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Mij
Senior Member (Voting Rights)
An Internist I saw in 1991 told me that my 'iron' was fine. I don't know if he tested my ferritin, and didn't know what ferritin was at time so didn't ask.
Then in 1996 when I was tested by a new GP, my ferritin was at 4. She asked if I was vegetarian, and when I told her I wasn't, she didn't believe me. She said "I only see this in vegetarians'. She gave me an rx for iron, and then accused me of not taking it because it took almost 9 months to increase my ferritin. I dropped her as a doctor.
Then in 1996 when I was tested by a new GP, my ferritin was at 4. She asked if I was vegetarian, and when I told her I wasn't, she didn't believe me. She said "I only see this in vegetarians'. She gave me an rx for iron, and then accused me of not taking it because it took almost 9 months to increase my ferritin. I dropped her as a doctor.
Arnie Pye
Senior Member (Voting Rights)
I've never had much difficulty getting ferritin tested. What I have difficulty getting is an iron panel. Ferritin was tested annually by my GP between 2010 (the earliest year I have results for) and 2013 (when it was done twice in consecutive months) and it dropped every time it was measured. What my GP didn't do was give me an iron panel, so my serum iron was never tested by her. But when I bought my GP records in 2014, I discovered that a hospital had tested my iron in 2010, and had alerted my GP (but not me) to the fact it was below range.
In the end I improved my own iron and ferritin, by paying privately for iron panels and buying my own prescription-strength iron tablets.
Merged thread
Could suspected low-grade inflammation in ME cause iron deficiency?
The following are: an article on iron deficiency from the Royal College of Physicians, an article on the role of low-grade inflammation in ME, and lastly, an article on activin family proteins as serum biomarkers for ME/cfs.
This third article reports:
"Interestingly, activin B is involved in inflammatory-induced anaemia via regulation of hepcidin expression [10], a function distinct from activin A."
Speculative wondering. Your comments are very much appreciated.
Thank you.
Here are the articles:
This article is from the Royal College of Physicians:
Iron deficiency without anaemia: a diagnosis that matters
Abdulrahman Al-Naseem, Abdelrahman Sallam, Shamim Choudhury and Jecko Thachil
DOWNLOAD PDF
DOI: https://doi.org/10.7861/clinmed.2020-0582
Clin Med March 2021
"Causes of iron deficiency
Iron has both a storage pool and a functional pool. The storage pool is the reticuloendothelial system which consists of the liver, spleen and lymph nodes. The functional pool consists of red blood cells, bone marrow and cardiac and skeletal muscle. Iron is absorbed in the duodenum via specific transporters and is carried by transferrin molecules to the storage and functional pools. Iron deficiency can be absolute or functional. AID is when the storage pool is iron-deficient due to reduced intake, increased needs, reduced absorption or excessive loss. AID also causes low iron levels within the functional pool. In FID the burden is the chronic inflammation, causing cytokine and hepcidin release. Hepcidin causes iron deficiency via the blockage of an iron exporter known as ferroportin. There are two ways in which this blockage causes ID. First, it reduces iron absorption in the duodenum; second, it causes iron retention within the storage pools. This means that despite normal iron levels within the storage pools, functional pools are iron deficient and cannot utilise the stored iron for vital body processes."2,10,12 (my bolding)
https://www.rcpjournals.org/content/clinmedicine/21/2/107
The role of low-grade inflammation in ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) - associations with symptoms
https://pubmed.ncbi.nlm.nih.gov/31901625/
Activin B is a novel biomarker for chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) diagnosis: a cross sectional study
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5353946/#!po=4.26829
"Interestingly, activin B is involved in inflammatory-induced anaemia via regulation of hepcidin expression [10], a function distinct from activin A."
ETA: added quotation marks
ETA #2: added title
Could suspected low-grade inflammation in ME cause iron deficiency?
The following are: an article on iron deficiency from the Royal College of Physicians, an article on the role of low-grade inflammation in ME, and lastly, an article on activin family proteins as serum biomarkers for ME/cfs.
