Guest guest Posted October 23, 2001 Report Share Posted October 23, 2001 >My son Drew (5 yo) has been chelating for about 2 months with good success. He just did his 6th session this weekend (3on 11 off, ending Sat pm) and Sun night and today has had significant nose bleeds. He had these when he was a toddler but hasnt had any nosebleeds of significance for about 2 years. We have him on a pretty standard DAN set of megavitamins. My wife seems to remember nosebleeds being mentioned as a symptom at the Atlanta DAN conference last spring. > >Does anyone have any thoughts on the triggers for nosebleeds during chelation (or not during chelation since the timing may be coincidental. > >Thank you > > on I have no idea what nose bleeds have to do with chelation, but I CAN recall other people asking this. (Not in droves, but at least a couple of times.) Moria Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 23, 2001 Report Share Posted October 23, 2001 > >My son Drew (5 yo) has been chelating for about 2 months with good > success. He just did his 6th session this weekend (3on 11 off, ending Sat > pm) and Sun night and today has had significant nose bleeds. He had these > when he was a toddler but hasnt had any nosebleeds of significance for > about 2 years. We have him on a pretty standard DAN set of megavitamins. > My wife seems to remember nosebleeds being mentioned as a symptom at the > Atlanta DAN conference last spring. > > > >Does anyone have any thoughts on the triggers for nosebleeds during > chelation (or not during chelation since the timing may be coincidental. > >My daughter who is 8 was diagnosed with Von Willebrand, Type I less than a year after autism diagnosis. She began having nosebleeds around 18-24 mos. VW can be genetic or acquired. I am very interested in finding out if nosebleeds or clotting factors can be affected by heavy metals(mercury). Does anyone have info. regarding that DAN conference where nosebleeds was brought up as a symptom? Also, we have only done a challenge test and are doing chelation as soon as we clear up yeast from 2 rounds of antibiotics for an infection. Thanks. > > > > I have no idea what nose bleeds have to do with chelation, but I > CAN recall other people asking this. (Not in droves, but at least > a couple of times.) > > Moria Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 23, 2001 Report Share Posted October 23, 2001 > >My son Drew (5 yo) has been chelating for about 2 months with good > success. He just did his 6th session this weekend (3on 11 off, ending Sat > pm) and Sun night and today has had significant nose bleeds. He had these > when he was a toddler but hasnt had any nosebleeds of significance for > about 2 years. We have him on a pretty standard DAN set of megavitamins. > My wife seems to remember nosebleeds being mentioned as a symptom at the > Atlanta DAN conference last spring. > > > >Does anyone have any thoughts on the triggers for nosebleeds during > chelation (or not during chelation since the timing may be coincidental. > >My daughter who is 8 was diagnosed with Von Willebrand, Type I less than a year after autism diagnosis. She began having nosebleeds around 18-24 mos. VW can be genetic or acquired. I am very interested in finding out if nosebleeds or clotting factors can be affected by heavy metals(mercury). Does anyone have info. regarding that DAN conference where nosebleeds was brought up as a symptom? Also, we have only done a challenge test and are doing chelation as soon as we clear up yeast from 2 rounds of antibiotics for an infection. Thanks. > > > > I have no idea what nose bleeds have to do with chelation, but I > CAN recall other people asking this. (Not in droves, but at least > a couple of times.) > > Moria Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 24, 2001 Report Share Posted October 24, 2001 and Moria, You may be aware that I'm pretty convinced that one of the effects of mercury toxicity, and maybe the most dangerous effect, may be its effects on sulfate transport, possibly leading to sulfate deficiency. In some children, from looking at plasma amino acid levels and getting a history of their growth, it looks like many with autism may be profoundly deficient in sulfate (more so than most children with autism)...so deficient that their body breaks down muscle to get at the sulfur stored there. Just a few stories from parents on such children who have had difficulty growing, but began chelation reported