I had this response on ferrritin elsewhere which i thought people would find interesting
Ferritin is stored iron and increases oxidative stress and DNA damage
Average lifespan for various ferritin levels
20-200 = 79 years old
200-399 = 76 years old
400-599 = 72 years old
600+ = 55 years old
for every 1 percent increase in ferritin 4 percent increase in heart attack
https://www.ahajournals.org/doi/abs/10.1161/01.CIR.86.3.803
Association between serum ferritin concentrations and levels of urinary 8-hydroxydeoxyguanosine (8-OHdG),
Donate blood or do therapeutic phlebotomy and target ferritin below 50-100
Any lower and you risk anemia.
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So, you agree with this earlier thread: Iron: an underrated factor in aging
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Well, my ferritin is 20 (I’m 68), and I am anemic (Hemoglobin 11.9, RBC 4.1, 'crit 34 - all a little under the normal range). The low ferritin is relatively recent, though I’ve been dealing with borderline anemia most of my adult life. Doctors go “you’re anemic!” when it drops below reference, then lose all interest when it goes a pixel into normal.
So, I dunno. My TIBC is normal, suggesting my iron intake is sufficient - as it should be given I don’t avoid red meat or iron enriched foods. I did have one doctor give me an iron supplement which I now regret taking especially since it made no difference. B12 hasn’t made a difference though I’m trying it again now.
We’ve never figured this one out. I did have about a third of my left femur removed a couple years ago. That might be a factor now though doesn’t explain the previous years.
In terms of longevity, I have the low ferritin going for me. However my RDW (negatively associated with longevity) is high so perhaps it’s a wash.
What are your recent RDW and MCV results?
I think ferritin is an interesting marker. I wonder to what extent my weekly blood tests in themselves have a health benefit. I dont think 10-20 ml a week is necessarily the whole story.
John Hemming -
RDW 17.3% (range 11.6-15.4%)
MCV 87.0 fL (range 79-97 fL)
RDW is, of course, a measurement of variations in MCV. What I found was that as I was managing to get my MCV (size of red blood cells) down from quite a high figure (99-100) my RDW went up because RBCs hang around for about 120 days and hence you can end up with smaller ones and larger ones which pushes up RDW.
Hence you need to look at the changes to see if you actually need to worry about RDW. If your MCV is pretty constant, but RDW high there may be an underlying issue to look at.
Sorry to be that guy but what is grg?
https://www.grg-supercentenarians.org/
There is a mailing list which is another useful source of discussion.
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Stiv
#10
I also have had a low ferritin for years. This year about 10. Was borderline anaemic so was refused my usual blood donation (do 4 a year).
It has never bothered me as a) seemed associated with longevity and b) I feel fine.
Have been investigated as obviously in a 59 yr old male it suggests suspicious blood loss but everything check out. I think Im a poor absorber.
The difference this time is that my RDW went to 17% (with normal MCV) which added years to my ‘biological’ age on the Morgan-Levine calculator. So Ive taken a course of ferrous sulphate, ferritin up to 50 a few weeks ago. Stopped the iron so will see if RDW improves after 120 days.
Interestingly I also get cyanosed at altitude. Might be related.
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How does one reduce MCV?
I’ve thought that regular blood donation might reduce RDW - but without solving the anemia issue that’s not an option.
I’ll check my numbers to see what the trends are. It’s a hassle to manually cross reference so much data - maybe ChatGPT can help here!
RDW is the variation in size of MCV. Blood donation may affect ferritin, but I don’t see a reason it would affect RDW.
dlkmd
#13
Yes ferritin is an iron storage protein but it is also and acute phase reactant. This means that it can be elevated from systemic INFLAMMATION. That may be the link here, ie not iron but inflammation from other causes, eg aging.
