Why some mid-thoracic subluxations become chronic: Iron metabolism - Part 2

Previously, I began a series that deals with the immune or reticuloendothelial system and each of its component organs. I started with the spleen, mentioning its various functions and how stress involving the levels of red and white blood cells and platelets can cause and perpetuate chronic recurring subluxations between T6 and T8. Needless to say, muscle contractions in this area cause a loss of the normal thoracic kyphosis or "flattening” between the shoulder blades commonly referred to as Pottenger's Saucer. I've written extensively of other visceral dysfunctions that can be involved in this area, including its involvement with digestive problems, hypoglycemia, and headaches among other common chronic symptom patterns.

Last month, I described iron metabolism from digestion to absorption, transport, and utilization in hemoglobin. I think it only appropriate to continue with interpretation of other very important blood tests needed to completely understand iron metabolism and its relationship to symptoms and subluxation patterns. When assaying iron levels in the body, we often look only at hemoglobin levels. Iron is essential for the formation of hemoglobin and its levels in the blood are determined by several factors: Proper acid environment in the stomach; absorption from the intestine; storage in intestine, liver, spleen, and marrow; breakdown or loss of hemoglobin; and synthesis of new hemoglobin.

But, as I stated, iron metabolism is completely dependent upon adequate ingestion, digestion, absorption, and liver function in order to be used by the body. So, after hemoglobin look at Serum Iron.

High levels of serum iron can indicate hemolytic disease (abnormal destruction of red blood cells). Much more commonly, this finding indicates protein deficiency, and that means that the iron must be deposited in the tissues. There are two conditions that can arise when that occurs:

• Hemochromatosis - abnormal deposits of iron in the tissues WITH damage as recognized by bronzing of the skin. This especially affects the liver, heart, lungs, and pituitary gland.
• Hemosiderosis - abnormal deposits of iron in the tissues WITHOUT damage. This results from multiple transfusions or excess iron administration and occurs primarily in the liver and lungs.

Low levels of serum iron indicates iron deficiency. While this may indicate chronic blood loss, for example in the digestive tract, it more commonly represents a nutritional iron deficiency anemia and can be confirmed by examining the results of a Complete Blood Count.

Next, needing to look at iron's means of transportation through the blood stream, we examine the TIBC (Total Iron Binding Capacity) test results. Since iron is transported by protein (transferrin) we'd like to know to what extent that transport mechanism is being utilized. The amount of iron that's bound to protein is then measured and compared to the amount of iron that would appear in plasma if all the transferrin were saturated with iron. This helps to:

• Evaluate nutritional status
• Estimate the ability to transport iron
• Distinguish iron deficiency anemia from chronic disease
• Aid in the diagnosis of hemochromatosis

High levels of TIBC are found with iron deficiency anemia and low serum iron. In other words, as serum iron levels decrease, protein saturation with iron decreases and TIBC increases.

Low levels of TIBC are found with RBC destruction or excess iron intake. The protein transport mechanism is saturated with iron. But I must point out that normal TIBC results may be found in some pathological conditions, such as in chronic inflammatory states like rheumatoid arthritis. For example, serum iron may be low in the presence of adequate body stores, but TIBC may be unchanged or may decrease to preserve normal saturation.

But, generally, serum iron increases and TIBC remains the same, which increases saturation. However, iron overload may not alter serum levels until relatively late in the development of the condition.

Finally, let's look at serum ferritin. The protein ferritin is the iron-storage protein and so normally only occurs in small quantities in blood. But, as the amount of iron stored in the body goes up so does the ferritin level, and vice versa. It's important to recognize that both serum iron and TIBC are of greater diagnostic usefulness when performed with a serum ferritin. The purpose of testing for ferritin then is threefold:

1. to measure iron storage,
2. to screen for iron deficiency and iron overload,
and
3. to differentiate between iron deficiency (low iron storage) and chronic inflammation (normal storage).

High levels of ferritin indicate pathology, such as hemochromatosis, hemosiderosis, alcoholic or inflammatory liver disease, Hodgkin's disease, and breast cancer.

Low levels of ferritin indicate iron deficiency anemia or severe protein deficiency. It would also be seen in patients undergoing hemodialysis.

In conclusion, remember that iron assimilation is entirely dependent on protein metabolism.

(Dr. Loomis can be reached by mail at 6421 Enterprise Lane, Madison, WI 53719-1116 or by phone at 800-662-2630. Visit his website at http://www.loomisenzymes.com.)