I have some Celitc news. It seems I have manifested the physiologic expression of a genetic mutation at C282Y (and H63D), which means that my body absorbs iron at an enhanced rate. People who know of such things surmise that the mutation originated in Scotland in the sixth or seventh century, and further, that it was somewhat of an adaptive development in environs which provided a low iron diet (and with relatively short longevity.) I apparently share this defect with more than one in ten of my Celtic brethren, and many Northern Europeans.

This phenomenon, known as hemochromatosis, causes a lifelong, gradual accumulation of iron. Adaptive though it may been at the time of its rise, a high iron diet coupled with longevity, leads to problems for us now. It is rarely detected in males until their mid-forties (me), and women in their mid-fifties. Although there may be vague symptoms such has abdominal and joint pain, the real trigger for diagnosis is elevated liver function test results, (specifically AST (SGTP).) This is because the iron accumulates in the liver as the erythrocytes are harvested for nutrient recycling at their end date. Elevated AST (caused by cellular damage in liver cells, releasing the AST enzymes) could indicate the need for another test for ferritin levels.

Now, although this defect of iron metabolism can cause cellular damage and lead to severe damage of the liver, pancreas, heart, and other organs, increasing the risk of liver and pancreatic cancer, it is easily treated with early intervention. The treatment: Phlebotomy -- Give blood, that's all! (Before the iron in the erythrocytes is re-absorbed.)

There you have it. Mudcat factlet for the day and public health service notice for "Celtic" descendents. Remember: simple treatment only with early detection.

- I am Iron Man