Very similar to my latest numbers. Your ferritin is slightly lower though.
“A study in Sweden found that older people with anemia (i.e., hemoglobin less than 12 g/dL in women and 13 g/dL in men) were 66% more likely to develop Alzheimer’s disease and have higher levels of biomarkers for Alzheimer’s than those who were not anemic (Valletta, JAMA 2026). However, this association does not prove cause-and-effect and there appeared to be little or no additional benefit to having much higher than adequate hemoglobin levels.”
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2847873
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Iron deficiency and dementia risk: evidence from the Swedish population-based cohort study AMORIS
Discussed just above:
Two exposure groups were defined: absolute iron deficiency (serum ferritin < 30 ug/L) and functional iron deficiency (transferrin saturation < 20% and serum ferritin ≥ 30 ug/L).
Compared with the reference group, absolute and functional ID was associated with increased dementia diagnosis (adjusted hazard ratio (HR) = 1.24, 95% confidence interval (CI): 1.18–1.42; HR = 1.21, 95% CI: 1.05–1.39, respectively), after adjusting for age, sex, education, and comorbidities.
That’s an interesting one @John_Hemming. So should one target transferrin saturation > 20% and serum ferritin ≥ 30 ug/L?
This is where the neural dopamine pathway comes in. I think that needs higher ferritin. 50-70 territory.
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Do you use topical or subq? Wouldn’t you expect the former to have a lesser effect on iron stores?
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No question. And it explains why extreme athletes like Lance Armstrong juice with EPO. Higher EPO equals higher HGB and a corresponding increase in performance.
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I’ve switched to topical compounded T cream, which is more expensive but should have a much less significant effect on hematocrit and iron stores (ferritin). In the mean time I’m also supplementing with heme iron and just playing the waiting game for ferritin to increase and hematocrit to gradually come down over the next couple of months.
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Dr. Greger does a deep dive into iron and health, ferritin and diabetes, cancer, neurological effects, anemia, optimal levels, supplementation and so forth.
The Iron Dilemma (via NutritionFacts.org)
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Summary
Greger’s iron episode argues a single thesis: most people carry more iron than is healthy, the “sweet spot” is a ferritin of 15–50, vegetarians sit closer to it, and excess iron drives diabetes and cancer via free-radical damage. He distinguishes iron stores (ferritin) from frank anemia, and closes with practical repletion advice for those who are actually deficient. The framing is consistently directional toward “less meat, more plants,” and the strength of evidence behind individual claims varies widely — the weakest claims carry the most rhetorical weight.
Key points as presented
- Ferritin measures stores; “normal” 30–300, but healthy ≈ 15–50; >50 starts toxicity risk, <12–15 too low.
- Iron is a pro-oxidant; we have no excretion mechanism, so stores rise with age.
- Higher iron → higher type 2 diabetes risk across the normal range (+20% at average ferritin, +43% at high), supported by Mendelian randomization and a small phlebotomy trial.
- Cancer as a “ferrotoxic disease”; a blood-donation RCT showed 60% lower cancer death.
- Vegetarians have lower ferritin but are not meaningfully more anemic (vegans 8% vs meat-eaters 9% in the British cohort).
- Iron deficiency without anemia has no demonstrated harms (one study, even showed “better memory”).
- Repletion advice: alternate-day dosing, vitamin C, bisglycinate, empty stomach; diet over supplements long-term.
What holds up
No iron excretion mechanism / stores accumulate with age — Correct. Regulation is absorption-only; men rise from adulthood, women post-menopause. (High)
Heme iron is less down-regulated than non-heme — Accurate, and it’s the mechanistic basis for heme iron tracking with cardiometabolic risk. (High)
Higher iron status associates with T2D, with some causal support — The observational association is robust (multiple meta-analyses), and MR provides some causal signal. Magnitudes (~20%/43%) are plausible. (Medium) — see caveats below.
Alternate-day dosing, vitamin C timing, bisglycinate tolerability — Aligns with current absorption/hepcidin science (Stoffel et al.). Bisglycinate’s ~2× bioavailability is reasonably supported. (Medium-high) — relevant to your own bisglycinate use.
~75% GI side effects / ~1-in-4 discontinuation on ferrous salts — In range for full-dose daily ferrous sulfate. (Medium-high)
Vegans not meaningfully more anemic than meat-eaters — Consistent with the EPIC-Oxford anemia data he cites; the anemia/low-stores distinction is correctly drawn. (Medium) — caveat: iron deficiency without anemia is genuinely more common in vegans, which he soft-pedals.
