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You are an intelligent person. Reread every word in my post at least three more times. Every word is true. We can currently track the relative gray matter shrinkage in infants from the first bottle of iron fortified formula milk. The pathology is underway before the kids have teeth and any other evidence of disease. The iron causes the gray matter shrinkage and is continuous throughout life. We can reverse the cell senescence with iron chelators and improve cognition/working memory in Down syndrome individuals.

I read it. I discounted it. Who is "We" in "We can". . . and where are these 50-60 articles published? I am curious because there are hundreds of "scientific journals" that publish on payment from the authors. . . and their "peer-reviewed" articles are bogus hokum. In other words, some published articles are not worth the spit to make spit wads out of them.

For example, how do you track the "shrinkage of gray matter over 30K years in the fossil record, when I know of very few human brains that have ever been fossilized. . . and there are VERY few fossils that are as young as 30K years.

That's just one of the reasons I discounted it: on the face of it, it's a false claim.

Secondly, the human body is an extremely efficient machine at extracting from normal dietary intake what it needs to include in its cellular structure and to remove from its structure what it does not need. It excretes what it doesn't need. . . especially iron. The effect of LEAD in the environment over the period in question is much more striking in the brains of children in our inner cities and it is HARD to quantify its effects. The effects of the drugs and alcohol their parents injected, ingested and inhaled while the child was in utero or the spermatozoa was being formed probably has one hell of a lot more effect on brain growth and size in the time that milk and bread had iron fortified vitamins added as a component than anything you can claim is caused by someone who really cannot make a causal relation based on any statistical claims. Correlation is NOT causation. . . even for oral spirochetes and the 95% correlation that Dr. McKlosky has identified until she applied Hills and Koch's criteria and proved it.

Complete cellular chelation of Iron would be very difficult considering Iron is a necessary component of blood. . . which anyone would know who has a basic understanding of the Oxygen transportation system in our bodies. One chelates people who suffer from Hemochromatosis, an over abundance of red blood cells either through illness or through transfusions. Iron Chelation can have serious side effects if not monitored by a qualified medical doctor. Yes, there does seem possible a benefit for some Down Syndrome persons. . . but at this point nothing has been clinically proved. Obviously you believe that diet can solve every problem. Would that were true. It isn't.

