WHEN YOUR BODY HOLDS ON TIGHT

The science behind inflammation, nutrient redistribution, and why the form of iron you eat matters more than the amount.

Most of us associate inflammation with something obvious — a swollen ankle, a sore throat, the redness around a cut. It flares up, does its job, and settles down. That kind of inflammation is healthy. It is your immune system working exactly as it should.

But there is another kind. It runs quietly in the background, at a low level, for months or years. There is no obvious swelling. No fever. Often no symptoms you would name as illness. Just a body that feels like it is running at 70%. Tired more than it should be. Slow to recover. Struggling to hold its nutritional baseline.

This low-grade, chronic inflammation is not rare. It is now considered one of the most common underlying patterns in modern adult health — driven by a combination of factors that most people encounter every day: diets high in refined and processed foods, disrupted sleep, sustained psychological stress, reduced physical movement, and excess body weight around the abdomen. None of these triggers are dramatic on their own. But when they run together, day after day, the immune system never fully switches off. It stays partially activated — and that has consequences that go well beyond how you feel in the moment.

One of those consequences involves how your body handles nutrients. Particularly iron, copper, zinc, and the vitamins that travel alongside them. Understanding this changes how you think about blood test results, about why supplements sometimes do not work, and about why the form in which you eat these nutrients matters more than most people realise.

WHAT INFLAMMATION DOES TO NUTRIENTS

When the immune system activates, the liver changes what it makes. This coordinated response — called the acute phase response — kicks in within hours. Some proteins are turned up. Others are deliberately turned down. The proteins that rise include ferritin, hepcidin, and CRP — markers your GP might measure. The proteins that fall are the ones responsible for carrying nutrients out to your tissues.¹

Transferrin (which carries iron), retinol-binding protein (which carries vitamin A), albumin — all drop when inflammation is active. The result is that iron, zinc, and vitamin A are pulled inward. They are held in the liver and immune cells rather than circulating freely. Serum levels fall — not because these nutrients have been used up, but because the body has moved them deliberately.¹

This is called nutritional immunity. Research published in Nature Reviews Microbiology describes it clearly: withholding iron and other transition metals from pathogens is an evolved defence mechanism. When your blood iron looks low during an infection or illness, that is often your immune system doing its job, not a sign that you are deficient.²

The problem is when that state becomes permanent. Acute inflammation is meant to resolve. The nutrient redistribution reverses. But in chronic low-grade inflammation — the kind driven by modern lifestyle factors — the acute phase response runs continuously at a lower level. The nutrient sequestration never fully switches off. That is the environment many people are living in when they get a blood test and wonder why their iron result looks normal but they feel exhausted.

THE IRON STORY: HEPCIDIN

Hepcidin is the hormone that decides whether iron moves. It is made in the liver, released in response to inflammation, and it works by attaching to ferroportin — the only known exit channel for iron out of cells — and breaking it down.³

When ferroportin is gone, iron cannot leave. The small intestine cannot export iron from food into the bloodstream. Immune cells sitting on recycled iron from old red blood cells cannot release it. Iron is locked inside — stores intact, but unavailable.⁴

This is called functional iron deficiency, and it is different from true iron deficiency. In true deficiency, the stores are genuinely empty. In functional deficiency, the stores are there but the body cannot reach them. Ferritin can look normal or even elevated. Serum iron is low. Transferrin saturation is low. On paper it can look like adequacy when it is anything but.⁴

The standard ferritin test alone cannot tell these two states apart when inflammation is present. The WHO reviewed population data from a project called BRINDA — pooling results from over 52,000 people across 16 surveys — and found that without accounting for inflammation, iron deficiency is routinely underestimated by 7 to 25 percentage points. They now recommend raising the adult ferritin cut-off to below 70 µg/L when CRP is elevated, rather than the standard 15–20 µg/L.^{5, 6}

Oral supplemental iron has its own challenge here. When hepcidin is elevated, the exit channel that would normally move absorbed iron into the bloodstream has been removed. Conventional iron supplements arrive at the gut wall and largely cannot get through. This is a plausible explanation for why many women describe taking iron supplements, tolerating them poorly, and seeing no improvement in their levels.^{3, 4}