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I think there is probably some link to inflammation of some form.
adssx
#15
My ferritin decreased a lot after starting dapagliflozin. It’s apparently well-known: Dapagliflozin Suppresses Hepcidin And Increases Erythropoiesis 2020
There was also a significant fall in ferritin concentrations by 32 ± 7% (from 10.75 ± 1.32 to 5.92 ± 0.88 ng/ml, placebo-corrected change of -4.23 ± 0.63 ng/ml P = 0.011 [Fig. 1]), while transferrin concentration increased by 11 ± 3% (from 298 ± 10 to 315 ± 11 mg/dl, placebo-corrected change = 22 ± 4 mg/dl, P = 0.027 [Fig. 1D]).
Consistent with this, transferrin saturation decreased by 22 ± 5% (P = 0.005), while total iron binding capacity increased by 10 ± 3% (P = 0.025 vs. baseline) and unsaturated iron binding capacity increased by 18 ± 3% (P = 0.013 [Table 1]).
More recent papers:
Iron deficiency and cardiovascular disease 2022
Whether the decline in ferritin reflects reduced iron availability due to increased red cell production or the anti-inflammatory properties of SGLT2i is uncertain.
Iron Deficiency in Heart Failure and Effect of Dapagliflozin: Findings From DAPA-HF 2022
Iron deficiency was common in DAPA-HF and associated with worse outcomes. Dapagliflozin appeared to increase iron use but improved outcomes, irrespective of iron status at baseline.
Potential Interactions When Prescribing SGLT2 Inhibitors and Intravenous Iron in Combination in Heart Failure 2023
In contrast, according to the “cytosolic iron repletion hypothesis,” the effect of SGLT2 inhibitors to decrease hepcidin and ferritin and increase transferrin receptor represents a direct action of these drugs: 1) to reverse inflammation-related increases in hepcidin and ferritin, and, thus, alleviate functional blocks on iron utilization; and 2) to increase in sirtuin-1 signaling, which suppresses hepcidin, accelerates the degradation of ferritin, and up-regulates transferrin receptor protein. […] The totality of clinical evidence supports the “cytosolic iron repletion hypothesis” because SGLT2 inhibitors elicit a full and sustained erythrocytosis in response to erythropoietin, even in overtly iron-deficient patients and in the absence of intravenous iron therapy. Therefore, the emergence of an iron-deficiency pattern of response during SGLT2 inhibition does not reflect worsening iron stores that are in need of replenishment, but instead, represents potential alleviation of a state of inflammation-related functional iron deficiency that is commonly seen in patients with chronic heart failure. Treatment with intravenous iron may be unnecessary and theoretically deleterious.
Sodium–Glucose Transporter 2 (SGLT2) Inhibitors and Iron Deficiency in Heart Failure and Chronic Kidney Disease: A Literature Review 2023
Furthermore, treatment with SGLT2 inhibitors leads invariably to a decrease in serum ferritin and transferrin saturation in laboratory findings that meet the typical current diagnostic criteria for an ensuing iron deficiency (Figure 2). After 12 months in the DAPA-HF trial, patients on dapagliflozin vs. placebo developed iron deficiency, according to the current diagnostic criteria, far more frequently (70%). However, dapagliflozin continued to induce uninterrupted, significant erythropoiesis and a rise in hemoglobin (Docherty et al., 2022) [21]. These intriguing findings raise the logical question about the clinical reliability of the laboratory diagnostic markers currently in use for iron deficiency, especially when patients are receiving SGLT2i.
How low is too low for iron (mine: 12 µmol/L), ferritin (19 µg/L) and transferrin saturation (16%)?
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AnUser
#16
Optimal ferritin levels according to Bryan Johnson’s team is 30-60 ug/L, so it is low and outside the reference range. He takes a ferritin supplement. I don’t know about the others.
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When you say “a ferritin supplement” is that to reduce ferritin, or increase it or is it “ferritin”. What is it?
AnUser
#18
I meant heme iron, to increase ferritin as his is/was low, he takes this, 10.5 mg a day:
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AIUI low is generally good as long as you are not actually anaemic.
Those are pretty low ranges according to Quest Diagnostics.
After taking rapamycin for some time I had to take an iron supplement to get back to 33ng/mL.
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