And to expand a little - we need iron to make hemoglobin and thus the red blood cells. Too little iron and we make fewer blood cells (and the ones that we do make tend to be smaller or “microcytic”). There are other things than low iron that would make us produce too few red blood cells too. There are also conditions that cause more destruction of red blood cells, from having an antibody reaction that targets the blood cells (autoimmune hemolytic anemia) to having an inherited abnormal form of hemoglobin. A fairly common form of the latter is beta thalassemia minor (or “trait” because it is caused by one normal and one abnormal copy of that hemoglobin unit), which is also microcytic like iron deficiency anemia. Because it looks like iron deficiency sometimes iron is advised to these people but it does them no good and theoretically could be causing too much iron. Having two abnormal copies of that hemoglobin unit, beta thalassemia major, will require regular transfusions and those people will as a result have too much iron in their system unless the iron is removed (chelation). Sickle cell is another form of abnormal hemoglobin that leads to greater destruction of red blood cells. And of course one can be anemic because of excessive blood loss, which can also result in an iron deficiency - such as from heavy menstrual flow, or some other source of chronic blood loss like from somewhere in the gut.
Let me check in here as somebody who actually did a rotation in the hematology ward of the NIH during residency and as somebody who has corrected a lot of misinformation about anemia and iron among patients. Here is my brief education.
Blood consists of several different types of cells and plasma, which is the surrounding liquid.
Red blood cells, or erythrocytes, are one of these types of cells.
Anemia is when you do not have enough red blood cells.
Anemia had many causes, but basically, it is caused by not making enough cells or losing too many.
You can lose cells through bleeding somewhere or if your body is destroying them (often through an autoimmune process)
Red blood cells are made in the bone marrow and contain iron as well as a protein caused hemoglobin.
If the body lacks any components needed to make red blood cells, you can have anemia.
Causes of productive anemia include:
Iron deficiency (most common) where you do not have enough iron for the cells, most commonly through bleeding
Abnormal hemoglobin production (sickle cell, thalessemias, protein C disease)
Hormonal problems that interfere with the production of red blood cells (thyroid disease, adrenal disease, low testosterone)
Bone marrow diseases (tumors, aplastic anemia)
Normally, the body absorbs only what iron is needed.  Once the body absorbs the iron, it is difficult to get rid of.
There are usually two ways that the body accumulates too much iron:
#1) The person has a form of anemia that is not low iron, such as thalassemia< and requires transfusions which gives them additional iron and since their iron levels are initially normal, te iron builds up in their body.
#2) The person has a disease such as hemochromatosis, so that the iron regulation is off and the body absorbs too much iron from the diet.
The ideal treatment for iron overload is phlebotomy, or removing blood. Excess iron leads to liver damage, joint pains and diabetes among other problems.
As you can imaging, removing blood is only effective when the patient is not already anemic. Therefore, for people with thalassemia and iron overload, chelation (which is selective removal of iron) is an option.
Chelation is not needed for people with hemachromatosis because they can be treated with phlebotomy.
98% of hemachromatosis is related to specific genetic defects.
Just because you have the defect does not mean you have iron overload and need treatment.
If genetic testing indicates that you have hemachromatosis, you should have a blood count and iron studies (iron, total iron binding capacity, ferritin levels, and possibly UIBC) done to determine your status.
If your counts are normal, you should be monitored; if they are high you should start treatment.
A hematologist is the specialist who most deals with this if your primary doctor is not comfortable with it.
*
And on review, I see that DSeid has basically typed the same thing.
Meanwhile. let me just say that the coolest patients at the NIH hematology ward are the thalessemics.  For those who don’t know how the NIH works-once they get a patient with a rare disease, they call them back every time they have a new study on the disease.  Some of the thalessemics have been coming in the same week every year for 20+ years.  It’s like a big family reunion.  Since they’re not actually sick (like some of the other patients) they treat it like a big party.  They’re off in the gym playing basketball and just hanging out with buddies from all across the country that they only get to see once a year. It was literally (and I do mean literally) the only hospital ward where they patients and the residents ordered Chinese take-out together (we did draw the line at beer although they tried) It’s seriously a wild and weird place.  When I was in the cardiology ward there, they were doing family studies and the schedule went something like this:
Sunday-parents and kids check in
Monday-echocardiograms in AM, stress testing in PM
Tuesday-tour white house in AM, EP studies in PM
Thursday-go to National Mall and tour museums
Friday-present data at conference
Saturday-further tests as needed, otherwise, free to see sights in DC
Sunday-check out and go home.*
Bolding mine.