WHY HEME IRON FOLLOWS A DIFFERENT PATHWAY

The form of iron found in animal tissue — called heme iron — is absorbed differently. Non-heme iron, the form in most plant foods and conventional supplements, enters the intestinal wall through a transporter and then relies on ferroportin to cross into the bloodstream. Hepcidin degrades ferroportin, blocking that final step.⁴

Heme iron is absorbed intact through separate transporter mechanisms that do not work the same way. The ferroportin step is still involved, but heme iron's distinct uptake route means it behaves differently in an inflamed environment compared to the non-heme forms most supplements rely on.⁴

This is the mechanistic basis behind the clinical observation that food-based iron is often better tolerated and more consistent in its effects — particularly for people dealing with chronic inflammation. It is not simply a bioavailability story. It is a delivery-route story.

Gram for gram, beef spleen contains significantly more heme iron than liver. This is why Somada's Iron Blend leads with spleen as the iron source. Liver's genuine strength lies elsewhere.

COPPER: THE NUTRIENT THAT GATES IRON

Copper and iron are more tightly connected than most people realise. An enzyme called ceruloplasmin — which carries roughly 95% of plasma copper — converts iron into the form that can be loaded onto transferrin for delivery to red blood cells. Without adequate copper, that step stalls. Iron may be present but cannot reach where it needs to go.¹

Copper deficiency can produce an anaemia that looks like iron deficiency and does not respond to iron supplementation — because the iron transport system itself is impaired. This is one reason persistent anaemia that does not resolve with iron is worth investigating further.

During inflammation, ceruloplasmin rises — the opposite of what iron and zinc do. That makes serum copper an unreliable individual marker during active illness. An elevated result may simply reflect the inflammatory response rather than genuine copper abundance.¹

The copper-to-zinc ratio in the blood rises predictably during inflammation and in population data correlates with cardiometabolic risk, though its use as an individual clinical marker is limited.⁷

Beef liver is one of the richest dietary sources of copper. The co-presence of heme iron and copper in the same food is not coincidental. It reflects how these nutrients naturally exist together in animal tissue — a relationship that does not exist in isolated synthetic supplements.

THE OTHER NUTRIENTS IN LIVER AND SPLEEN

Vitamin A (retinol). Liver contains preformed retinol — the most usable form of vitamin A. Retinol plays a direct role in iron metabolism: vitamin A insufficiency is linked to reduced red blood cell production and impaired release of iron from liver stores, independent of iron status itself.⁸

During active inflammation, the protein that carries retinol in the blood is suppressed, causing circulating vitamin A to fall regardless of what is stored in the liver. BRINDA research across 22 population surveys found that once inflammation is accounted for, estimated vitamin A deficiency fell by 6 to 22 percentage points — meaning a large portion of what looks like deficiency is actually redistribution.⁹

One note for pregnancy: preformed retinol has an upper safe limit of 3,000 µg RE per day. Liver-based products at typical serving sizes sit well below this threshold, but worth noting for those who are pregnant or planning to be.

Vitamin B12. Total serum B12 can paradoxically rise during inflammation because one of its carrier proteins behaves as a positive acute-phase protein. A normal or high B12 result does not rule out functional deficiency. More reliable markers are holoTC (the active fraction of B12) and methylmalonic acid, which your GP can test for.¹⁰

B12 absorption also depends on a multi-step process — gastric acid, intrinsic factor, and a specific receptor in the terminal ileum. Gut conditions including atrophic gastritis, H. pylori, and Crohn's disease affecting the terminal ileum can compromise this at different points.¹⁰

Folate. Unlike most of the nutrients discussed here, folate is not significantly redistributed during inflammation — it is one of the more reliable markers even when CRP is elevated. Erythrocyte folate, which reflects three to four months of status, is the preferred test for chronic adequacy.¹¹

Inflammation does increase folate demand through faster immune cell turnover and mucosal repair. FSANZ note for label purposes: claims on liver products must use the word "folate" — "folic acid" is not permitted on liver products under the FSANZ Code.

