I wanted to get my thoughts down on the topic even though it needs some key answers. If it proves out then I will write it up in a web page. Here is the basic concept, C282Y causes a misfolded protein which no longer can exit the cell wall to get to its receptor in order to request the production of Hepcidin. Given that LDL cholesterol serves the purpose of cell repair and HDL cleans up the mess, does it follow that these misfolded proteins must be 'cleaned' up by cholesterol? If so, then a C282Y mutation would be autosomal dominant for elevated cholesterol AND that cholesterol would be necessary for cell health. Meaning that artificially lowered cholesterol from statin use could leave the body unable to keep up with repairs. Of course these proteins would only be produced while the body thinks it has too much iron - so keeping us in maintenance with a Ferritin under 50 may stop the creation of these misfolded proteins and reduce cell stress. Not so for those who go undiagnosed and continue to produce these misfolded proteins all of their lives. A statin seems like it could do even more harm in such cases.
Late night thoughts on the night before a blood donation. Aren't I the life of the party.
Late night thoughts on the night before a blood donation. Aren't I the life of the party.
Further info - I had a chance to discuss this with my wife's doctor who also treats many HH patients. He agreed with my line of reasoning here but emphasized that the cholesterol increase should be thought of as a baseline increase and is not likely enough to be called 'high' on its own. Further he corrected me that LDL does not do repair, it is the delivery mechanism for the molecules that actually do the repair. And HDL goes to the site of the repair and provides transport for the remnants of the repair.