Iron, together with thyroid, is probably one of the things most improperly tested for. With thyroid, doctors only measure TSH, which gives you almost no clue of actual thyroid function. Similarly with iron, doctors mainly test ferritin and then prescribe iron supplementation or phlebotomy based on just one marker. Pretty dangerous if you ask me.
A quick story. There was a man with significantly elevated ferritin, yet he was anemic. The doctor prescribed phlebotomy for years and the patient just got worse and his ferritin barely dropped. After a couple of years he had to quit his job and was administrated to a psychiatric hospital. After more than a decade they did some more tests and concluded that he was very low in copper and ceruloplasmin, which is needed to mobilize iron (ferritin) from the tissue for utilization in the body. For many years the doctors mainly tested ferritin and prescribed phlebotomy, whereas his problem was not mobilizing the iron and thus he got severe iron buildup everywhere in his body, including his brain, which caused him to get all kinds of brain damage and psychiatric issues.
Point being, it’s dangerous to test only ferritin. Both an iron deficiency and an excess can be harmful.
Iron is needed for neurotransmitter synthesis (dopamine, serotonin, etc), cytochrome c (energy production), thyroid hormone conversion, testosterone production, DNA synthesis, cellular replication and growth, catalase and peroxidase enzymes, which neutralize free radicals, etc.
However, iron excess can cause cardiovascular disease, arterial disorders, brain damage (and can contribute to Alzheimer’s and Parkinson’s disease), fatigue, lethargy, reduced hormone production, inflammation all over, ED, liver fibrosis, diabetes, infections, bacterial overgrowth, etc.
Iron excess is much worse than iron deficiency.
The total amount of iron in a 70kg man is about 3500–4000mg, corresponding to an average concentration of 50–60mg of iron per kg of body weight. The vast majority (2300mg, 65%) of iron in the body is found in the hemoglobin of erythrocytes. About a tenth of total iron (350mg) is present in the myoglobin of muscle and enzymes and cytochromes of other tissues. Of the remainder, approximately 500mg is found in macrophages of the reticuloendothelial system (RES), about 200–1000mg is stored in hepatocytes in the form of ferritin, while 150mg of iron is found in the bone marrow.
We need about 1-2mg of iron per day and only about 10% of ingested iron is absorbed, so we need to eat roughly 10-20mg of iron per day. A highly acidic environment in the stomach is needed to free the iron from food for proper absorption.
There are two forms of iron present in food, heme iron ((Tim?) ferrous iron; Fe2+) and non-heme iron (ferric iron; Fe3+).
The Fe2+ can immediately be absorbed whereas the Fe3+ has to be converted to Fe2+ first in order to be absorbed, thus Fe2+ is much better absorbed than Fe3+ iron. The way vitamin C aids in Fe3+ iron absorption is that it donates an electron to Fe3+, which is then converted to dehydroascorbate and Fe2+ respectively, making the iron absorbable. So vitamin C only enhanced Fe3+ absorption and not Fe2+.
Hepcidin, which is created by the liver, regulates iron absorption. The more iron you have in your body, the more hepcidin is created and the less iron is absorbed. Once iron is absorbed, it is stored as ferritin, an intracellular iron storage protein, in the body. When there is a low demand for iron in the body, absorbed iron is stored within the enterocyte in the form of ferritin. Ceruloplasmin mobilizes the stored iron, creating Fe3+, which is then taken up by transferrin. Transferrin transports the iron around in the body to places where it is needed, such as the bone marrow, cells (for energy production), liver, spleen, etc.
A proper iron panel checks for:
- Ferritin
- Serum iron
- Transferrin (Tf)
- Transferrin saturation (TfS)
- Serum transferrin receptor (TfR)
- Serum copper
- Ceruloplasmin
- Hemoglobin & hematocrit – Reticulocyte (immature red blood cells) hemoglobin content reflects the iron status more sensitively, however TfS is a better clinical marker for iron supplementation therapy (R). The low accuracy of Tf and TfS in the diagnosis and management of iron deficiency conditions does not permit definitively recommending their use (R).
Ferritin
Ferritin can be elevated when you have high iron stores or during inflammation. A good range for ferritin is between 50-150ng/mL. Ferritin is a marker of inflammation rather than iron status in overweight and obese people (R).
Transferrin
Transferrin is usually elevated when there is little iron in the blood and reduced when there is a lot of iron in the blood.
Transferrin saturation is usually elevated when there is elevated free iron, Fe3+, in the blood and vise versa. Transferrin saturations of less than 20% indicate iron deficiency, while transferrin saturations of more than 50% suggest iron overload. Transferrin and transferrin saturation is usually inversely correlated. Ideally you want TfS at the low end of the range as high TfS could increase the risk of cardiovascular mortality (R). However, inflammation lowers TfS as well as serum iron.
Serum transferrin receptor is elevated when there is low iron in the blood and vise versa.
