New guy on the site and new to researching
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Figured I would say HI. I have started researching with my wombat using GLP3.
Only 5 weeks in and there has been a 6% weight loss in him. There has ben a 5% drop in waist/belly measurement (visceral fat indicator). This has started a chain reaction of physiological changes including a drastic reduction in sleep apnea episodes, cessation of snoring, more energy, etc. The apnea reduction has caused pulse and BP drops into Orthostatic Hypotension, leading us to begin reducing the ACE inhibitor and beta-blocker we were researching for the last three years.
A side note, the lab work done before starting GLP3 research led to finding high ferritin (iron) levels, also caused by metabolism stress to the liver (compensation for high insulin resistance), that are being dealt with by phlebotomy and are rapidly resolving as well. Lastly, lab tests comparing A1C and hemoglobin from now to 5 weeks ago show marked improvement in both. All good things!
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Figured I would say HI. I have started researching with my wombat using GLP3.
Only 5 weeks in and there has been a 6% weight loss in him. There has ben a 5% drop in waist/belly measurement (visceral fat indicator). This has started a chain reaction of physiological changes including a drastic reduction in sleep apnea episodes, cessation of snoring, more energy, etc. The apnea reduction has caused pulse and BP drops into Orthostatic Hypotension, leading us to begin reducing the ACE inhibitor and beta-blocker we were researching for the last three years.
A side note, the lab work done before starting GLP3 research led to finding high ferritin (iron) levels, also caused by metabolism stress to the liver (compensation for high insulin resistance), that are being dealt with by phlebotomy and are rapidly resolving as well. Lastly, lab tests comparing A1C and hemoglobin from now to 5 weeks ago show marked improvement in both. All good things!
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@valgal You asked for it lol:
My Ferritin Journey: How I Was Misdiagnosed with "Incurable" Hereditary Hemochromatosis
The Discovery
In March 2026, routine bloodwork through a preventive health service revealed my ferritin at 725 ng/mL — nearly double the upper limit of normal (380) and about 6x higher than optimal (under 120). Everything else in my iron panel was completely normal: serum iron 102 mcg/dL (normal), TIBC 318 mcg/dL (normal), and iron saturation 32% (normal). That pattern matters — I'll come back to it.
The Misdiagnosis
A hematologist (blood specialist) in my area told me my elevated ferritin was "100% hereditary and incurable" and that I would need phlebotomy (blood removal) for the rest of my life. He pointed to my HFE gene testing from 2017, which showed I'm homozygous for the H63D mutation — meaning I carry two copies of this variant.
I was told this was hereditary hemochromatosis. Case closed, lifelong patient, see you every few months.
Why He Was Wrong
Here's what the doctor either didn't know or didn't mention:
Classical hereditary hemochromatosis (HH) is caused by the C282Y mutation, not H63D. C282Y homozygous accounts for 60-90% of clinical HH cases. I am C282Y negative. My genotyping confirmed this in 2017 — the same test the doctor used to diagnose me.
H63D homozygous accounts for only about 1% of biochemical HH cases, and fewer than 2% of people with this genotype ever develop clinical iron overload. It's a minor variant, not a diagnosis.
My iron saturation was 32%. In true hereditary hemochromatosis, iron saturation is typically above 45% — often much higher. Mine was normal. This single number effectively rules out the classical HH mechanism, where the body absorbs too much iron from food and the iron builds up in organs.
My ferritin was elevated for a completely different reason. Ferritin isn't just an iron storage marker — it's also an acute phase reactant, meaning it rises with inflammation, metabolic stress, and liver fat accumulation. My full metabolic picture told the real story:
BMI 42 (severe obesity)
HOMA-IR 3.63 (significant insulin resistance)
ALT 56 (elevated liver enzyme, consistent with fatty liver/NAFLD)
Triglycerides 179, HDL 34 (classic metabolic syndrome lipid pattern)
hs-CRP 1.0 (systemic inflammation actually low — suggesting the ferritin is hepatic, not systemic)The correct diagnosis is dysmetabolic iron overload syndrome (DIOS) — also called metabolic hyperferritinemia. The liver, stressed by fat accumulation and insulin resistance, releases excess ferritin. The solution isn't lifelong phlebotomy — it's fixing the metabolic dysfunction driving the elevation. Phlebotomy can accelerate ferritin reduction, but the root cause is metabolic, not genetic.