This third article reports:
"Interestingly, activin B is involved in inflammatory-induced anaemia via regulation of hepcidin expression [10], a function distinct from activin A."
Speculative wondering. Your comments are very much appreciated.
Thank you.
Here are the articles:
This article is from the Royal College of Physicians:
Iron deficiency without anaemia: a diagnosis that matters
Abdulrahman Al-Naseem, Abdelrahman Sallam, Shamim Choudhury and Jecko Thachil
DOWNLOAD PDF
DOI: https://doi.org/10.7861/clinmed.2020-0582
Clin Med March 2021
"Causes of iron deficiency
Iron has both a storage pool and a functional pool. The storage pool is the reticuloendothelial system which consists of the liver, spleen and lymph nodes. The functional pool consists of red blood cells, bone marrow and cardiac and skeletal muscle. Iron is absorbed in the duodenum via specific transporters and is carried by transferrin molecules to the storage and functional pools. Iron deficiency can be absolute or functional. AID is when the storage pool is iron-deficient due to reduced intake, increased needs, reduced absorption or excessive loss. AID also causes low iron levels within the functional pool. In FID the burden is the chronic inflammation, causing cytokine and hepcidin release. Hepcidin causes iron deficiency via the blockage of an iron exporter known as ferroportin. There are two ways in which this blockage causes ID. First, it reduces iron absorption in the duodenum; second, it causes iron retention within the storage pools. This means that despite normal iron levels within the storage pools, functional pools are iron deficient and cannot utilise the stored iron for vital body processes."2,10,12 (my bolding)
https://www.rcpjournals.org/content/clinmedicine/21/2/107
The role of low-grade inflammation in ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) - associations with symptoms
https://pubmed.ncbi.nlm.nih.gov/31901625/
Activin B is a novel biomarker for chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) diagnosis: a cross sectional study
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5353946/#!po=4.26829
"Interestingly, activin B is involved in inflammatory-induced anaemia via regulation of hepcidin expression [10], a function distinct from activin A."
ETA: added quotation marks
ETA #2: added title
Last edited by a moderator:
Arnie Pye
Senior Member (Voting Rights)
Could suspected low-grade inflammation in ME cause iron deficiency?
I think inflammation could cause low iron in anyone, with or without ME - but I'm making a distinction between serum iron and ferritin (iron stores).
Ferritin is an "Acute Phase Protein". This means it rises in the presence of infection or inflammation.
It increases because the body moves iron into ferritin to reduce the ability of pathogens to reproduce. Iron is locked up very tightly in ferritin and pathogens can't access the iron, whereas serum iron can be "stolen" by pathogens.
You might find this link of interest :
https://irondisorders.org/anemia-of-chronic-disease-2/
I think inflammation could cause low iron in anyone, with or without ME - but I'm making a distinction between serum iron and ferritin (iron stores).
Ferritin is an "Acute Phase Protein". This means it rises in the presence of infection or inflammation.
It increases because the body moves iron into ferritin to reduce the ability of pathogens to reproduce. Iron is locked up very tightly in ferritin and pathogens can't access the iron, whereas serum iron can be "stolen" by pathogens.
You might find this link of interest :
https://irondisorders.org/anemia-of-chronic-disease-2/
Jonathan Edwards
Senior Member (Voting Rights)
I think the problem is that these studies did not find low grade inflammation in ME. The second study sounds as if it did but it actually had no controls so tells us nothing about ME having low grade inflammation. It talks about correlations with symptoms but although it picks out the few instances where there was some correlation it seems that is a whole there were no correlations - at least with fatigue. So hidden behind the text it says - we more or less did not find any inflammation that related to ME symptoms.
The third study is even clearer. Despite the raised Activin B, everything else was normal - so no inflammation. So it is a bit difficult to know what to make of the Activin - certainly not a relation to inflammation.
The first paper claims that iron deficiency without anaemia is very important but there is precious little support for this in the actual paper. It admits that symptoms are too vague to now whether they are due to iron deficiency or the disease causing the iron deficiency.
I cannot get excited about this I am afraid.
