MOM and behaviors/ reply to Kathy, , and Deanna

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So why do you think the oxalates seem to bother Miralax'd children and not bother a non-miralax'd child? Deanna, notice the stiffnes, it's called tetnay, this is the side affect that your doctor tried to get away diagnosing as Guillian Bare Syndrome, there is plenty of research showing that tetnay and stiffening of the muscles are a side affect from peg, it depletes the magnesium resulting in tetnay, you might want to research this and give it to him.....I don't think he's researched the side affects of PEG............... I am concerned that because this medication IS absorbed and we don't have the WHOLE story, we are missing VIP information regarding what happens.........now. We don't have any information on where it goes, or what it does, when in fact it is absorbed? Below is just a tid bit of information of fact, that

this medication indeed causes these side affects..................Do any of these symptoms sound familiar? The 6 patients intolerant to IFN- (Table 5) were removed from the study for the following reasons: grade 3 toxicity with necrotizing skin reactions at the sites of injections (patient 1); grade 3 fatigue and difficult concentration, grade 2 joint aches, and shortness of breath (patient 9); grade 3 fatigue, aches, and depression, grade 2 nausea and stiffness (patient 14); grade 3 depression and grade 2 fatigue (patient 17); grade 3 pulmonary toxicity (patient 18); and grade 3 irritability and depression, and grade

2 fatigue and muscle and bone aches (patient 20). Side effects Toxicities at each dose level are detailed in Tables 2 and 3. At the dose level ranges of PEG IFN--2b 0.75 to 4.5 µg/kg SQ weekly, side effects were mild to moderate and included flulike symptoms (fever, chills) most prominent with the first injection, lasting for 24 to 48 hours and subsiding, fatigue, and aches. Tolerance to fever and flulike symptoms developed after multiple injections, although fatigue tended to increase. Only one patient experienced grade 2 nausea at

4.5 µg/kg, and another had grade 2 skin rash at 4.5 µg/kg (not shown for simplification). No other patients experienced such toxicities at these levels or at dose levels of 6 to 9 µg/kg. http://bloodjournal.hematologylibrary.org/cgi/content/full/98/6/1708 Description/Abstract Tissue distribution, disposition, and metabolism of /sup 3/H-cyclosporine were studied in rats after single and repeated oral doses of 10 and 30 mg/kg and after an iv dose of 3 mg/kg.^The oral doses of 10 and 30 mg/kg were dissolved in polyethylene glycol 200/ethanol or in olive oil/Labrafil/ethanol.^Absorption from both formulations was

slow and incomplete, with peak /sup 3/H blood levels at 3-4 hr.^Approximately 30% of the radioactive dose was absorbed, which is consistent with oral bioavailability data for cyclosporine.^More than 70% of the radioactivity was excreted in feces and up to 15% in urine.^Elimination via the bile accounted for 10 and 60% of the oral and iv doses, respectively.^Since unchanged cyclosporine predominated in both blood and tissues at early time points, the half-lives of the distribution phases (t 1/2 alpha) of parent drug and of total radioactivity were similar.^In blood, kidney, liver, and lymph nodes, t 1/2 alpha of cyclosporine ranged from 6-10 hr.^Elimination of radioactivity from the systemic circulation was multiphasic, with a terminal half-life of 20-30 hr.^/sup 3/H-Cyclosporine was extensively distributed throughout the body, with highest concentrations in liver, kidney, endocrine glands, and adipose tissue.^The concentrations of both total radioactivity and parent drug

were greater in tissues than in blood, which is consistent with the high lipid solubility of cyclosporine and some of its metabolites.^Skin and adipose tissue were the main storage sites for unchanged cyclosporine.^Elimination half-lives were slower for most tissues than for blood and increased with multiple dosing.^The amount of unchanged drug was negligible in urine and bile. http://www.osti.gov/energycitations/product.biblio.jsp?osti_id=6125031 Tell me this isn't scary.......................... Almost any molecule can be modified in this way. Not only are therapeutic proteins and peptides such as growth factors and blood products now being pegylated for medicinal purposes, but, because of the safety of the method, substances such as liposomes used in foods and cosmetics are also being

pegylated. Human beings could thus find themselves coming into daily contact with PEGs. 3-D Structure Interferon Look at the similarities with EG poisoning, and they can't make the connection? This is beyond unbelievable................. * Under actual conditions of use in a veterinary practice ethylene glycol (EG)poisoning may be diagnosed without using the commercial test kit ormeasurement of serum levels. While test kit results can be read in 30 minutesthe steps involved can be labor intensive. It is impractical to wait for testresults (from a diagnostic laboratory) thereby delaying treatment for this

lifethreatening emergency. History, clinical signs, etc. are practical ways ofdiagnosing suspected EG poisoning. Clinical signs present upon admission includedataxia, central nervous system depression, vomiting, disorientation, dehydration,nystagmus, polyuria and polydipsia. Sixty-three of the 105 animals had no clinicalsigns present. Of the 38 total confirmed cases, 32 had a combination of theseclinical signs present. Abnormal clinical laboratory findings included increasedserum osmolality, metabolic acidosis, hyperglycemia, calcium oxalate crystalluria,increased BUN and creatinine. http://www.fda.gov/cvm/FOI/936.htm So with all that said, how does oxalates bring out Miralax behaviors other than it still being in the system? I've read that the oxalates can cling onto virus's and when eliminating the oxalates

the virus re-occurs, do you think that this is the case with the peg? When eliminating the oxalates it could be re-releasing the peg? Jeanie Hudson wrote: Hi , You are SO right about oxalates in foods bringing about similar symptomsas while on miralax. Abby has been on a low/moderate for awhile, but recently wasgiven recipes for some great pasta/macaroni & cheese dishes. I don't know what I wasthinking but gave her a ton of soy cheese

in these dishes. Huge mistake. Soy is highin oxalates and she was having stomach aches, more constipation, more behavioral issues,itching and scratching, not sleeping well...............I think it was due to the soy.This reminder is helpful to me that she needs to stay low to moderate LOD.Kathyp.s we are at our one year miralax free anniversary !!!! Re: MOM and behaviors?LOD stands for low-oxalate diet...not a diet to lose weight but dietin the meaning of, what you consume... miralax can raise oxalatelevels is the theory and yes, for some sensitive individuals, foodscan contribute to oxalate build up in the body as well. So the

LowOxalate Diet means that you are eating the foods that are known to below-producers of oxalates, in an effort to not overburden thesensitive individuals body with too many oxalates. Too many oxalatesseems to result in similar symptoms like constipation, and the neuroand behavioral changes. Oxalates would explain why post-miralax,there would be some times where I would get a miralax flashback withmy son-- there would be a day or a moment where it was like, wow, ishis body just clearing out some of the old miralax, because this islike a deja vu... well, the more I learned about the oxalate theorywith miralax, then it made sense that chances are, that he was havingoxalate overload again, but instead of from the 17 grams of miralaxper day, it was coming from elsewhere...probably the foods he waseating at the time.