Hereditary hemochromatosis
Hereditary hemochromatosis is a Mendelian disorder of iron regulation — most often HFE-related (C282Y homozygous, or compound heterozygous C282Y/H63D), with rarer non-HFE forms involving TFR2, HJV, HAMP, or SLC40A1 (ferroportin). The shared substrate defect is hepcidin insufficiency — relative or absolute — which removes the normal brake on intestinal iron absorption. Iron progressively accumulates in the liver, heart, pancreas, joints, anterior pituitary, and skin over years to decades, driving the classic late presentations: cirrhosis with hepatocellular carcinoma risk, restrictive then dilated cardiomyopathy with arrhythmia, 'bronze diabetes,' arthralgia in the second and third metacarpophalangeal joints, hypogonadotropic hypogonadism, hypothyroidism, and skin hyperpigmentation. Therapeutic phlebotomy is the gold-standard treatment — first-line, weekly during induction until ferritin <50 ng/mL, then maintenance every 2-4 months — and has been since the 1950s. AASLD 2018 + 2024 + EASL + ACG guidelines. Iron in supplements explicitly contraindicated. Raw seafood avoidance (Vibrio vulnificus sepsis >50% mortality in iron overload) load-bearing. Family screening mandatory for first-degree relatives. Rusfertide (PTG-300) hepcidin mimetic + mini-hepcidins emerging therapeutic class targeting upstream defect. Iron Disorders Institute + American Hemochromatosis Society + Canadian Hemochromatosis Society. Thirty-fifth deliberate non-elevation.
What changes during this transition
Juno covers hemochromatosis because users with the diagnosis (or with a first-degree relative diagnosed) regularly probe the peptide space for adjunct interventions — and the honest answer is consistent enough that it deserves a substrate. The honest answer is this: phlebotomy is the gold standard, has held that position for seventy years, and shows no sign of being displaced. No peptide currently in community circulation addresses the upstream defect (hepcidin insufficiency driving inappropriate intestinal iron absorption). The peptides users encounter — BPC-157 framed as 'liver healing,' TB-500 framed as 'cardiac anti-fibrotic,' NMN framed as general-aging NAD+ support, SS-31 framed as mitochondrial-protective, Cerebrolysin in its multi-jurisdictional neuroprotection register — all address downstream consequences (fibrosis, mitochondrial damage, end-organ injury) without touching the iron-loading driver. The disease-specific load-bearing therapeutic horizon is hepcidin agonism — not the peptides currently in community circulation. Rusfertide (PTG-300), a hepcidin mimetic, has advanced through Phase 3 in polycythemia vera with an FDA submission, and parallel programs target hereditary hemochromatosis. Mini-hepcidins and other hepcidin mimetics are in earlier clinical development. This emerging therapeutic class targets the upstream defect directly — restoring the absent regulatory signal rather than chasing downstream organ damage. If a disease-specific peptide therapy reaches approval for hereditary hemochromatosis in the next several years, it will almost certainly come from this class. That makes 'wait for hepcidin agonists; manage with phlebotomy in the meantime' the editorially honest current posture. Deliberate non-elevation. This is the thirty-fifth life-stage substrate where Juno's editorial decision is to provide /ask grounding without elevating peptides as a discovery surface. Phlebotomy plus dietary management plus family screening is the protocol Juno would direct a user toward, and that protocol does not involve peptides. Elevating BPC-157 or TB-500 or SS-31 as discovery cards under 'hemochromatosis' would imply they belong in the management conversation; they do not. Multi-jurisdictional posture applies here in a specific way. Cerebrolysin's clinical register across EU jurisdictions, China, and Russia is real evidence within its registered indications (stroke, TBI, vascular dementia, Alzheimer-spectrum cognitive decline). Honoring that register properly means honoring its bounds — and the bounds do not include hereditary iron-overload disorders. The same principle applies in the opposite direction: BPC-157's Croatian and broader peer-reviewed work is real evidence within the GI-injury and musculoskeletal-injury contexts where it was characterized. That legitimacy does not propagate to a Mendelian iron-regulation disorder. Multi-jurisdictional respect means specificity, not blanket extension. Who this surface serves. The user who arrives at /ask asking 'is BPC-157 a good idea for my hemochromatosis?' gets a substantive, accurate answer pointing them back toward their hepatologist, toward the load-bearing dietary safety threads (iron in supplements, raw seafood and Vibrio vulnificus, vitamin C with iron-rich meals), and toward the hepcidin-agonist horizon as the disease-specific therapeutic frontier.