HOW YOUR GUT CHANGES THE EQUATION

When inflammation is at the absorptive surface itself, the problem compounds. Normal absorption needs intact intestinal villi, functioning transporter proteins, and a healthy mucosal lining. Gut inflammation disrupts all three at once.

Coeliac disease destroys the villi in the upper small intestine — precisely where iron, folate, and calcium are absorbed. Active inflammatory bowel disease produces mucosal damage and directly suppresses the transporter proteins that handle iron, zinc, and B12 at different sites along the gut.¹²

Coeliac disease affects approximately 1 in 70 Australians, with around 80% undiagnosed. Crohn's & Colitis Australia's 2025 report estimates 179,420 Australians are living with IBD — and 30% of inpatients are anaemic.^{13, 14} This is not a peripheral population. And it illustrates why gut health and nutrient status cannot be assessed separately.

WHOLEFOOD SOURCES

The nutrients most disrupted by inflammation — iron, copper, zinc, vitamin A, B12, folate — are concentrated in organ meats in the co-factor arrangements the body already knows how to handle.

Values are approximate. Absorption is influenced by overall diet, inflammation status, and individual physiology.

DAILY REQUIREMENTS

Source: NHMRC Nutrient Reference Values for Australia and New Zealand.¹¹ RDI = Recommended Dietary Intake. AI = Adequate Intake. The Upper Level represents the highest daily intake considered unlikely to cause harm.

WHAT AFFECTS ABSORPTION

What helps. Vitamin C consumed alongside non-heme iron significantly increases absorption by keeping iron in its soluble form in the gut. Animal tissue eaten alongside plant iron sources can also support uptake. Adequate stomach acid is a prerequisite for releasing both iron and B12 from food protein — which is one reason proton pump inhibitors, when used long-term, can quietly impair both.

What competes or inhibits. Phytates in wholegrains and legumes, polyphenols in tea and coffee, and high doses of calcium can all reduce non-heme iron absorption at the same meal. High-dose zinc supplementation over months can deplete copper by binding it in the intestinal wall before it is absorbed. The NHMRC sets the zinc upper level at 40 mg/day specifically to protect against this.¹¹

The gut microbiome factor. Butyrate — produced by gut bacteria fermenting dietary fibre — is the preferred energy source for colon cells. It supports mucus production, tightens the intestinal barrier, and helps regulate the local immune response. Depletion of butyrate-producing bacteria is consistently seen in IBD and contributes to the cycle where inflammation impairs absorption, which worsens nutritional status, which worsens inflammation. The evidence here is still developing, but the direction is consistent.¹²

COMMON QUESTIONS

Does inflammation mean my iron test results are wrong?

Not wrong — but potentially incomplete. During active inflammation, ferritin rises as a positive acute-phase protein, which can mask true depletion. Serum iron falls, which can suggest deficiency when stores are actually adequate. The WHO now recommends raising the adult ferritin cut-off to below 70 µg/L when CRP is elevated, rather than the standard 15–20 µg/L. For a reliable picture, ferritin should be paired with CRP and ideally transferrin saturation. If your test was taken during an illness, after surgery, or while managing a chronic inflammatory condition, it is worth retesting after things have settled — generally two to four weeks after recovery.^{5, 6}

Why might iron supplements not be working?

When hepcidin is elevated — which happens during inflammation — the exit channel that normally moves absorbed iron into the bloodstream has been broken down. Conventional iron supplements arrive at the gut wall and largely cannot cross. This is compounded if the iron form also irritates the gut, which can itself drive local inflammation. Heme iron from animal tissue follows a different absorption route that is less directly dependent on this pathway, which is part of why food-based sources tend to be more effective for many people who have not responded to conventional supplementation. If iron supplementation genuinely is not working, elevated hepcidin from chronic inflammation is worth raising with a practitioner.^{3, 4}

If copper is needed for iron transport, do I need to supplement both?

For most people who eat meat regularly, dietary copper intake is adequate. The issue is more likely to arise when iron supplements are taken at high doses for extended periods without attention to copper, or when copper absorption is impaired by gut disease. Foods that naturally contain both copper and heme iron — beef liver and spleen are the best examples — provide these nutrients in the ratios they naturally co-exist in. If you have a confirmed deficiency in either mineral, working with a practitioner on the specific gap is a better approach than broad self-supplementation.^{1, 11}

Does high-dose vitamin C help with iron absorption?