Hey Swordmaker, 60 Iron chelation studies published in just 2014 Nobody but a liberal would conflate CHELATING EXCESS IRON into chelating all iron. Get yourself a couple more PhD's in cell biology and biochemistry and maybe you can broaden my horizons a little. Zn/Ga-DFO iron-chelating complex attenuates the inflammatory process in a mouse model of asthma. http://www.ncbi.nlm.nih.gov/pubmed/25009783 ambient air pollutants on longitudinal changes in exhaled nitric oxide (FeNO), a potentially useful biomarker of eosinophilic airway inflammation, http://www.ncbi.nlm.nih.gov/pubmed/24696513 The concentration of iron in real-world geogenic PM₁₀ is associated with increased inflammation and deficits in lung function in mice. http://www.ncbi.nlm.nih.gov/pubmed/24587402 Iron Chelators Increase IKBα Expression, Modulate CDK2 and CDK9 activities and Inhibit HIV-1 Transcription. http://www.ncbi.nlm.nih.gov/pubmed/25155598 pediatric cancer patients, and report our experience with Iron Chelation Therapy (ICT). http://www.ncbi.nlm.nih.gov/pubmed/25154390 The iron chelator, DFX, can decrease the concentrations of iron and ferritin after cerebral hemorrhage and can thereby decrease the incidence of hydrocephalus. In addition, after IVH, the gene expression of Wnt1 and Wnt3a was enhanced, with protein expression also upregulated; DFX was able to suppress both gene and protein expression of Wnt1 and Wnt3a in brain tissue. http://www.ncbi.nlm.nih.gov/pubmed/25152462 Our results show that more than 50% of children with SCD have inadequate control of iron overload with DFX. http://www.ncbi.nlm.nih.gov/pubmed/25138173 It is concluded that iron chelation therapy can improve the efficacy of EPO to alleviate EPO resistance in patients wtih anemic MDS, decrease the pathological level of EPO, enhance Hb levels and reduce the dependency on blood transfusion. http://www.ncbi.nlm.nih.gov/pubmed/25130822 There are current clinical trials of minimally invasive hematoma removal and iron chelation which may limit such dysfunction. Understanding the mechanisms underlying the initial hemorrhage and secondary BBB dysfunction in ICH is vital for developing methods to prevent and treat this devastating form of stroke. http://www.ncbi.nlm.nih.gov/pubmed/25120903 Iron scavengers (chelators) offer therapeutic opportunities in anticancer drug design by targeting the increased demand for iron in cancer cells as compared to normal cells. http://www.ncbi.nlm.nih.gov/pubmed/25100578 Pulmonary hypertension associated with hemolytic disorders was moved from WHO group I to group V PH diseases. Treatment strategies are also unique and include blood transfusion, iron chelation, http://www.ncbi.nlm.nih.gov/pubmed/25077000 Treatment of iron overload requires robust estimates of total-body iron burden and its response to iron chelation therapy. Compliance with chelation therapy varies considerably among patients, and individual reporting is notoriously unreliable. http://www.ncbi.nlm.nih.gov/pubmed/25064711 gaba chelates iron http://www.ncbi.nlm.nih.gov/pubmed/1755517 Potentially, diets rich in polyphenols might be beneficial for patients groups at risk of iron loading by limiting the rate of intestinal iron absorption. http://www.ncbi.nlm.nih.gov/pubmed/25058155 Our data show that TPEN induces cell death by chelating copper to produce TPEN-copper complexes that engage in redox cycling to selectively eliminate colon cancer cells. http://www.ncbi.nlm.nih.gov/pubmed/25047035 Chlamydia trachomatis (Ct) is a bacterial human pathogen responsible for the development of trachoma, the worldwide infection leading to blindness, and is also a major cause of sexually transmitted diseases. As iron is an essential metabolite for this bacterium, iron depletion presents a promising strategy to limit Ct proliferation. http://www.ncbi.nlm.nih.gov/pubmed/25027937 We previously showed that ceruloplasmin knockout (CP KO) mice exhibit Parkinsonian neurodegeneration (~30% nigral loss) by 6 months, which is prevented by iron chelation. http://www.ncbi.nlm.nih.gov/pubmed/25011704 Zn/Ga-DFO iron-chelating complex attenuates the inflammatory process in a mouse model of asthma. http://www.ncbi.nlm.nih.gov/pubmed/25009783 Iron Chelating Strategies in Systemic Metal Overload, Neurodegeneration and Cancer. http://www.ncbi.nlm.nih.gov/pubmed/25005181 Iron chelators induce autophagic cell death in multiple myeloma cells. http://www.ncbi.nlm.nih.gov/pubmed/24998390 Iron-enhanced coagulation is attenuated by chelation A thrombelastographic and ultrastructural analysis. http://www.ncbi.nlm.nih.gov/pubmed/24991945 We hypothesized that the robust immune response to Ent and Lcn2 requires iron chelation rather than the Ent+Lcn2 complex itself and also can be stimulated by Lcn2-evasive siderophores. http://www.ncbi.nlm.nih.gov/pubmed/24980968 Antioxidant properties investigated included scavenging of free radicals, iron chelation and the inhibition of lipid peroxidation http://www.ncbi.nlm.nih.gov/pubmed/24976244 iron in excess impaired differentiation, but this antiadipogenic effect was less pronounced than under iron chelation. Of interest, expression of several genes involved in mitochondrial biogenesis occurred in parallel with expression of iron-related genes both during adipogenesis and in human adipose tissue. http://www.ncbi.nlm.nih.gov/pubmed/24973963 To investigate the retinal-protective effects of the oral iron chelator deferiprone (DFP) in mice lacking the iron regulatory hormone hepcidin (Hepc). http://www.ncbi.nlm.nih.gov/pubmed/24970260 Iron chelation therapy with deferasirox in the management of iron overload in primary myelofibrosis. http://www.ncbi.nlm.nih.gov/pubmed/24959339 Although there is currently not enough evidence to support clinical use of iron chelation in MS, an overview of studies of iron chelation or antioxidant therapies will be also provided. http://www.ncbi.nlm.nih.gov/pubmed/24929968 