Important caveat
Hereditary hemochromatosis is a hepatologist- or hematologist-managed Mendelian disorder. Therapeutic phlebotomy is the gold-standard first-line treatment — weekly during induction until ferritin falls below 50 ng/mL, then maintenance every 2-4 months — and is established as the cornerstone of management by AASLD 2018 and 2024 guidelines, EASL, and ACG. No peptide in community circulation addresses the upstream hepcidin-regulation defect. Adjunct peptide use does not substitute for phlebotomy, does not change phlebotomy cadence, and does not change disease trajectory in ways supported by current trial evidence. IRON IN SUPPLEMENTS IS EXPLICITLY CONTRAINDICATED. Any oral supplement containing elemental iron, ferrous sulfate, ferrous gluconate, ferrous fumarate, ferric pyrophosphate, heme iron polypeptide, or any iron salt is contraindicated in hereditary hemochromatosis at any dose. This includes standard multivitamins, prenatal vitamins, gummy vitamins, 'energy' formulations, 'greens' powders that contain iron, and many 'longevity stack' products. The supplement-channel risk is the load-bearing safety thread that makes NMN (or any general-aging supplement program) hazardous-by-association in this disease — the issue isn't usually the headline supplement itself, it's the iron-containing co-supplements that travel with it. Audit every label of every supplement currently in your cabinet with your specialist before continuing any program. High-dose vitamin C with iron-rich meals significantly enhances non-heme iron absorption and should be discontinued or separated from meals. RAW SEAFOOD AVOIDANCE — VIBRIO VULNIFICUS SEPSIS RISK. Iron overload dramatically increases susceptibility to Vibrio vulnificus, a marine bacterium that causes overwhelming sepsis with mortality rates above 50% in hemochromatosis patients. Raw or undercooked oysters, clams, mussels, and shellfish are the dominant exposure route. This is not a theoretical risk — it is documented across the hemochromatosis literature as one of the diet-attributable mortality threads specific to this disease. Raw seafood is contraindicated for life in hereditary hemochromatosis regardless of ferritin status or phlebotomy adequacy. FAMILY SCREENING. Hereditary hemochromatosis is autosomal recessive (C282Y/C282Y is the most common genotype). First-degree relatives — full siblings, children, parents — should receive genetic counseling and HFE testing (C282Y, H63D, S65C). Early-identified relatives can begin monitoring and, if needed, prophylactic phlebotomy before end-organ damage occurs; this is the highest-leverage prevention intervention in the disease. HCC surveillance. If cirrhosis is established, hepatocellular carcinoma surveillance with liver ultrasound and AFP every 6 months is standard of care. Iron Disorders Institute + American Hemochromatosis Society + Canadian Hemochromatosis Society are legitimate patient-organization resources. WADA athletes: BPC-157 (S0) and TB-500 (S2) prohibited at all times. Pregnancy: hemochromatosis pregnancy generally well-tolerated; iron is naturally redistributed during pregnancy; prenatal vitamins should be iron-free in known hemochromatosis patients; hepatology + maternal-fetal medicine coordination. Hepcidin agonist pipeline (rusfertide, mini-hepcidins) is the disease-specific therapeutic frontier — that conversation belongs with your hepatologist, not with a peptide clinician.
Want this list to grow? The library is editorial — if there’s a peptide you think belongs on this page with documented or mechanistically-clear evidence, send us a note with the citation and we’ll review it under the same evidence-tier discipline as every other entry.