The 21st Century is … weird. 
That was a marvelous approachable summary starting from just about a zero baseline and ending up at most of the high level info a patient probably needs. Bravo Good Sir.
Whole blood is the usual way to eliminate iron. Blood centers won’t accept donations if you have a blood disorder but many will perform ‘therapeutic phlebotomies’ and may use the blood for testing. Chelation can create problems for some people, phlebotomies are quick and harmless. Initially you may need to lose a lot of iron to reduce the ferritin levels in your liver which are holding iron for you, maybe a lot since you don’t need to use that reserve. Your physician should provide a minimum hematocrit or hemoglobin level where it’s safe for a phlebotomy. You may need them frequently at first but after a while your iron reserves should diminish and then you can look into further treatment. I often meet hemochromatosis patients in for a phebotomy when i get mine for erythrocytosis, a similar but less problematic disorder.
I believe that vitamin C and most varieties of alcohol tend to increase absorption of iron while coffee, green tea, curcumin, dark chocolate, red wine, and other polyphenol-rich foods tend to hinder iron absorption.
And don’t attempt phlebotomy on yourself even if you have access to sterile equipment. If you happen to faint at the sight of blood (vasovagal syncope) you could easily bleed to death.
You can have enough red cells but with unusual hemoglobin. People with sickle cell anemia have a normal red-cell count, but their hemoglobin doesn’t work as well as the baseline variants.
In the end it isn’t exactly about how much iron or about how many red cells, it’s about whether the amount and type you have works correctly or not. Both “low iron” and “not enough red blood cells” are shorthands for something that’s much more difficult to measure.
I’ve got thalasemia superminiminor and one of the consequences of The Year My Tonsils Were Trying To Kill Me was ferropenic (low-iron) anemia. I still had superhigh red cell counts, but I didn’t have enough for me.
I have hemochromatosis. My treatment consists of phlebotomies about every three months or so, they take about a pint of blood each time. It’s basically like donating blood. They give you a drip via a needle in the arm, drop the tube and bag over the side of the bed/chair and gravity takes care of the rest. It’s not especially painful in and of itself (at least if you get a good nurse who can insert the needle painlessly), but not terribly comfortable either, particularly if you hate needles. I have mine done in a hospital. The nurses also wrap heated towels around my arm for a while beforehand to help prep the vein, take my blood pressure before and after, and put a heart rate monitor clip on one of my fingers to keep an eye on my vitals during. It’s just an outpatient thing so I can go home straight after.
Drink lots of water beforehand and during to help replace the lost fluid. My blood pressure tends to drop significantly during so sometimes they give me a saline drip afterwards to help replace the lost fluid faster. If you’re nervous or really hate needles, your body may feel extremely exhausted the first couple of times so you’ll want to just go home and sleep. Whether or not you can return to work or your normal activities afterwards depends on how well you handle it. It’s best not to do anything too stressful or physically strenuous afterwards as it takes 24-48 hours for your body to replace the lost blood (so I was told anyway) so you don’t want to put any more pressure on yourself than you need to. I always take the rest of the day off and take it easy. You can drink alcohol afterwards if you really want to but you will get drunk quicker because your blood volume is lower. You may also dehydrate yourself more in the process and delay your body’s recovery so it’s better to lay off the beer that night.
Your GP should be able to refer to a hematologist to advise the best treatment for your individual case. I get a blood test a few days before every phlebotomy and discuss results with my hematologist on the day before she sends me off to the nurses to get it done. That way, my hematologist can keep an eye on my iron levels and blood count to assess how much needs to be taken that session. Where you go to have it done and how often will all depend on your individual circumstances and what the health care system is like where you live.