adverse reactions to chelation. There stories have convinced me that some children need to get their sulfur chemistry to recover to some extent before beginning chelation. Chelation itself may strain the sulfur chemistry because DMSA has been found to be excreted in a form where it drags two cysteine's with it. Cysteine is the precursor of sulfate. Treating yeast infections may also challenge this chemistry. To highlight THAT effect, I'm putting below a paragraph I wrote four years ago when I was a caregiver for my father who had Alzheimers disease. ------------------------------- I just got back from Memphis where my father had started a round of diflucan to treat a fungal infection he has had for years. He has been on Ticlid, an anticoagulant, for three years, but on the third or fourth day of diflucan, he started to have nosebleeds, and one morning I found him with his entire shirt saturated with blood. Neither his doctor, pharmacy, or the local pharmacy school could tell me of a potential interaction, but a letter to Dr. Bill Shaw brought the suggestion that both drugs might be using the same detoxification pathway. It may be that when diflucan started " using up " that detoxification chemistry, my father might have ended up with too much active anticoagulant in his system because his body was suddently not breaking down this drug properly, even though he had been taking it without any problems for three years. This sort of phenomenon is relevant to what has been telling us about " suboptimality " issues. Things can have unanticipated effects when they occur together. ======================================= Van Willebrand factor has a lot to do with sulfated molecules, and is very related with the sort of lipid related receptors that may explain the relationship that the cholesterol disease Lemli-Opitz and the Reelin story have to autism. I've put some abstracts below investigating the role that Vwf has to do with various sulfated GAGs. If chelation and/or antifungal medication are putting a strain on sulfation chemistry, then you might expect some of these relationships to get strained. Please note the article on platelets. J Biol Chem 2001 Apr 13;276(15):11970-9 Cell surface heparan sulfate proteoglycans participate in factor VIII catabolism mediated by low density lipoprotein receptor-related protein. Sarafanov AG, Ananyeva NM, Shima M, Saenko EL. Holland Laboratory, American Red Cross, Rockville, land 20855, Washington University, Washington D.C. 20037, USA. We have demonstrated previously that catabolism of a coagulation factor VIII (fVIII) from its complex with von Willebrand factor (vWf) is mediated by low density lipoprotein receptor-related protein (LRP) (Saenko, E. L., Yakhyaev, A. V., Mikhailenko, I., Strickland, D. K., and Sarafanov, A. G. (1999) J. Biol. Chem. 274, 37685-37692). In the present study, we found that this process is facilitated by cell surface heparan sulfate proteoglycans (HSPGs). This was demonstrated by simultaneous blocking of LRP and HSPGs in model cells, which completely prevented fVIII internalization and degradation from its complex with vWf. In contrast, the selective blocking of either receptor had a lesser effect. In vivo studies of clearance of (125)I-fVIII-vWf complex in mice also demonstrated that the simultaneous blocking of HSPGs and LRP led to a more significant prolongation of fVIII half-life (5.5-fold) than blocking of LRP alone (3.5-fold). The cell culture and in vivo experiments revealed that HSPGs are also involved in another, LRP-independent pathway of fVIII catabolism. In both pathways, HSPGs act as receptors providing the initial binding of fVIII-vWf complex to cells. We demonstrated that this binding occurs via the A2 domain of fVIII, since A2, but not other portions of fVIII or isolated vWf, strongly inhibited cell surface binding of fVIII-vWf complex, and the affinities of A2 and fVIII-vWf complex for the cells were similar. The A2 site involved in binding to heparin was localized to the region 558-565, based on the ability of the corresponding synthetic peptide to inhibit A2 binding to heparin, used as a model for HSPGs. PMID: 11278379 [PubMed - indexed for MEDLINE] Ter Arkh 1998;70(3):67-71 [Leukocyte and thrombocyte glycosaminoglycans in hemophilia A and von Willebrand's disease]. [Article in Russian] Kharchenko MF, Egorova LV, Bitiukova ES, Tutova II, Nazarova NS, Papaian LP, Kargin VD. AIM: The study of glycosaminoglycanes (GAG) in leukocytes