Menorrhagia as leading IDA cause in menstruating women — Correct for that population. (High)
What doesn’t hold up (or is overstated)
The “60% lower cancer death from donating blood” claim — This is the load-bearing overstatement. The source is the FeAST trial (Zacharski). Reality: 1,277 symptomatic peripheral-arterial-disease patients, mean age 67, 98.5% male — not healthy general-population volunteers, and “calibrated phlebotomy,” not voluntary blood donation. Critically, no difference was documented between treatment groups in all-cause mortality and the secondary outcome of death plus nonfatal MI and stroke — the trial’s primary endpoint was null. Cancer was a secondary substudy: reduced cancer incidence (HR 0.65, 6.0% vs 9.3%) and the cancer-mortality HR ≈0.39 that yields his “60%.” Single trial, unreplicated, secondary endpoint, narrow population. Presenting it as “a thousand cancer-free individuals randomized to donate blood” is misleading framing. Holds weakly; the framing does not hold. (Low) ScienceDirect + 3
Ferritin as a clean iron marker for the diabetes/cancer claims — Major omission: ferritin is an acute-phase reactant. It rises with inflammation, insulin resistance, fatty liver, and alcohol. Much of the “elevated ferritin → diabetes” association is confounded/reverse-causal — insulin resistance raises ferritin. MR partly addresses this, but MR results for iron→T2D are mixed across studies, not the settled “genetic evidence supports a causal link” he asserts. (Medium that some causal effect exists; Low for the clean magnitude he implies)
The n=6 phlebotomy/insulin-sensitivity study — Real (Fernández-Real), but six men. The ~40% effect is directionally consistent with MR but the study itself is far too small to “demonstrate” anything. He presents underpowered evidence as confirmatory. (Low as standalone proof)
“Iron deficiency without anemia is harmless” — Overstated via cherry-pick. The single study he leans on (the “better memory” finding is almost certainly a multiple-comparisons artifact) is contradicted by several RCTs (Verdon 2003, Krayenbuehl 2011, Vaucher 2012) showing iron repletion reduces fatigue in non-anemic iron-deficient women. The honest statement is “evidence is mixed,” not “no conclusive evidence of harm.” (Does not hold as stated)
The 15–50 “sweet spot” / “>50 = toxicity” — A defensible minority position presented as established. The optimal ferritin range is genuinely contested; mainstream deficiency cutoffs (<30, sometimes <45 with inflammation) and the upper bound are debated. Treating 50 as a toxicity threshold is the aggressive end of the literature. (Low-medium)
Bottom line
The mechanistic spine (no excretion, heme vs non-heme, iron as pro-oxidant) and the practical dosing advice are sound. The disease-prevention thesis rests disproportionately on one null-primary-endpoint trial’s secondary analysis and on a biomarker (ferritin) confounded by inflammation — neither acknowledged. It’s a reasonable hypothesis dressed as a settled conclusion. Net: directionally plausible, evidentially oversold. (Overall confidence in his strong causal framing: Low-medium.)
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Looking at this and not watching the video he does not seem to mention dopamine. Arguably that wants ferritin at 70. (whichever units)
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Sustained dysregulation of iron and glutathione homeostasis induces chronoferroptosis, a persistent ferroptotic adaptation in neuronal cells
https://www.nature.com/articles/s41420-026-03208-6
“Although iron accumulates in brain regions impacted by neurodegenerative diseases such as Alzheimer’s and Parkinson’s, how chronic elevated iron levels contribute to neuronal dysfunction remains unclear. Here, we show that sustained iron overload, but not acute exposure, leads to a state of ferroptotic stress where nerve cells remain viable but become hypersensitive to oxidative injury. Retinoic acid-differentiated SH-SY5Y neuronal cells were exposed to acute (6–8 h) or chronic (9 days) iron loading to model transient versus prolonged age-related iron stress. While acute iron exposure produced minimal biochemical changes and did not sensitize cells to oxidative or ferroptotic challenges, chronic iron exposure induced ferritin upregulation, mitochondrial superoxide accumulation, suppression of GPX4 expression, elevated lipid peroxidation and loss of cellular glutathione (GSH). In addition, chronic but not acute GSH depletion by buthionine sulfoximine (BSO) recapitulated the iron-induced phenotype. Cells under chronic ferroptotic stress exhibited increased sensitivity not only to the ferroptosis inducer RSL-3 but also to hydrogen peroxide. Ferrostatin-1 significantly mitigated these effects suggesting that lipid peroxidation drives this state. Together, these findings demonstrate that, in contrast with acute exposure, chronic disruption of iron homeostasis with consequent GSH depletion remodels cellular redox homeostasis over time, inducing a state we term chronoferroptosis: a persistent ferroptotic adaptation characterized by coordinated alterations in iron-handling and antioxidant defense proteins that may represent early vulnerability to neurodegenerative pathology. Thus, these studies highlight the importance of sustained stress paradigms for modeling the progressive nature of neurodegenerative diseases.”
Pop-sci article.
Long-Term Iron Accumulation Strips Neurons of Disease Resilience
"Neurodegenerative conditions like Alzheimer’s and Parkinson’s diseases afflict tens of millions of people worldwide, driven by a complex web of cellular vulnerabilities that scientists are actively racing to untangle. For years, an intriguing clue has hovered at the edges of neurodegeneration research: the gradual, progressive buildup of iron inside aging neurons. While this mineral accumulation appears harmless early in life, it eventually transforms into a catalyst for slow, widespread neuronal demise.
