for four different carboxylases (enzymes) to catalyze their specific metabolic reactions. Can only be synthesized by bacteria, yeasts, molds, algae, and some plant species. Important to hair.

beta-keratin - the main protein in nails, skin and hair. Contains cysteine.

lipoic acid - a coenzyme involved in the decarboxylation of pyruvic acid and other keto acids

coenzyme A directly involved in the metabolism of carbohydrates, proteins, and lipids, and plays a role in all the energy-requiring processes of the body

Oxytocin (the "love hormone") - has a disulfide linkage between cysteine residues, which helps form an internal ring structure.

inorganic sulfate

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Kim,

 

Thanks for highlighting the beauty in my baby! It truly was (and still is) an instant love affair, just like you read about in great literature. He is still the twinkle in my eye, despite my sarcastic comments! (I secretly loved his fluffy duck hair.... and when he was first learning to talk we would ask, "Are you a boy or a girl?". He would always tell us, "I'm a duck!".)

 

Yes, my son is PANDAS, although it is not as difinitive a diagnosis as some others here. His tics were definitely triggered by a nasty case of strep. The doctors agree that there is a correlation. However, after TONS of testing, we realize that he had underlying factors which caused him to be more at risk for a PANDAS type of reaction.

 

It's interesting that this whole thing is linked to sulfur metabolism. My son can't handle excess sulfur, but perhaps it's because his body can't process it correctly. I do think that if the molecules of sulfur are not being converted into beneficial chemicals, some could get stuck in the sulfite stage and cause toxicity. The toxins can further inhibit the activity of PST enzymes.

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Sunshine,

 

I happen to think we all have a genetic susceptabilty to gorgeous kids here :blink:

 

As always don't count on complete or accurate info here. I'm always learning and revising opinions on all of this, but here's a few thoughts. And BTW thank you to all who responded. Michelle and Myrose, I hope there is something here that you find interesting or useful.

 

Cheri and I were talking about this on the glaucoma thread. We were discussing scar tissue in relationship to all of this. My son has a friend who has basically been his best friend since 3 yr. preschool. This friend has had some mild tics. They were particularly noticable after chickenpox and mono. He cut his arm rather badly this summer. He has scar tissue almost bubbling out of the scar where the stitches were. I called his mom and asked her if he had had an infection in the cut. She said no, it looked great until the stitches came out, then all of this scar tissue appeared, but she did say that he was allergic to sulfa medications. I'm not sure how sulfa drugs fit in, but it seems it might be important.

 

I'm not sure if you have been reading Carolyn N's thread, but it looks to me like the CBS mutation and the MTHFR both could factor into this. Since your son had a + - for CBS (is that right?) It seems we are right back to methylation. Is the CBS mutation responsible for "turing off" the ability of the EXT gene to expression of heperan sulfate?

 

In one of two articles posted there (Elizabeth Waring and Susan Owens have done the most research on this, that I'm aware of) It says that you need methinione and cystein to make sulfur. With MTHFR you have a problem with B12 which results in a problem with methionine synthesis. With CBS you have a problem with converting homocystein to cystein. Lack of cystein would equal yucky nails, I believe. There has to more more involved though. Oldest son is the one with the benign tumor, youngest had the nail problem. So....?

 

The articles posted there gives some other examples of how one could end up with low sulfation. Chlorine which is being discussed on yet another thread can further reduce sulfation apparently. One more thing, it looks to me like the role of sulfate diminishes in neuronal synapsis as you age.

 

If these conditions are hereditary, why has the incidence of tics increased? You may see family members with the same mutations, but no tics. Now, remember, we have 3 studies that show higher numbers of kids that tic, with higher amts. of thimerosal (just one thing that comes to mind, I'm sure there are many environmental toxins that could be increasing odds of this, but if there is ONE thing that has been acknowledged in those studies, it was increase in tics). That bugs me. It is SO NOT focused on.

 

Now since you are a fellow bony tumor parent look at this.......bolding mine

 

http://www.researchcrossroads.com/index.ph...rant_id=3210354

 

We found that the GluR1 subunit of AMPA-type glutamate receptors binds heparin, and that surface expression of AMPA receptors is drastically reduced in EXT1-deficient neurons in vitro. Abnormalities in the glutamate receptor system have been implicated as a potential cause of autism spectrum disorders. Based on these observations, we hypothesize that neuronal HS deficiency causes abnormal glutamatergic synaptic transmission, which in turn results in the development of autistic traits. In this project, we aim at demonstrating that genetic disruption of HS synthesis results in social interaction deficits and impaired glutamate receptor function of the animal.