and platelets of patients with hereditary coagulopathy. MATERIALS AND METHODS: GAG concentration, composition and fraction identification were made in 25 patients with hemophilia A and 10 patients with Willebrand disease. RESULTS: In hemophiliacs, leukocytes contained low concentrations of GAG. In those with bleeding and synovitis GAG levels were lower than the average, in those with extensive hematomas in the absence of locomotor disorders the above levels were close to normal. Chondroitinsulphate dominated in GAG composition though it was less polydisperse. Heparin sulphate levels were elevated. Platelet GAG characteristics were close to normal. In Willebrand disease leukocyte GAG content and composition was similar to those in hemophilia A except some differences in electrophoretic properties of small GAG components. CONCLUSION: Metabolism and/or release of GAG from blood cells may be involved in pathogenesis of hemophilia A and Willebrand disease. PMID: 9575593 [PubMed - indexed for MEDLINE] Biochim Biophys Acta 1987 Dec 10;931(3):286-93 Platelet surface glycosaminoglycans are an effective shield for distinct platelet receptors. Steiner M. Division of Hematology/Oncology, Memorial Hospital of Rhode Island, Pawtucket 02860. The presence of glycosaminoglycans on the platelet surface was demonstrated by electronmicroscopy and biochemical analysis. Chondroitin ABC lyase was able to remove a substantial portion of the Ruthenium red-stained outer coat of platelets. Analysis of the reaction product released by the enzyme revealed chondroitin 4-sulfate. To determine the biological function of this glycosaminoglycan coat, binding studies with a variety of potential platelet ligands were performed. In decreasing order of effectiveness, chondroitin ABC lyase was able to increase the binding sites of von Willebrand factor, fibrinogen, antibody to platelet-specific antigen P1A1, Fc fragments of IgG, and monomeric IgG. No change in binding was observed with F(ab)2 fragments of IgG, wheat germ agglutinin and pokeweed mitogen. These studies indicate that glycosaminoglycans shield some platelet receptor sites from their respective ligands. Upon release of the heteropolysaccharide from the platelet surface more of these sites become accessible to the ligand. It may be significant that especially glycoproteins involved in platelet adhesion and aggregation are involved in this process. PMID: 2823910 [PubMed - indexed for MEDLINE] At 10/24/2001 +000004:09 AM, you wrote: > > > >My son Drew (5 yo) has been chelating for about 2 months with good > > success. He just did his 6th session this weekend (3on 11 off, >ending Sat > > pm) and Sun night and today has had significant nose bleeds. He >had these > > when he was a toddler but hasnt had any nosebleeds of significance >for > > about 2 years. We have him on a pretty standard DAN set of >megavitamins. > > My wife seems to remember nosebleeds being mentioned as a symptom >at the > > Atlanta DAN conference last spring. > > > > > >Does anyone have any thoughts on the triggers for nosebleeds during > > chelation (or not during chelation since the timing may be >coincidental. > > >My daughter who is 8 was diagnosed with Von Willebrand, Type I >less than a year after autism diagnosis. She began having nosebleeds >around 18-24 mos. VW can be genetic or acquired. I am very >interested in finding out if nosebleeds or clotting factors can be >affected by heavy metals(mercury). Does anyone have info. regarding >that DAN conference where nosebleeds was brought up as a symptom? >Also, we have only done a challenge test and are doing chelation as >soon as we clear up yeast from 2 rounds of antibiotics for an >infection. Thanks. > > > > > > > > I have no idea what nose bleeds have to do with chelation, but I > > CAN recall other people asking this. (Not in droves, but at least > > a couple of times.) > > > > Moria Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 24, 2001 Report Share Posted October 24, 2001 | Not sure if this will apply but nose bleeds can actually be a sign of dehydration. Also a sign of allergy. Could your kid be allergic to some supplement? My daughter's not on milk thistle due to allergy. You can spray a pure saline solution (not the preservative polluted stuff they sell - dump it out of the spray bottle and replace) to stop the bleeding. K. Quote Link to comment Share on other sites More sharing options...
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