None of the below should be considered medical advice - we are describing the questions people ask about this site. Always consult a qualified medical professional.

• How do I delete my data?We'd prefer the data is not deleted because we use it to teach the system how to calculate the "age at symptoms". However, you do have the "Right to be Forgotten" and this function is present in the system but a bit hidden away. To delete your data please follow this instructions.
  1) On the results page click Checkiron-home menu option (if you've left the system, then re-upload your data and let it process to get to the results page)
  2) Then scroll down until you see Results. Scroll further and you'll see "Privacy function- right to be forgotten". Under that is the delete button
  3) Press the delete button and all record of your visit original data and results will be deleted, including any information you've provided.
  4) If you get an error saying "incorrect session" its because you've tried to delete the data more than 30 mins after it was processed. To resolve this you must reload your data, let it process, and then click checkiron-home and find the delete button again. This will then work - this is the only way we can check its you deleting your own data.
• Why have you created this site?. We are an iron overload prevention site. We want to increase awareness of the most common genetic disorder (Hemchromatosis Type 1) for people of Northern European descent, which can over years cause iron overload in the organs and eventually organ damage. In the US there are 4.2M people with this genetic disorder and many could die of organ damage before they are diagnosed. Hemochromatosis is easily and safely treated for most people, if caught before organ damage has occurred. But we believe prevention is even more important, if the 4.2M people who have the genes are aware of it in early life, then simple lifestyle changes (eg doing blood donation and small diet changes) early in life would mean that a person might never need any treatment at any stage in life. This site will tell people their risks and allow them to choose if they think simple lifestyle changes will work.
• What are the lifestyle changes. If you go on a Hemochromatosis forum you may see people saying it does not matter what you eat because you just get a phlebotomy (or venescetion for UK people) to treat it. This may be correct advice is you are fully loaded with iron but we believe that in some cases prevention is possible before anyone gets fully loaded. So we would suggest all people at risk (ie with the mutations but do not suffer from symptoms) use lifestyle changes early enough that they less likely to get excessive iron in their organs. This would involve being a regular blood donor and avoiding fortified foods such as breakfast cereals, avoiding taking vitamin C supplement, drinking milk when eating a steak and avoiding offel based foods such as sausages or black pudding. NB clearly all people are different and some will need treatment, if the lifestyle changes are insufficient. All people with this condition will need regular medical checkups to ensure iron levels are within the safe limits and some will need to resort to Plebotomies (venesections in the UK).
• What are differences between CheckIron V1, V2.2, V3, V3.1,V3.5 and V3.6. In CheckIron V1 we looked at just 18 mutations for HH Type 1. V2 expands this to 139 mutations and includes the rarer forms of Hemochromatosis Types 1-5. In July 2020 in V2.2 we introduced the effect of the difference between men and women too. One of our goals is to use DNA to predict when someone will overload iron - this of course is fraught with problems becasue we are ignoring effects of what people eat and other related conditions. In V2.x we create an Age at Symptoms estimate currently using only the HH Type 1 data. This data is an estimate and inevtiably wrong, but if you provide feedback we hope to improve on it over time and use all the input data we have. In April 2021 we released V3 which has 28 inflammatory diseases and 960 mutations. We also now allow each disease to compare with the average uploader of data - this can help because some V2 and V3 had a completely new way of displaying the results using graphs and text and in V3 we added loading speed indicators. In V3.1 we increased add the gene JAK2 to Polycythemia and added ALS as another inflammatory disease. In 3.5 we added support for Nebula Whole Genome data, we added support for Inflammatory Heart Diseases and added Hemolytic Anemia, beta-thalassemia Anaemia and Sideroblastic Anemia to the Anemia section. In V3.6 we updated the % better and %worse underlying data to bring it up to date.
• What do you do with my data?. We're very much concerned about your privacy. We do not ask you to register and do not know who you are. We do store the DNA data you give us and ask the optional questions about symptoms and diagnosis because we are trying to spot patterns between the main mutations causing the disorder and other genes which modify the rate at which you get iron overload. We do use the data you give us into Research for Hemochromatosis, but the data will never be shared in full. Certain very fully anonymised even from our internal anonymised data small (so small, that there is insufficient information to identify anyone) subsets (to prove a scientific feature) may be shared for the purpose of publishing science papers. If you really are concerned about us storing your data, we provide a delete button - please follow the instructions in the first FAQ above. If you click this all your data and results are deleted forever.
• If I have the mutations do I have the disorder?. Many people say "No, not necessarily" in answer to this question, but it is more correct to say you have it but you may not suffer the symptoms in normal lifetime. The most common mutation causing Iron Overload disorder is the homozygous C282Y mutations (ie having 2xC282Y). If you have this pair of gene mutations you will have lower hepcidin production than people without it. However, the effect of the lower hepcidin differs between individuals and other genes controlling the absorption and transport of the iron to the organs also have an effect and these modifiers can make a massive difference to how old you are when the iron has built up enough to cause damage. Also lifestyle (what you eat and whether you are menstruating and/or a blood donor) also make massive differences.
• How do you calculate the analysis results. A DNA file from the current suppliers will typically contain about 600-700K DNA SNPs details and from Nebula there are 3.5B DNA SNPs. We are currently looking at just 960 of these which pertain to Hemochromotosis Types 1-5 plus other inflammatory genetic diseases and the production of proteins which control the absorbtion and transport of iron in its various formats. We then tell you which Hemochromatosis related SNPs you have and give you the SNPedia relevant text associated with those SNPs. We are not a diagnosis site, we do provide some description of the mutations you have based round increased or decreased risk or comparison with the average person who has submitted data. We may well increase the number of SNPs we look at as we learn more from this research. Experimentally we do calculate the "age at symptoms" using only the DNA data - this is NOT accurate but is an indication of your risks. We do find currently that for many people it will only be a few years out and for a small number it can be as much as 30 years out. We believe the 30 years out group is due to a missing ingredient which could be lifestyle or another disease we have yet to consider. Note also there can be many more mutations of a gene than we analyse because if a mutation has no reported effect we do not include it in the analysis - it is important to point this out as it seems some analysis sites do include every known mutation in which case we find some people get concerned about a mutation which has no effect.
• Which DNA supplier has the highest accuracy. For the non-whole genome suppliers, accuracy is actually the wrong word but "coverage" is a better measure. All the current DNA suppliers cover slightly different SNPs and we've done the following analysis specifically for Hemochromatosis (HH) mutations, associated iron metabolism genes and associated inflammation mutations. The important HH Type 1 mutations are C282Y, H63D and S65C - these are the gatekeepers to the Hepcidin Defiency which causes HH Type1. If you have one or more of these mutations then you load iron according to which one(s) and then other iron metabolism mutations. We are now looking at 960 mutations in total and the results are shown in the table below where we measure them by disease type. One thing we have notice is that data from FTDNA and Ancestry in 2017 and before did not cover the Hemochromatosis mutations at all. It appears during 2018 (still to find exact dates) both started to include all 3 Type 1 mutations whereas 23andMe only had and continues to have 2 of the mutations
  
• What do you mean by coverage. In V2.x we looked at just 139 SNPs and in V3 960 SNPs in the hundreds of thousands of SNPs in the data files and we now look for evidence of a Y-chromosome to determine if the person is male or female- only Ancestry and 23andMe suppliers support this feature and for the other suppliers we assume the person is a man. Each supplier has support for different sets of SNPs. We have now added support for Whole Genome Sequencing (WGS) from Nenula in V3.5-theortically coverage is 100% for these but the format we use to read you data does not support that measurement so its not reported in the results.