A breakthrough study finally unmasked the temporal mechanics behind this heavy-metal threat. By engineering the first-ever progressive cellular model of long-term iron accumulation, the team discovered that chronic iron exposure systematically dismantles a neuron’s internal defense systems over time. This chronic depletion leaves the cells fragile, defenseless, and highly vulnerable to secondary environmental stressors, a distinct, time-dependent degenerative pathway the researchers have named chronoferroptosis."
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In short I just want to say loudly:
Reducing iron works!
I want to share my daily experiences with this. Papers and research are always welcome, but direct experience is crucial to understanding.
Good news: I was able to reduce my iron down into range and it helped many things!
Bad news: To do this I had to take risks beyond the scope most people would accept.
Specifically, I used EGCG and this needed a lot of other support including b-vitamins, zinc, molybdenum. Getting too much or too little of any of these factors would lead to problems. It also upset my gut, so the clear cost if I would do this long term is microbial adaptation at the moment.
However, I am very glad to see success from lowering iron so clearly.
Quite simply, before I got the labile iron down I had: balding from scalp inflammation, tendons not healing at all, POIS, joint aches including knees and weak stomach acid.
After getting iron down and zinc in, all those went away. As iron crept up again over 2-4 weeks, all except the POIS came back.
A lot of this thread is theory. I just want to share that this is my daily experience, and the feedback is very clear to me.
I measured my free iron in the blood before and after and saw that number go down. I also have HTMA hair tests which, while not reliable, also point in that same direction. Then of course I also have all the symptoms pointing in the same direction too, so it all looks very convincing to me that I was successful. I can share the numbers if interested.
However, I have to find gentler ways to manage iron. So I’m now testing Apolactoferrin and researching IP6. Blood donation isn’t reliable for me, though I will keep trialing from time to time.
**Please tell me about your experiences with IP6. **
I also have a hypothesis to share:
- zinc deficiency
leads to - iron and copper going where they shouldn’t be: dysregulation,
- with iron in particular blocking zinc the most
My reasoning is that zinc is the biggest soil deficiency in the world, so it makes sense to start here. The others in the books recommended near the start of this thread explain the specifics on from this better than I can.
I expect if children are simply given enough zinc, that this iron accumulation may not happen. I’d like to see that hypothesis tested.
Due to wild changes in temperature this year, and also I’m also pretty confidence that I have a pathogenic bacteria in my gut that is weakening my stomach acid to increase iron. I don’t think it’s H.Pylori as it’s a little bit subtle. I believe I picked this up a few years ago from Bali , but that it’s been sitting unactivated during the cold weather. The reason why I’m so confident of this is that I can battle this gut bacteria with various means (probiotics, prebiotics, antibiotic-like supplements and foods), and this affords me less indigestion problems. This combined with the hot weather link and it looks very clear.
Overall I’m very happy to have discovered a fix to this problem and I’m looking forward to finding an even better one.
In terms of IP6 I’ve seen some concern that iron gets to the liver, but struggles to go further. Can anyone feedback a little on their experiences with IP6?
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Useful conversations need measurements.
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I don’t know if anyone has mentioned this yet but GLP1’s have been reducing ferritin levels for a lot of people anecdotally. Potentially could be another mechanism for why they reduce cardiovascular events. That being said, people need to make sure they don’t get too low on GLP1’s.
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It’s because sema and tirz reduce LDL-cholesterol by 5-10% and retatrutide by up to 20%.
Well yea that’s a much larger factor for CVD reduction along with reduced blood pressure. I’m just saying lower iron could add more to that reduction if someone had a higher iron status to begin with.
John Hemming: Bearing in mind costs,
What measurements do you think would be most useful for me to track and when? For example, I initially measured a standard iron panel, but when I retested I just tested for labile iron.
233ug/dL before down to 165ug/dl after. Ferratin, tibc in range.
The issue with this is that these are just blood test results. They’re not tissue samples. What else is good to test?
I can share my HTMA results before and after as well, but HTMA has a repeatability problem, so they are not used in consensus science. However, I believe it is conceivable that if we only consider samples from the same lab and relative, not absolute changes, then there could be some value that can’t be captured from any other means?
Please also feel free to mention more expensive testing as well, just to consider.
In addition, I’m in Hong Kong. If anyone knows anything about pairing with a university to get access to testing equipment, please let me know.
If anyone knows anything about testing metal excretion in urine too, please let me know as well.
While I value studies and papers, I’d like to see more people sharing their experiences with lowering iron. Experimentation is the backbone of science. Get hands-on. Even if it’s only measurement at first, starting with that free iron blood test.
Ferritin is a useful figure. Just because a lab says it is in range does not mean there is not an issue. One problem with ferritin is that if you are inflamed ferritin will be higher. Micrograms per deciliter sounds unusual units.
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