I’m not good with needles - I don’t mind flu shot type of needles but blood tests and phlebotomies irk me. I just hate the thought of people taking my vital fluids. When I arrange the time off work, I tell my boss I have to visit Dr Dracula again.  However, at my local hospital, Hematology is on the same ward as Oncology and is technically part of the Cancer Care Unit, so while I’m busy trying not to freak out at the drip in my arm, most of the other patients around me are getting chemo, so it helps to put things in perspective. It could be worse…
  However, at my local hospital, Hematology is on the same ward as Oncology and is technically part of the Cancer Care Unit, so while I’m busy trying not to freak out at the drip in my arm, most of the other patients around me are getting chemo, so it helps to put things in perspective. It could be worse…
OK, hi. I have worked in clinical genetics laboratories for many years, and I have tested many hundreds of samples for hereditary hemochromatosis, which is associated with variants in the HFE gene.
First off, we need to clarify which mutations you’re carrying. There are three commonly reported variants: C282Y, H63D, and S65C. Most of the time, you are only at risk if you have two copies of C282Y or one C282Y and one H63D. S65C is a minor risk factor, but most people consider it not worth worrying about.
Secondly, even if you have a risk-associated genotype, the odds are very good that you’ll never actually develop the disease. I’d need to look this up to confirm, but my memory is saying that it’s about 80% of people with the mutations never have any actual symptoms or problems.
This is to say do not take any action whatsoever without getting checked by a doctor. They can test the actual iron levels in your blood to see if there’s a problem. A genetic result is not sufficient by itself.
Understanding why takes us a bit into the molecular biology of the disease. The body has no way of selectively getting rid of iron. Iron levels are controlled completely at the uptake level - we absorb more when we need more. The system managing this exists in the cells lining the gut. Imagine a gut epithelial cell - one face is exposed to the food sliding past, and has proteins that can reach out and grab iron and get it into the cell. The opposite face is exposed to the bloodstream. The HFE protein sits on this side of the cell. It’s transmembrane, so part of the protein is sticking out into the blood, while the rest is inside the cell. The sticky-out bit can bind to iron in the blood (technically to iron-bound proteins, but that’s not important). When it has bound iron, the inner bit of the protein sends out a “we have enough iron, everyone!” message. This prevents the cell from taking up more iron.
The mutations we’re discussing prevent the HFE protein from getting into the membrane where it’s supposed to be. Technically, they interfere with the binding of a peptide known as beta-2-microglobin, which acts as sort of a postage stamp to tell the cell that a protein is supposed to get to the membrane. Less protein in the membrane means less “we’re OK” signal, and so the cell is constantly grabbing as much iron as it can. Over time - and we’re talking decades here - iron levels can build up enough to overwhelm the body’s systems to keep it under control, and it can start doing tissue damage. Iron is a very reactive substance and can do lots of wild chemistry, including becoming a free radical.
So why do many mutation carriers not get the disease? Part of the answer is simply “we don’t know yet”. There may be other genetic factors at play we haven’t figured out yet. But another big part of it is environment and diet. The body can’t absorb iron unless we eat it, so many people manage the condition by eating a low-iron diet - no red meat, that sort of thing.
On the plus side, it’s easily managed once you know you have it. As has been said, theraputic phlebotomy can get iron levels under control fairly easily. Personally, I find it sort of satisfying on some level to know that modern genetic testing has taken us back full circle to using bloodletting to cure a disease.
Anyway, check with a doctor before assuming you actually have the disease.
I added bolding - I too looked at my raw genetic data and found that combination of mutations. So I am getting the more specific iron testing to see what is what.
If you suspect you suffer from Hemochromatosis, please confirm via a qualified physician. He/She will guide you through the initial diagnosis and treatment, perhaps referring you to a specialist familiar with the malady.
Well intentioned as people’s comparisons with (their) other particular metabolic (iron) imbalances may be, they are irrelevant as related to Hemochromatosis. It is a life threatening condition that is incomparable to anything else, and warrants specific treatment.
If you wish personal insight from one who has Hemochromatosis, please PM me.