Can GH Cause My...
Please note that this page is where my current efforts are going. It is not complete, but has enough value for me to publish. I will remove this statement when I have the page in a completed state. Thank you for your patience and please feel free to ask me questions. I am happy to research any topic.
It is very common when finding out that one has a genetic issue to attempt to identify exactly how much can be blamed on it. But the question is really not that simple. There are a variety of stages and genetics involved making it so there are very few global answers. I will try to explain this better in these few paragraphs.
Hemochromatosis as explained on my First Terms page is a term that really talks about being in a state of having too much iron stored in a person's body. Basically saying that Serum Ferritin (SF) is greater than 300. The initial goal in understanding this issue (or phenotype) was for doctors to find a way to keep us from approaching or exceeding a SF of 1000 which is where organ damage is significant risk. So the question 'Can GH be the cause of my ... elevated liver enzymes', when asked by someone who has a SF > 1000 seems like a very easy answer. But after treatment and when in maintenance our SF can be less than 20 which would be considered anemic for other folks. At that point it is much less likely that the elevated liver enzymes would be caused by GH.
So the first thing to do is realize what question you are asking. This is not as simple as it may seem. Many of us with hereditary hemochromatosis (or Type I) just say we have hemochromatosis and this question would really mean something like, "I am a c282y homozygote in controlled maintenence (SF < 50, TS ~65%), could this still be causing my ..?". Which is a very different question from, "I am a c282y, h63d compound heterozygote and have just been diagnosed with a SF > 1000 and a TS of 96%, could this be why I have ...?".
Typically, a doctor looking at these questions would hear something different like "my SF is greater than 300, could this cause ankle pain". Their answer would completely ignore the genetics because it would not really factor in to what was asked.
So what can we know? We can break our group into sub groups and try to understand what challenges each relate to. Here is a nice list of possible symptoms (phenotypes): pdf.
C282Y - The C282Y mutation essentially stops the protein created by the HFE gene from being able to exit its cell. The creation process in the gene is triggered when a high amount of iron is present, so at those times these proteins are created by the cell and die since they are unable to escape the cell. At this point an enzyme called ALK3 is locked inside the cell by the HFE protein. This causes damage to the cells and general stress. And what is called on to repair damaged cells? Cholesterol. LDL cholesterol is the transport mechanism for the molecules necessary to do these repairs and HDL transports the clean-up molecules after the cell has been repaired. So C282Y on its own implies that a person should have a higher baseline value for LDL and HDL cholesterol due to the constant repair cycle. There may also be a correlation for this person between iron intake in their diet and elevated cholesterol values. But on the other side of the coin, C282Y causes the cells of the body to increase their cholesterol storage. So this person may actually have low cholesterol except when the body is doing extensive repairs to itself. That would make the LDL cholesterol value especially important for a C282Y.
It is very common when finding out that one has a genetic issue to attempt to identify exactly how much can be blamed on it. But the question is really not that simple. There are a variety of stages and genetics involved making it so there are very few global answers. I will try to explain this better in these few paragraphs.
Hemochromatosis as explained on my First Terms page is a term that really talks about being in a state of having too much iron stored in a person's body. Basically saying that Serum Ferritin (SF) is greater than 300. The initial goal in understanding this issue (or phenotype) was for doctors to find a way to keep us from approaching or exceeding a SF of 1000 which is where organ damage is significant risk. So the question 'Can GH be the cause of my ... elevated liver enzymes', when asked by someone who has a SF > 1000 seems like a very easy answer. But after treatment and when in maintenance our SF can be less than 20 which would be considered anemic for other folks. At that point it is much less likely that the elevated liver enzymes would be caused by GH.
So the first thing to do is realize what question you are asking. This is not as simple as it may seem. Many of us with hereditary hemochromatosis (or Type I) just say we have hemochromatosis and this question would really mean something like, "I am a c282y homozygote in controlled maintenence (SF < 50, TS ~65%), could this still be causing my ..?". Which is a very different question from, "I am a c282y, h63d compound heterozygote and have just been diagnosed with a SF > 1000 and a TS of 96%, could this be why I have ...?".
Typically, a doctor looking at these questions would hear something different like "my SF is greater than 300, could this cause ankle pain". Their answer would completely ignore the genetics because it would not really factor in to what was asked.
So what can we know? We can break our group into sub groups and try to understand what challenges each relate to. Here is a nice list of possible symptoms (phenotypes): pdf.
C282Y - The C282Y mutation essentially stops the protein created by the HFE gene from being able to exit its cell. The creation process in the gene is triggered when a high amount of iron is present, so at those times these proteins are created by the cell and die since they are unable to escape the cell. At this point an enzyme called ALK3 is locked inside the cell by the HFE protein. This causes damage to the cells and general stress. And what is called on to repair damaged cells? Cholesterol. LDL cholesterol is the transport mechanism for the molecules necessary to do these repairs and HDL transports the clean-up molecules after the cell has been repaired. So C282Y on its own implies that a person should have a higher baseline value for LDL and HDL cholesterol due to the constant repair cycle. There may also be a correlation for this person between iron intake in their diet and elevated cholesterol values. But on the other side of the coin, C282Y causes the cells of the body to increase their cholesterol storage. So this person may actually have low cholesterol except when the body is doing extensive repairs to itself. That would make the LDL cholesterol value especially important for a C282Y.