 

So it looks like if you have a deficiency in sulfate (heparan sulfate in this case) you have drastically reduced AMPA receptors, if their hypothesis proves correct. I suspect we are "lite" on heparan sulfate. I think that situation gets worse during illness, allergy season, diet could play a part too. I don't think PST is our biggest problem though, a factor maybe, but not the pathway that is MOST affected.

 

These GAGS are shed when there is inflammation. They are also involved in what type of infection fighters are called up, if I'm reading this right.

 

bolding mine

 

http://www.jimmunol.org/cgi/content/abstract/154/2/871

 

Heparan sulfate initiates signals in murine macrophages leading to divergent biologic outcomes

LE Wrenshall, FB Cerra, RK Singh and JL Platt

Department of Surgery, University of Minnesota, Minneapolis 55455.

 

We have previously shown that the interaction of heparan sulfate (HS), a constituent of cell surfaces and extracellular matrices, with murine macrophages causes activation of the macrophages leading to the production of cytokines and PGE2 and profound changes in the cellular immune responses triggered by the macrophages. Here we describe the molecular mechanisms that underlie these immunoregulatory changes. We demonstrate that HS delivers signals to macrophages through at least two pathways, one involving the activation of a tyrosine kinase and of nuclear factor-KB, and the other involving the activation of protein kinase C and the elevation of intracellular calcium. The former pathway is associated with the production of IL-6, and the latter pathway is associated with the production of PGE2. Our findings suggest a model in which components of the microenvironment, such as HS, may determine the functional state of an APC, thereby modifying immune responses

 

 

If you are born with a lack of sulfate, it looks like you have gut vulnerability because these things are found extensively in the gut, and they protect the lining from toxins and pathogens fungus parasites etc. Since these carbohydrate chains are negatively charged, they repel each other (in the case of chondrotin sulfate as they repel each other they cushion joints), and mediate in what type of bacteria/virus are attracted to the cell expressing them and looks like they play a role in which virus/bacteria are able to enter.

 

Cheri, if you made it this far...I'm wondering if the floppy larynx and the concave chest that you described with your affected son was cartilage that was not formed exactly right? It will try to find something to show what I'm getting at there. I'll try to get back to that.

 

As far as the finger/toe nails. I think my youngest son had MORE damage from having a hereditary condition that was worsened from day one, by getting the HEP B birth dose (oldest son didn't receive that until I believe week 5). I SAW the reaction with him flaying his head around with his mouth open. I think he tured orange and had a problem with the measles vaccine at one year because of an inability to utilize/convert beta carotein and inadequte cystein (wouldn't surprise me a bit to see CBS mutation here either) which was probably due to low stores of vit A (vit A is well known to be important in dealing with measles) His sulfur deficiency and gut damage was not allowing proper nutrient abosorbtion or adequate ability to handle

protein. He shunned it, and stopped eating normally. The weird thing, this child who is SO taste sensitive almost craves garlic and onion, both sulfur containing foods.

 

Well, If I read this back, I'll probably delete it, so I'm just going to hit send, spelling mistakes and all. There is lot's more where all of this came from, so if anyone has questions, please feel free to ask.

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Ran across this while looking for something else, had to post for anyone with limited eaters. My youngest son showed CLEAR regression in this dept, not from birth. Totally wonderful eater, until something changed. I can't help but to think of how many vaccines list anorexia in the adverse events section. That's not to say that naturally occuring illness couldn't precipitate also though.

 

http://lib.bioinfo.pl/pmid:17823502

 

Neuroendocrinology. 2007 Sep 7; : 17823502 (P,S,E,:blink: Regulation of Food Intake by Inflammatory Cytokines in the Brain.

 

Jessica B Buchanan, Rodney W Johnson

A number of inflammatory cytokines are synthesized and released after activation of the immune system. In addition to other biological effects, these cytokines can potently inhibit food intake. Cytokine-mediated inhibition of food intake is of particular importance because excessive production of peripheral inflammatory cytokines is often associated with the cachexia-anorexia syndrome seen in some chronic diseases. The weight loss in cachexia is associated with an increase in morbidity and mortality. Understanding how cytokines regulate food intake may be crucial in enhancing quality of life and facilitating recovery in patients exhibiting cachexia. This review describes the main inflammatory cytokines that influence food intake and explores how peripheral cytokines communicate with hypothalamic nuclei to influence feeding. Copyright © 2007 S. Karger AG, Basel.

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Sunshine,

 

I was hoping you would take a look at this. Geeeez Louise!