The Access Barrier
Even after I understood my own condition better than the specialist who diagnosed me, I hit a practical wall: I couldn't find a doctor in my area (rural northern Alabama) willing to write a therapeutic phlebotomy order. The blood bank would accept me as a regular donor, but regular donations are limited to once every 8 weeks — at that pace, reducing ferritin from 725 to my target of 150-200 would take 6-10 months.
Therapeutic phlebotomy allows draws every 1-2 weeks, cutting that timeline to 6-10 weeks. But it requires a doctor's order, and the local providers I approached either weren't familiar with the protocol or wanted me to go through the hematologist (the same one who misdiagnosed me).
How I Solved It
I researched which blood banks in my area accept therapeutic phlebotomy orders and found that LifeSouth Community Blood Centers has a formal therapeutic phlebotomy program. I had an AI health assistant help me draft a detailed clinical letter explaining my iron panel, HFE genotyping, metabolic context, and phlebotomy protocol — complete with ICD-10 codes and physician signature lines. I brought the letter to my primary care provider (a nurse practitioner), who reviewed it and signed the order the same day. LifeSouth approved the order within a week.
Where I Am Now
First blood bank donation completed April 16, 2026. Pre-donation hemoglobin: 15.6 g/dL (normal range, down from 17.2 a month earlier — likely related to resolving my obstructive sleep apnea through weight loss).
Therapeutic phlebotomy order approved by LifeSouth — I can now draw every 1-2 weeks on a medical schedule.
First therapeutic draw scheduled for April 25, 2026.
Concurrent weight loss: Down from 328 to 309 lbs in 7 weeks through medication (Retatrutide), dietary changes, and lifestyle overhaul. As my metabolic health improves, the underlying driver of the elevated ferritin is being addressed at the root cause — not just managed with blood removal.
Target: Ferritin below 150-200 ng/mL. I expect to reach this in 2-3 months between therapeutic phlebotomy and metabolic improvement.The Lesson
If a doctor tells you an elevated ferritin is "100% hereditary and incurable," ask these questions:
What is my iron saturation? If it's under 45%, classical hemochromatosis is unlikely regardless of HFE genotype.
Am I C282Y homozygous? That's the mutation that actually causes clinical HH. H63D alone rarely does.
What's my metabolic picture? BMI, insulin resistance, liver enzymes, triglycerides — metabolic syndrome and NAFLD are the most common causes of elevated ferritin with normal iron saturation.
Is this DIOS? Dysmetabolic iron overload syndrome is far more common than hereditary hemochromatosis and is driven by metabolic dysfunction, not genetics.Don't accept a lifelong treatment plan without understanding the root cause. The doctor who told me I'd need phlebotomy forever was treating a lab number without understanding why it was elevated.
-
@valgal You asked for it lol:
My Ferritin Journey: How I Was Misdiagnosed with "Incurable" Hereditary Hemochromatosis
The Discovery
In March 2026, routine bloodwork through a preventive health service revealed my ferritin at 725 ng/mL — nearly double the upper limit of normal (380) and about 6x higher than optimal (under 120). Everything else in my iron panel was completely normal: serum iron 102 mcg/dL (normal), TIBC 318 mcg/dL (normal), and iron saturation 32% (normal). That pattern matters — I'll come back to it.
The Misdiagnosis
A hematologist (blood specialist) in my area told me my elevated ferritin was "100% hereditary and incurable" and that I would need phlebotomy (blood removal) for the rest of my life. He pointed to my HFE gene testing from 2017, which showed I'm homozygous for the H63D mutation — meaning I carry two copies of this variant.
I was told this was hereditary hemochromatosis. Case closed, lifelong patient, see you every few months.
Why He Was Wrong
Here's what the doctor either didn't know or didn't mention:
Classical hereditary hemochromatosis (HH) is caused by the C282Y mutation, not H63D. C282Y homozygous accounts for 60-90% of clinical HH cases. I am C282Y negative. My genotyping confirmed this in 2017 — the same test the doctor used to diagnose me.
H63D homozygous accounts for only about 1% of biochemical HH cases, and fewer than 2% of people with this genotype ever develop clinical iron overload. It's a minor variant, not a diagnosis.
My iron saturation was 32%. In true hereditary hemochromatosis, iron saturation is typically above 45% — often much higher. Mine was normal. This single number effectively rules out the classical HH mechanism, where the body absorbs too much iron from food and the iron builds up in organs.
