We requested an iron panel as it was clear his GP wasn’t going to offer even though husband falls asleep at the drop of a hat. I’m glad we asked because his ferritin is very low having fallen from his usual 50-90 over the years
26/07/22
Ferritin 19.2 (22 -322)
Serum iron 21.4 (14 - 31.3) 42.77%
According to rT3 adrenals, in men, nearer 70% is better
Transferrin 2.52 (2.15 - 3.65) 24.67% I think this might be considered low and therefore shows a lack of capacity for more iron, according to rT3
% Saturation 37 (16 - 50) Again, rT3 says in men, nearer 45% is better
Our iron intake from food is good and we also supplement with iron but I’ve recently discovered that the dose we both take is only a maintenance for those who already have good levels. We vary between 13mg and 25mgs depending on the product at the time and have also been experimenting with alternate days because of latest suggestions but also constipation issues. Husband isn’t a rigid as me at taking it because of work travels
It’s possible levels have dropped because of the low dose taken only on alternate days and it’s also clear there are likely absorption issues which will need to be addressed but for now I’d like help interpreting the labs please
If transferrin is suggesting lack of capacity but his ferritin and serum iron need help, what to do?!!
Iron saturation being reasonable also confuses the picture somewhat. Or at least I’m confused by it
Thank you
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Noelnoel
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Yes, your husbands iron levels and reserves are low.
The transferrin is low because his serum iron is only 42.77% through range. In a healthy person transferrin might increase to encourage more iron to be procured from which ever source (food, ferritin, etc) but inflammation can stop transferrin increasing. The ‘lack of capacity for more iron’ means there is no more room to keep iron safely bound as obviously ‘free’ iron would be toxic.
T/S% is a calculation of other iron values and often becomes meaningless when iron mechanism aren’t working well except to confirm they aren’t working well!
Low doses of iron are often tolerated better than high to prevent the bodies safety mechanisms coming into play. Maybe taking less iron but twice a day with some vitamin C, or else Betaine HCL with pepsin that improves gastric acid levels and iron absorption. Alcohol also improves iron absorption 😉.
If this were me I would ask GP for FBC that assesses RBC's & haemoglobin levels for investigative aenemia markers, and other inflammation markers such as CRP & ESR
The transferrin is low because his serum iron is only 42.77% through range
It looks as though you’re saying his transferrin is low because his serum iron is
You then go on to say:
inflammation can stop transferrin increasing
Am I correct to say his transferrin is low but ought to be higher, that it isn’t low because his serum iron is low but because of the possibility of inflammation which may be preventing a rise in transferrin thus disabling uptake of iron
I’m confused, which, believe me isn’t difficult. I find the whole iron panel thing a minefield but I need some clarification on these two points before I can begin to unravel it and understand
I’m not sure exactly what you are asking 😁 but I'll try explaining again.
Once heme iron is absorbed (with help from HCL + Vit C) ferroportin takes it to transferrin for transportation around the body to bone marrow, tissues, etc. Almost all circulating plasma iron is bound either to ferritin or transferrin, and your liver should produce more transferrin to encourage more circulating iron when stores run low.
But bodily inflammation caused by insulin resistance, gut issues, even COVID infections, etc, causes the liver to release damaging cytokines such as hepciden & IL6 (IL6 is extremely common in Hashi & why we aim to keep antibodies low).
Ferroportin can be very vulnerable to these cytokines and stops the iron reaching the transferrin. This is when labs should show transferrin going up (inverse relationship with iron) as it tries to encourage more iron but on this forum we often see transferrin remaining low in the presence of low serum iron, and this is also related to bodily inflammation known as Anaemia of Inflammation (or Chronic Disease). It just means the inflammation is preventing intricate iron mechanisms from working correctly in several different ways.
There are many forms of anaemia & they often cross over into each other as the full impact of deficiencies cause issues in so many different areas, and it can be difficult to unravel what is causing what. For instance in someone with Vit B12 deficiency anaemia that prevents good erythropoiesis, serum transferrin levels should increase to prevent unused iron from going into tissue iron overload but in the presence of other health issues causing bodily inflammation transferrin may remain low. This is why an iron panel is essential and when symptomatic other blood chemistry must also be considered.
Usually the body controls iron levels (to an large extent) by absorption. Calcium is an iron absorption inhibitor (both heme & non-heme) so it's best not to have milk with your steak & chips but a glass of orange juice for instance.
Thank you radd, I really appreciate your efforts to explain. It’s clear you have a lot of knowledge on iron but for someone like me who doesn’t, small and simple explanations work best. Others can absorb and digest quickly, I can’t so intricate introductions of mechanisms are wasted on me
As I begin to grasp the various concepts there will be more questions and I really do understand if you don’t have the stomach for the long haul, maybe someone else will chip in to help
I need to firstly clarify what you’re trying to explain in the statement below:
The transferrin is low because his serum iron is only 42.77% through range
You appear to be saying that low serum iron is causing low transferrin
Followed by:
inflammation can stop transferrin increasing
Meaning that inflammation also causes low transferrin. Is my understanding correct?
