Thanks for the link to the calculator. According to my values, I should supplement 72 mg of iron biglycinate EOD. Did you work out what your equivalence would be in heme?
I ended up using a combo - 1 Proferrin with 25-50mg of iron bisglycinate and 600mg lactoferrin EOD. I’ll be retesting next month to see how much it moved the needle.
Per Claude, looks like 1 Profferin (10.5mg heme) might do the trick:
72 mg iron bisglycinate → ~20% elemental iron = ~14–15 mg elemental iron → absorbed at ~20% = ~3 mg actually absorbed
Proferrin ES at ~30% absorption: 3 mg ÷ 0.30 = ~10 mg elemental heme iron needed
That’s essentially 1 tablet of Proferrin ES (10.5 mg elemental), which would likely deliver equivalent or slightly better absorbed iron than 72 mg bisglycinate.
One tablet is also conveniently the minimum recommended dose, so it’s a clean swap.
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From all of the research I have reviewed, get your levels just inside the lowest acceptable level at which you feel appropriately well. From some causal and considerable population evidence, low-ish ferritin, etc. is geroprotective.
My levels are in check now but I can validate the “nasty experience” for those who have not experienced it. Mine centered on one big toe. I had no earthly idea that a toe could be so painful. It was excruciating and I have a decently high pain threshold.
It can be a lot more painful and disabling than that.
On the other hand it is an incredibly simple problem to define. I am not sure the reason exactly why it happens has been properly researched. I think it probably links to a movement in metabolism that drives people to be more acidic, but that has not as far as I know been researched.
I asked a couple of questions of chatGPT and will copy the response below. However, I think it misses the fact that urate is more soluble in neutral or alkaline urine (as long as there is enough volume). Hence even if stones are not created less urate will be excreted in acidic urine.
chatGPT:
The best evidence supports this distinction:
Acidic urine is well linked to uric acid kidney stones in people with gout or hyperuricaemia, but it is not established as a primary cause of gouty arthritis itself. Gout is primarily driven by systemic urate burden and monosodium urate crystal deposition in joints and tissues; low urine pH mainly changes what happens in the urinary tract, where it promotes uric acid crystallization. (PMC)
On the kidney stone side, the evidence is strong. Reviews consistently describe low urinary pH as the major or overriding determinant of uric acid stone formation. This is because acidic urine shifts dissolved urate toward the less soluble protonated form, uric acid, making crystallization much more likely; risk is especially high around urine pH ≤5.5. (PMC)
On the gout side, the key driver is different. Reviews of gout pathophysiology describe gout as arising when serum/tissue urate supersaturation leads to monosodium urate crystal formation in and around joints, followed by inflammation. Those sources do not treat acidic urine as a main determinant of joint gout in the way it is for uric acid stones. (PMC)
There is also direct evidence that many patients with gout do indeed have low urinary pH. A 2022 study found that about half of the gout patients studied had acidic urine, and more acidic urine was associated with nephrolithiasis and worse renal findings. A systematic review likewise notes that gout is associated with lower urinary pH, which theoretically predisposes to stones. (PMC)
Mechanistically, the best-supported explanation is impaired urinary buffering, especially reduced renal ammonium excretion, often in the setting of insulin resistance/metabolic syndrome. That explains why gout, obesity, diabetes, and uric acid stones often cluster together. It also explains why acidic urine is more strongly tied to stone risk than to articular gout itself. (PMC)
One especially useful piece of evidence on causality is that lowering serum urate does not necessarily normalize urine pH. In a prospective study of gout patients treated with febuxostat for 6 months, serum urate fell substantially, but urine pH did not significantly change. That argues against a simple model where gout or hyperuricaemia alone directly causes acidic urine; instead, low urine pH appears to reflect a related metabolic/renal phenotype that often coexists with gout. (PubMed)
There is some literature suggesting that local acidity in tissues could favor monosodium urate crystallization or inflammation, but that is different from urine becoming acidic. The strongest evidence you asked for points to this conclusion: acidic urine is mainly a marker and mechanism for uric acid nephrolithiasis, not a proven direct driver of gouty arthritis. (PMC)
My bottom line:
- Best-supported link: gout ↔ low urinary pH ↔ higher risk of uric acid stones. (PMC)
- Much weaker / not established: low urinary pH as a direct cause of joint gout. Gout itself is mainly about systemic urate supersaturation and MSU crystal deposition in tissues, not urinary acidity. (PMC)
A practical way to think about it is:
- Serum urate / tissue urate supersaturation → gout risk
- Urine pH, urine volume, urinary uric acid load → uric acid stone risk (PMC)
I can also turn this into a compact table: “evidence for acidic urine causing stones” versus “evidence for acidic urine causing gout,” with the strongest papers in each column.
Ya, my goal is 50.
BTW, you may have noticed, but for others, they added a thyroid calculator and male hormone calculator at https://www.longevity-tools.com/.
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My pH naturally runs close to five . I prefer that end of the scale but closer to 6.0-6.5. I found that switching my magnesium formulation from glycinate to citrate (1 tab AM/2 tanb evening for a total of 400 mg elemental) maintains pH ~6.0.
I would panic at 5