 

Again, this is from the osteo study. The two things that are supposed to be stuck in the Golgi (instead of making it to the cell surface and the extra cellular matrix) were GlcNAc and GlcA. I've been kind of ignoring the GlcA, trying to understand heparan sulfate and I still don't know where GlcNAc comes from. Does your body make it, or does it come from diet? Anyway, look at what wiki says about GlcA

 

http://en.wikipedia.org/wiki/Gluconic_acid

 

Gluconic acid occurs naturally in fruit, honey, kombucha tea, and wine. As a food additive (E574[1]), it is an acidity regulator and

The gluconate anion chelates Ca2+, Fe2+, Al3+, and other heavy metals.

 

 

I'm wondering if this means that all the boys need for a long healthy life is nicotine and wine. Ok, just trying to keep it light, this all get a bit intense at times.

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Not sure how I missed this thread, but once again my son just as Chemar's has "stong thick hair and nails."

 

Oh! And what is this about Cheri's son having a concave chest? My son has the concave chest too. Tho for some reason seems to be less pronounced since weight lifting.

 

C.P.

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CP,

 

Now remember, I don't know what I'm talking about 1/2 of the time so take this as such, ok?

 

You know what I've been looking at, so I'm just looking for any common ground. Doesn't mean there is any although, some things that I read sound quite striking with other situations here. Just wish I could understand/explain better. Anyway in the 2nd article that HSPG is "heparan sulfate protoglycans."

 

First this

 

http://www.wecare4lungs.com/pe.htm

 

What is Pectus Excavatum?

 

A pectus excavatum may be caused by an excessive overgrowth of costal (rib) cartilage, low bone densities, poor nutrition and muscle imbalances. It is found more often in boys then girls. Pectus excavatum becomes more noticeable once the child enters periods of rapid growth such as during early adolescence. It is not uncommon for a child with a pectus excavatum to also have curvature of the spine (scoliosis), a hunched over posture (kyphosis) or Vitamin D deficiency (rickets).
and

 

Pectus excavatum is the medical term for an abnormality of the rib cage that results in a caved-in or sunken appearance of the chest. This condition, which is present at birth (congenital), is due to abnormal growth of the connective tissue joining the ribs to the breastbone (sternum). Usually, the abnormality is mild and needs no treatment.

 

Now this

 

 

Several human cartilage disorders are due to loss-of-function mutations in specific ECM and cell-surface HSPG genes such as syndromes resulting from mutations in the Pln and glypican-3 genes3,4. Gene disruption of Pln and glypican-3 in mice resulted in various skeletal abnormalities analogous5-7 to the clinical features observed in humans

 

Here more of that copy

 

http://www.pubmedcentral.nih.gov/articlere...i?artid=1387052

 

Several human cartilage disorders are due to loss-of-function mutations in specific ECM and cell-surface HSPG genes such as syndromes resulting from mutations in the Pln and glypican-3 genes3,4. Gene disruption of Pln and glypican-3 in mice resulted in various skeletal abnormalities analogous5-7 to the clinical features observed in humans (chondorodystrophias/mandibular hypoplasia). Another syndrome, hereditary multiple exostoses, the most common type of tumor disorder developing primarily in long bones and characterized by inappropriate cartilage growth, results from mutations in the EXT gene family encoding for enzymes involved in HS chain assembly on proteoglycan core proteins8,9. Chondrogenesis is a complex process involving the coordinated action of many players including growth factors, their receptors, and molecules controlling their bioactivity both extracellularly and intracellularly.

 

Many chondrogenic growth factors share the property of selectively binding to HSPGs present at the cell surface and in the ECM. In several cases, these high affinity interactions lead to localized increases in soluble HS-binding growth factors to concentrations or conformations optimal for interaction with signaling receptors10. Many studies describe the expression and involvement of HS-binding growth factors during the steps leading to chondrocyte differentiation11-13. Notable examples include bone morphogenetic proteins (BMPs), fibroblast growth factor-2, and heparin-binding growth-associated molecule-pleiotrophin / midkine family members.

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Kim,

My daughter (PANDAS) allergic to sulfonamides, which do contain sulfur. Does that have anything to do with your theory on sulfur metabolism? She was give a sulfonamide for an ear infection when she was about 1 1/2 and broke out in head to hives. Just wondering when I read these posts. Thanks, Colleen

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Kim,

 

Yes, we have that under COMPOUNDS OF BACTERIAL OR YEAST/FUNGAL ORIGIN.

 

Son was very very low for both.

 

Only thing high in that compound was Hippurate. (Part of his failing to digest protein)

 

C.P.

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