The third study is even clearer. Despite the raised Activin B, everything else was normal - so no inflammation. So it is a bit difficult to know what to make of the Activin - certainly not a relation to inflammation.
The first paper claims that iron deficiency without anaemia is very important but there is precious little support for this in the actual paper. It admits that symptoms are too vague to now whether they are due to iron deficiency or the disease causing the iron deficiency.
I cannot get excited about this I am afraid.
Thank you @Arnie Pye for your comments and the link.
Arnie Pye
Senior Member (Voting Rights)
People might like this video, which just came out today, on "Blood Tests For Iron Status".
The speaker is not the most compelling speaker I've ever heard, but his information was interesting. He discusses iron studies and ferritin in a general way, then starts to discuss results you might see in sickness, including inflammation. Towards the end of his talk he discusses haemochromatosis.
The speaker is not the most compelling speaker I've ever heard, but his information was interesting. He discusses iron studies and ferritin in a general way, then starts to discuss results you might see in sickness, including inflammation. Towards the end of his talk he discusses haemochromatosis.
Arnie Pye
Senior Member (Voting Rights)
Copied post
I had to do my own diagnosis for my chest pain. When the standard tests for heart attack showed I wasn't having one - and this happened several times - I was eventually asked if I was "anxious" and I said no. I could tell I wasn't being believed.
At the same time this was going on I also had a GI bleed that had been going on for several years. Eventually (it took three hospitals to find it) I had what was described as a "giant polyp" removed which had very fragile blood vessels. I discovered eventually that my GP records suggested that I was seeking treatment for piles (which I wasn't - the blood was much too dark for that) which was why nobody was taking it seriously.
In the end I had to fix my own low iron and low ferritin. It took nearly two years because I absorbed iron poorly, and during that time my chest pain reduced and reduced. I no longer get it now. If you look at links for anaemia the fact that it can cause chest pain and tachycardia is barely mentioned. It certainly isn't given any prominence. I didn't exactly diagnose the cause of my chest pain. I paid for testing, saw I had low iron and ferritin, started fixing that, and ended up fixing the chest pain in the process, as an added bonus.
I had to do my own diagnosis for my chest pain. When the standard tests for heart attack showed I wasn't having one - and this happened several times - I was eventually asked if I was "anxious" and I said no. I could tell I wasn't being believed.
At the same time this was going on I also had a GI bleed that had been going on for several years. Eventually (it took three hospitals to find it) I had what was described as a "giant polyp" removed which had very fragile blood vessels. I discovered eventually that my GP records suggested that I was seeking treatment for piles (which I wasn't - the blood was much too dark for that) which was why nobody was taking it seriously.
In the end I had to fix my own low iron and low ferritin. It took nearly two years because I absorbed iron poorly, and during that time my chest pain reduced and reduced. I no longer get it now. If you look at links for anaemia the fact that it can cause chest pain and tachycardia is barely mentioned. It certainly isn't given any prominence. I didn't exactly diagnose the cause of my chest pain. I paid for testing, saw I had low iron and ferritin, started fixing that, and ended up fixing the chest pain in the process, as an added bonus.
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Moved posts
Interesting. One of my aunts ( without ME/.CFS ) has developed chest pains . Concurrently she has high ferritin ( iron panel ok, no heamachromatosis) . I wonder if there is a related mechanism .
Interesting. One of my aunts ( without ME/.CFS ) has developed chest pains . Concurrently she has high ferritin ( iron panel ok, no heamachromatosis) . I wonder if there is a related mechanism .
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Arnie Pye
Senior Member (Voting Rights)
High ferritin with an okay iron panel could be a sign of inflammation. Ferritin is an acute phase protein (aka acute phase reactant) :
https://en.wikipedia.org/wiki/Acute-phase_protein
But having said that, I don't think knowing it is very helpful because it doesn't tell you whereabouts in the body the inflammation is or anything about the cause of a problem.