Sorry to have jumped in on your post and thank you for asking the question, which is pertinent to my situation too. I think the idea is that your husband is likely to have some form of inflammation/ill health/other anaemia preventing his transferrin raising. My low B12 has been confusing the picture with my low iron for years. Best wishes
Uncomplicated iron deficiency: Serum transferrin (and TIBC) high, serum iron low, saturation low. Usual causes of depleted iron stores include blood loss, inadequate dietary iron. RBCs in moderately severe iron deficiency are hypochromic and microcytic. Stainable marrow iron is absent. Serum ferritin decrease is the earliest indicator of iron deficiency if inflammation is absent.
Anemia of chronic disease: Serum transferrin (and TIBC) low to normal, serum iron low, saturation low or normal. Transferrin decreases with many inflammatory diseases. With chronic disease there is a block in movement to and utilization of iron by marrow. This leads to low serum iron and decreased erythropoiesis. Examples include acute and chronic infections, malignancy and renal failure.
(note - LabCorp is US based so any reference ranges shown on their site may not apply to the UK)
Thanks for the helpful explanations. What would you suggest as a suitable low dose, if I were to try a twice a day regime? I have been using Spatone (two sachets for a month, then three for a couple of months, but every other day) but iron panel still pitiful and TIBC 28%. (Ferritin 4.63%, serum iron 14.35% and saturation 18.7%).
Very interested that you mention both covid and IL6, as I've had covid, likely twice in 4 months, and was supplementing hard beforehand but recent test which was straight after 2nd (unconfirmed but symptomatic) bout was as bad as ever. I am genetically predisposed to higher IL6 anyway. No blood signs of inflammation (what would HDL do re. inflammation please?) and on autoimmune diet with benefit. Just bought a new iron supplement to try in addition to the Spatone but it was expensive (for me) so want to use it in the best way I can.
I can't offer you my experiences regarding the doses for iron supplementation because have haemochromatosis, and that that is why I have knowledge on how iron works.
Regarding HDL .......
'During inflammation multiple changes in HDL structure occur leading to alterations in HDL function. In the short term, these changes may be beneficial resulting in an increase in cholesterol in peripheral cells to improve host defense and repair but over the long term these changes may increase the risk of atherosclerosis'.
Are you able to say if my understanding of those two points is right. It would be helpful if you could because I get in a real muddle with iron and when we speak with our GP l want to be sure I’m clear on what to ask for
Apologies that I’ve been unable to appreciate properly the rest of what you wrote but once I have the answer for the above I’ll feel better equipped to move on to look at it in more depth and I really don’t expect you to hold my hand as I do that, I’ll just re-post
No, low serum iron doesn't necessarily cause low transferrin. Possibly liver issues but usually inflammation (from auto immune disease) is the most likely cause of low transferrin on this forum,
Ideally transferrin should match that of adequate iron levels for transportation and to keep it bound. When iron becomes low, transferrin should increase to encourage more iron into circulation. but low iron by its very nature is indicative of unwellness, and risks misaligned iron/transferrin mechanisms.
Further variations come about because of the 'healthy' volatile nature of ferritin's relationship with the immune system (ie ferritin withholding iron in the presence of infection to starve bacteria by creating 'healthy' inflammation) and the 'unhealthy' & damaging influence of auto-inflammation inhibiting transferrin from raising.
Remember not all inflammation is healing and skewed iron results are rarely simple.
It’s still a way from being solidly compounded/embedded in my head but these explanations are helping me piece it together
A test about a month ago that included CRP showed 0.8 (0 - 5) but does this definitively rule out inflammation or would ESR have to be carried out too, a bit like having the two antibody tests for Hashi’s
We know that his thyroid has been struggling for at least four years but probably longer because I’d been watching his decline for some time, finally getting suspicious about his thyroid gland from what I kept reading on here. Eventually he listened and got tested
April 2018
TSH 6.09 (0.27 - 4.2)
FT4 13.2 (12 - 22)
The consultant then advised husband’s GP should follow up.10 weeks later GP repeated
June 2018
TSH 5.3 (0.35 - 5.5)
FT4 15.4 (10 - 19.8)
Dec 2021
TSH 6.68 (0.35 - 5.5)
FT4 14 (10.5 - 21)
FT3 4.5 (3.5 - 6.5)
All very unsatisfactory
B12 733 (211 -911) supplements
Folate 8.9 > 5.38 supplements
GP said the usual, TSH needs to be higher before thyroid replacement. We know where this trajectory is leading but for some reason we have to wait till his gland starts failing and he’s feeling really unwell. What a fab policy that is!
So, we are now at the point where other labs (iron panel) are showing up problems which perhaps could’ve been avoided if thyroid treatment had already commenced but it’s no good crying over the proverbial
Rather than wait until he’s on his knees I’m wondering about getting him started on the same glandulars as me to see what happens, alongside trying to address the iron panel problems. Is it possible that if glandulars start to raise his thyroid hormones and he continues with low dose iron, that his iron panel could start to improve. I know about the chicken and egg possibility of which came first; struggling thyroid gland or low nutrients but if we address both at the same time …?
I should also mention his TPOab is low within range but he’s never had the other Hashi antibody test. However, when he returns next week he’ll be doing the medichecks test which includes it
This is part of recent FBC. I hope I’ve covered everything
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