For non-heme iron, yes — meaningfully. Vitamin C keeps iron in the form that the intestinal transporter handles, increasing uptake at the gut wall. The advice about having orange juice with a plant-based iron meal has a genuine mechanism behind it. That said, this applies specifically to non-heme iron. Heme iron works through a different pathway and is not enhanced by vitamin C in the same way. Very high-dose vitamin C above roughly 1 g per day has diminishing returns — the gut's absorption capacity saturates, and the excess is cleared by the kidneys.¹⁵

BRINGING IT ALL TOGETHER

Inflammation does not just make you feel unwell. It reorganises how your body handles the nutrients that keep you functioning — pulling iron out of circulation, redirecting zinc, suppressing the carrier proteins that move vitamins to your tissues. The lab results this produces are genuinely difficult to read without context. Feeling depleted while your blood test looks normal is not imaginary. It is a specific, describable physiological process.

The form in which nutrients arrive matters in this environment. Heme iron enters the intestinal wall through a different route than the non-heme iron most supplements rely on. Copper and retinol exist in liver in concentrations and arrangements that support the iron system rather than working in isolation. This is not a marketing claim — it is what whole food is.

The practical starting point is not a supplement. It is making sure fatigue has been properly investigated — with CRP alongside ferritin, not ferritin alone. From there, consistently eating the foods that carry these nutrients in their most usable forms is what the evidence most reliably supports.

This article provides general nutrition information only and is not intended as medical advice. If you have concerns about your iron, copper, zinc, or vitamin levels, consult a qualified health practitioner.

REFERENCES

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2. M. I. Hood and E. P. Skaar, "Nutritional immunity: transition metals at the pathogen–host interface," Nat Rev Microbiol, vol. 10, no. 8, pp. 525–537, 2012. https://doi.org/10.1038/nrmicro2836

3. E. Nemeth, E. V. Valore, M. Territo, G. Schiller, A. Lichtenstein, and T. Ganz, "Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein," Blood, vol. 101, no. 7, pp. 2461–2463, 2003. https://doi.org/10.1182/blood-2002-10-3235

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6. WHO, WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations, Geneva: WHO, 2020. https://www.who.int/publications/i/item/9789240000124

7. A. Kerkadi, H. Raïq, M. S. Prince et al., "Zinc and copper levels and CVD risk markers, Qatar Biobank," Front Cardiovasc Med, vol. 10, p. 1305588, 2024. https://doi.org/10.3389/fcvm.2023.1305588

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9. L. M. Larson, J. Guo, A. M. Williams et al., "Approaches to assess vitamin A status in settings of inflammation: BRINDA project," Nutrients, vol. 10, no. 8, p. 1100, 2018. https://doi.org/10.3390/nu10081100

10. E. Andrès, K. Serraj, J. Zhu, and A. J. M. Vermorken, "The pathophysiology of elevated vitamin B12 in clinical practice," QJM, vol. 106, no. 6, pp. 505–515, 2013. https://doi.org/10.1093/qjmed/hct051

11. NHMRC, Nutrient Reference Values for Australia and New Zealand (2006; sodium/fluoride update 2017). https://www.eatforhealth.gov.au/nutrient-reference-values

12. A. Fasano, "Zonulin, regulation of tight junctions, and autoimmune diseases," Ann NY Acad Sci, vol. 1258, no. 1, pp. 25–33, 2012. https://doi.org/10.1111/j.1749-6632.2012.06538.x

13. Coeliac Australia, Coeliac disease — overview. https://coeliac.org.au/learn/coeliac-disease/

14. Crohn's & Colitis Australia, IBD State of the Nation 2025. https://crohnsandcolitis.org.au/advocacy/our-projects/ibd-state-of-the-nation/

15. M. Levine, C. Conry-Cantilena, Y. Wang et al., "Vitamin C pharmacokinetics in healthy volunteers," Proc Natl Acad Sci USA, vol. 93, no. 8, pp. 3704–3709, 1996. https://doi.org/10.1073/pnas.93.8.3704