Low/normal ferritin, low/normal transferrin and elevated transferrin saturation could indicate enhanced iron mobilization from tissue and then ceroluplasmin might be too high. Lower copper first before supplementing iron.
Elevated ferritin and low transferrin saturation could indicate reduced iron mobilization from tissue and then ceruloplasmin might be too low. Restore copper levels first before donating blood. Low ceruloplasmin could also lead to elevated liver enzymes, low hemoglobin and increased TfR. If ceruloplasmin is normal, and ferritin is still high, you might have inflammation, so check for hsCRP, GGT and other liver enzymes. Inflammation should be lowered as fast as possible as it causes iron accumulation in tissue, which could further promote inflammation.
Low ferritin, low transferrin saturation and elevated serum transferrin receptor, could indicate that you might have low iron stores and might benefit from eating more iron rich foods or considering a supplement.
How to resolve iron dysregulation or low iron
Recent research found that giving people a supplement with multiple vitamins and minerals is much better than giving them only folate or B12 or both, like they used to do in the past.
“We found that 40-75% of the patients were deficient in A, C, D and selenium and 28-38% of the patients had low levels of B vitamins and folate.”
– from (Nutritional deficiencies in iron overloaded patients with hemoglobinopathies)
Vitamin B2 is needed for iron mobilization and low vitamin B2 can cause elevated ferritin and low transferrin saturation.
Vitamin B12
“After cobalamin therapy, serum iron levels (59.1 ± 30 µg/dL), serum ferritin levels (44.9 ± 38.9 ng/mL) and transferrin saturation values (17.5 ± 9.6 %) decreased, and serum UIBC levels (295.9 ± 80.6 µg/dL) increased.” (R)
Vitamin A supplementation may increase hemoglobin and ferritin in people with low retinol (R).
Vitamin D might decrease serum iron and increase hemoglobin or at least prevent its degradation during intense training, but otherwise, it doesn’t seem to affect iron markers all that much (R, R, R).
Zinc is able to lower elevated serum iron and thus TfS (R).
Adding iodine to your iron supplementation dramatically increases ferritin and transferrin more than just iron supplementation alone (R).
Low selenium can cause elevated TfS (R) and iron supplementation increases the requirements for selenium (R).
Low iron can be caused by:
- Ulcers
- Hookworms
- Intestinal bleeding
- Not enough stomach acid
- Infection by helicobacter pylori causes gastric atrophy, which reduces iron absorption
- Inflammation, which increases hepcidin
- Or simply, eating low iron food
If you are iron deficient and are consuming lots of iron rich foods, but cannot seem to increase your iron, then take a safe iron supplement, such as:
However, be careful with iron supplementation as it can significantly increase oxidative stress in the body:
“However, the glutathione peroxidase (GSH-Px) and antioxidant vitamins A, C and E were found significantly decreased (P < 0.01) in all treated groups. Lipid peroxide levels (LPO), protein carbonyl (PC), conjugated dienes (CD), lipid hydroperoxide (LOOH) and oxidized glutathione (GSSG) levels were found significantly increased (P < 0.01) after oral iron (100mg ferrous sulphate) supplementation groups.” (R)
“Co-supplementation of ferrous salts with vitamin C exacerbates oxidative stress in the gastrointestinal tract leading to ulceration in healthy individuals, exacerbation of chronic gastrointestinal inflammatory diseases and can lead to cancer.” (R)
So in summary, don’t take huge amounts, such as over 100mg and don’t take it with vitamin C. Get your vitamin C from natural sources, such as pineapple, kiwi, oranges, etc., as those foods also have natural anti-oxidants that will protect the gut from oxidative damage. Fruit intake is associated with an increase in ferritin and hemoglobin (R).
Calcium, phytic acid, and polyphenols, such as grape seed extract, green tea extract, curcumin, coffee, etc., are iron absorption inhibitors, but small amounts of these compounds, as found in whole foods, should not pose a problem if consumed in moderation (R, R, R, R, R). For example, drinking tea or milk with a meal containing iron does not inhibit its absorption.
To lower iron, you can do/use the following:
- Give blood – this will probably work the fastest
- Aspirin
- Qizhufang (R)
-
Alpha lipoic acid
-
Hesperidin
-
Cranberry
-
Tetracycline
-
Lactoferrin
As always, thanks so much for reading my article. Let me know if this article was helpful in the comments below.
If you found it helpful and insightful please like and share so others can also benefit from this information and feel free to leave a comment down below if you have any questions for me.
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Great article hans, ive gotta aplaude you. This is so much better than what ive learned on my medical school.
Thanks man, appreciate it!
I am impressed with all of the information in your articles. It has been something I have been trying to figure out for years. I appreciate how you separated the topics. The complicated issue of ED can not be fixed with one medication for everyone. The medications become the cause of the problems. There is not enough education for doctors or health care professionals on the effect of copper, iron, NO, and toxins on ED. The thyroid is always evaluated on tsh. We need better steps to treat early ED than NO boosters. Is there somewhere I can find this info in medical journals? Thank you for the information.