My ferritin was elevated for a completely different reason. Ferritin isn't just an iron storage marker — it's also an acute phase reactant, meaning it rises with inflammation, metabolic stress, and liver fat accumulation. My full metabolic picture told the real story:
BMI 42 (severe obesity)
HOMA-IR 3.63 (significant insulin resistance)
ALT 56 (elevated liver enzyme, consistent with fatty liver/NAFLD)
Triglycerides 179, HDL 34 (classic metabolic syndrome lipid pattern)
hs-CRP 1.0 (systemic inflammation actually low — suggesting the ferritin is hepatic, not systemic)The correct diagnosis is dysmetabolic iron overload syndrome (DIOS) — also called metabolic hyperferritinemia. The liver, stressed by fat accumulation and insulin resistance, releases excess ferritin. The solution isn't lifelong phlebotomy — it's fixing the metabolic dysfunction driving the elevation. Phlebotomy can accelerate ferritin reduction, but the root cause is metabolic, not genetic.
The Access Barrier
Even after I understood my own condition better than the specialist who diagnosed me, I hit a practical wall: I couldn't find a doctor in my area (rural northern Alabama) willing to write a therapeutic phlebotomy order. The blood bank would accept me as a regular donor, but regular donations are limited to once every 8 weeks — at that pace, reducing ferritin from 725 to my target of 150-200 would take 6-10 months.
Therapeutic phlebotomy allows draws every 1-2 weeks, cutting that timeline to 6-10 weeks. But it requires a doctor's order, and the local providers I approached either weren't familiar with the protocol or wanted me to go through the hematologist (the same one who misdiagnosed me).
How I Solved It
I researched which blood banks in my area accept therapeutic phlebotomy orders and found that LifeSouth Community Blood Centers has a formal therapeutic phlebotomy program. I had an AI health assistant help me draft a detailed clinical letter explaining my iron panel, HFE genotyping, metabolic context, and phlebotomy protocol — complete with ICD-10 codes and physician signature lines. I brought the letter to my primary care provider (a nurse practitioner), who reviewed it and signed the order the same day. LifeSouth approved the order within a week.
Where I Am Now
First blood bank donation completed April 16, 2026. Pre-donation hemoglobin: 15.6 g/dL (normal range, down from 17.2 a month earlier — likely related to resolving my obstructive sleep apnea through weight loss).
Therapeutic phlebotomy order approved by LifeSouth — I can now draw every 1-2 weeks on a medical schedule.
First therapeutic draw scheduled for April 25, 2026.
Concurrent weight loss: Down from 328 to 309 lbs in 7 weeks through medication (Retatrutide), dietary changes, and lifestyle overhaul. As my metabolic health improves, the underlying driver of the elevated ferritin is being addressed at the root cause — not just managed with blood removal.
Target: Ferritin below 150-200 ng/mL. I expect to reach this in 2-3 months between therapeutic phlebotomy and metabolic improvement.The Lesson
If a doctor tells you an elevated ferritin is "100% hereditary and incurable," ask these questions:
What is my iron saturation? If it's under 45%, classical hemochromatosis is unlikely regardless of HFE genotype.
Am I C282Y homozygous? That's the mutation that actually causes clinical HH. H63D alone rarely does.
What's my metabolic picture? BMI, insulin resistance, liver enzymes, triglycerides — metabolic syndrome and NAFLD are the most common causes of elevated ferritin with normal iron saturation.
Is this DIOS? Dysmetabolic iron overload syndrome is far more common than hereditary hemochromatosis and is driven by metabolic dysfunction, not genetics.Don't accept a lifelong treatment plan without understanding the root cause. The doctor who told me I'd need phlebotomy forever was treating a lab number without understanding why it was elevated.
@kj4otu this is amazing information! My husband was tested 6 years ago with a ferritin level of 1200. Diagnosed with hemochromatosis as well.
after a few rounds of therapeutic phlebotomy, his ferritin levels went way down, then he lost interest in following through with any kind of treament.
now we are with a new functional medicine practitioner. Bloodwork came back with a ferritin level of 1100. This provider has been doing a therapeutic phlebotomy and is testing his levels again next week. She is taking one step at a time with diagnosing and recommendations of follow up treatment.
Thanks for sharing all this info. I'll dive into all of his bloodwork and share the info with our functional medicine provider.