Intranasally-administered deferoxamine mitigates toxicity of 6-OHDA in a rat model of Parkinson׳s disease. http://www.ncbi.nlm.nih.gov/pubmed/24928620 Benzylidene acylhydrazides inhibit chlamydial growth in a type III secretion- and iron chelation-independent manner. http://www.ncbi.nlm.nih.gov/pubmed/24914180 iron sensing. Part 2. Experimental detection of free iron concentration (pFe) in urine samples. http://www.ncbi.nlm.nih.gov/pubmed/24883429 Major preclinical and clinical trials have shown advances in iron-chelation therapy for the treatment of iron-overload disease as well as cardiovascular and chronic inflammatory diseases. http://www.ncbi.nlm.nih.gov/pubmed/24888568 We found that AT101 caused caspase-independent, non-apoptotic MPNST cell( malignant peripheral nerve sheath tumor cells) death, which was accompanied by autophagy and was mediated through HIF-1α induced expression of the atypical BH3-only protein BNIP3. These effects were mediated by intracellular iron chelation, a previously unreported mechanism of AT101 cytotoxicity. http://www.ncbi.nlm.nih.gov/pubmed/24824755 We found rHuEPO to be a potent scavenger of HO˙ (kr = 1.03-1.66 × 1011 m-1 s-1 ) with the capacity to inhibit Fenton chemistry through catalytic iron chelation. http://www.ncbi.nlm.nih.gov/pubmed/24811856 Patients presenting with resectable or advanced OAC could be considered as candidates for a clinical trial of iron chelation therapy as an addition to standard neoadjuvant or palliative treatments. http://www.ncbi.nlm.nih.gov/pubmed/24780018 effective iron chelators are now available, including preparations that can be taken orally. This has resulted in substantial improvement in mortality and morbidity for patients with severe chronic iron overload. http://www.ncbi.nlm.nih.gov/pubmed/24726864 A few studies have shown that iron and proteins related to iron metabolism are closely related to HILI, and iron chelation may exert protective effects on HILI. http://www.ncbi.nlm.nih.gov/pubmed/24649714 Currently, the goal of iron chelation has shifted from treating iron overload to preventing iron accumulation and iron-induced end-organ complications, http://www.ncbi.nlm.nih.gov/pubmed/24646011 Early chelation of blood-derived iron and antioxidant treatment mitigated early motor-neuronal injury. Our data suggest that BSCB breakdown contributes to early motor-neuron degeneration in ALS mice and that restoring BSCB integrity during an early disease phase retards the disease process. http://www.ncbi.nlm.nih.gov/pubmed/24591593 Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction. http://www.ncbi.nlm.nih.gov/pubmed/24586712 Diethylenetriaminepentaacetic acid-D-deoxy-glucosamine (DTPA-DG) was synthesized and examined for its activity as a cell-permeable iron chelator in human hepatocellular carcinoma (HEPG2) cell line exposed to high concentration of iron sulfate and compared with deferoxamine (DFO), a prototype iron chelator. http://www.ncbi.nlm.nih.gov/pubmed/24554907 Cur(Que)min: a neuroactive permutation of curcumin and quercetin for treating spinal cord injury. http://www.ncbi.nlm.nih.gov/pubmed/24524922 Metal chelator combined with permeability enhancer ameliorates oxidative stress-associated neurodegeneration in rat eyes with elevated intraocular pressure. http://www.ncbi.nlm.nih.gov/pubmed/24509160 The last decade has ushered in a new era in iron chelation therapy. Coupled with advances in tissue iron quantitation, there is tremendous promise of an individually tailored approach to chelation, and subsequent reduction in morbidity and mortality. http://www.ncbi.nlm.nih.gov/pubmed/24504090 Therapeutic phlebotomy and iron chelation are the cornerstones of therapy. The average survival is less than a year in untreated patients with severe cardiac impairment. However, if treated early and aggressively, the survival rate approaches that of the regular heart failure population. http://www.ncbi.nlm.nih.gov/pubmed/24503941 Iron homeostasis in breast cancer. http://www.ncbi.nlm.nih.gov/pubmed/24486738 R2 and R2* are equally effective in evaluating chronic response to iron chelation. http://www.ncbi.nlm.nih.gov/pubmed/24452753 Iron chelation and multiple sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/24397846 Measuring LPI before starting conditioning can offer an opportunity to predict toxicity and, perhaps, the need for chelation therapy. http://www.ncbi.nlm.nih.gov/pubmed/24335268 Iron chelation is a promising, novel adjunctive therapeutic strategy for MRSA and VISA infections. http://www.ncbi.nlm.nih.gov/pubmed/24292099 Furthermore, we have demonstrated that synthetic iron chelators and a genetic iron chelator are neuroprotective against proteasome inhibitor-induced DA neuron degeneration, suggesting that iron chelation might be a promising therapeutic target for PD. http://www.ncbi.nlm.nih.gov/pubmed/24262171 Iron overload as a major targetable pathogenesis of asbestos-induced mesothelial carcinogenesis. http://www.ncbi.nlm.nih.gov/pubmed/24257681 Targeting chelatable iron as a therapeutic modality in Parkinson's disease. http://www.ncbi.nlm.nih.gov/pubmed/24251381 In this study, we have assessed whether high-affinity iron chelators of the pyridoxal isonicotinoyl hydrazone (PIH) class can restrict the growth of clinically significant mycobacteria. http://www.ncbi.nlm.nih.gov/pubmed/24243647 The effect of iron loading and iron chelation on the innate immune response and subclinical organ injury during human endotoxemia: a randomized trial. http://www.ncbi.nlm.nih.gov/pubmed/24241495 Pharmacological handling of monocyte migration into the CNS combined with chelators that neutralize the effects of extracellular iron occurring due to the release from dying macrophages as well as intraneuronal chelation may denote good possibilities for reducing the deleterious consequences of iron deposition in the CNS. http://www.ncbi.nlm.nih.gov/pubmed/24218010