Another cause of high ferritin is : https://en.wikipedia.org/wiki/Anemia_of_chronic_disease
These might be of interest :
https://bootcampmilitaryfitnessinst...m-ferritin-levels-koperdanova-cullis-2015.pdf
https://www.oxfordshireccg.nhs.uk/p.../S59-3-investigation-of-a-raised-ferritin.pdf
https://mft.nhs.uk/app/uploads/2019/07/high-ferritins-for-GP-guide-FINAL.pdf
https://academic.oup.com/metallomics/article/6/4/748/6015473
Thank you.
I had suggested inflammation to let her discuss with GP. GP pretty uninterested,- seems to happen more and more once you are classed as " elderly"
I shall check out the links - thanks again
For another ne of my aunts the high ferritin has probably been sussed out. Inflammation a definite .
After years of back pain, put down to bring constantly on her feet as a florist, she finally got GP to take note via a letter from her chiropractor.
She has osteo arthritis. Meds have made a huge difference.
My ME aunt however had not got tobthe bottom of hers
After years of back pain, put down to bring constantly on her feet as a florist, she finally got GP to take note via a letter from her chiropractor.
She has osteo arthritis. Meds have made a huge difference.
My ME aunt however had not got tobthe bottom of hers
Art Vandelay
Senior Member (Voting Rights)
My ferritin has been very high ever since I got ME/CFS. I've been tested for haemochromatosis many times because no-one can quite believe it. Fatty liver was also ruled out early on.
My Father's ferritin has been very high also but only over the last 7-8 years. His GP seems to have lost interest in exploring the reason why.
Mij
Senior Member (Voting Rights)
Merged
Iron deficiency goes unnoticed in too many U.S. female adolescents
Typically, 15 μg/L is the cutoff used to diagnose iron deficiency, says Laura Murray-Kolb, a nutrition scientist at Purdue University in West Lafayette, Ind., who was not involved in the study. The WHO set that cutoff based on when the body’s iron stores in bone marrow are already depleted. Without enough iron, bone marrow can’t produce more hemoglobin.
But the standard may not be the most effective measure of iron deficiency, Weyand says, because it doesn’t capture “how much iron our [bodies] think we need.” Weyand has treated patients with symptoms of iron deficiency who have ferritin levels above the 15 μg/L cutoff.
In the new study, about 40 percent of participants met the 25 μg/L criteria for iron deficiency. Only 17 percent would qualify based on the 15 μg/L standard set by the WHO, which is roughly in line with previous estimates. Six percent met criteria for anemia, with both ferritin levels below 25 μg/L and hemoglobin levels below the standard cutoff of 12 milligrams per deciliter.
https://www.sciencenews.org/article/iron-deficiency-goes-anemia-us-female-adolescents
Iron deficiency goes unnoticed in too many U.S. female adolescents
Typically, 15 μg/L is the cutoff used to diagnose iron deficiency, says Laura Murray-Kolb, a nutrition scientist at Purdue University in West Lafayette, Ind., who was not involved in the study. The WHO set that cutoff based on when the body’s iron stores in bone marrow are already depleted. Without enough iron, bone marrow can’t produce more hemoglobin.
But the standard may not be the most effective measure of iron deficiency, Weyand says, because it doesn’t capture “how much iron our [bodies] think we need.” Weyand has treated patients with symptoms of iron deficiency who have ferritin levels above the 15 μg/L cutoff.
In the new study, about 40 percent of participants met the 25 μg/L criteria for iron deficiency. Only 17 percent would qualify based on the 15 μg/L standard set by the WHO, which is roughly in line with previous estimates. Six percent met criteria for anemia, with both ferritin levels below 25 μg/L and hemoglobin levels below the standard cutoff of 12 milligrams per deciliter.
https://www.sciencenews.org/article/iron-deficiency-goes-anemia-us-female-adolescents
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Arnie Pye
Senior Member (Voting Rights)
For people who have a Twitter account and can read replies this thread is really shocking :
It's very long and it is just report after report from women that doctors have dismissed their ferritin levels under 10 as not being important.
In my own experience doctors don't treat low ferritin as long as haemoglobin is in range.
It's very long and it is just report after report from women that doctors have dismissed their ferritin levels under 10 as not being important.
In my own experience doctors don't treat low ferritin as long as haemoglobin is in range.