Iron and Anaemia: Why Iron Tablets Are Not Always the Answer

Iron deficiency is one of the most common nutritional problems worldwide, affecting more than 1.2 billion people. Yet many people are prescribed iron supplements without anyone asking a more important question:

Why is the iron low in the first place?

Iron deficiency can be caused by poor dietary intake, impaired absorption, chronic inflammation, infections, digestive disorders, heavy menstrual bleeding, pregnancy, endurance exercise, medications and chronic disease.

Simply taking iron tablets without understanding the underlying driver often leads to frustration, digestive side effects and incomplete recovery.

Understanding how iron is regulated within the body provides valuable insight into why iron deficiency develops and why some people remain symptomatic despite apparently “normal” iron levels.

Why Iron Matters

Iron is involved in far more than the production of red blood cells.

It plays essential roles in:

• Oxygen transport via haemoglobin

• Myoglobin production within muscle tissue

• ATP production and mitochondrial energy generation

• Cytochrome P450 enzymes involved in liver detoxification

• Dopamine, noradrenaline and serotonin synthesis

• Thyroid hormone regulation

• Immune function

• Cognitive performance and concentration

  
  

Iron sits at the final stages of the electron transport chain within the mitochondria. Without sufficient iron, cells struggle to generate ATP efficiently, leading to fatigue, poor exercise tolerance, brain fog and reduced resilience.

Iron Is Constantly Recycled

Many people assume iron comes solely from food.

In reality, the majority of iron used each day is recycled.

Red blood cells survive for approximately 120 days before being removed by macrophages in the spleen. The haemoglobin is dismantled, the iron is recovered and returned to circulation for reuse.

Around 20-25mg of iron is recycled daily from old red blood cells.

By comparison, only around 1-2mg of dietary iron is absorbed each day.

This recycling system is remarkably efficient and explains why disturbances in iron regulation often matter more than dietary intake alone.

Iron Absorption Begins in the Stomach

Iron absorption starts with stomach acid.

Dietary ferric iron (Fe3+) must be converted into ferrous iron (Fe2+) before absorption can occur.

Factors that impair this process include:

• Low stomach acid

• Proton pump inhibitors (PPIs)

• H. pylori infection

• Ageing

• Chronic antacid use

• Excess tea consumption

• Tannins

• Certain medications

  
  

Vitamin C enhances iron absorption, while tannins found in tea and coffee can significantly reduce it.

This is one reason why many individuals taking iron supplements continue to struggle if digestive function has not been addressed.

Heme vs Non-Heme Iron

Not all iron is absorbed equally.

Heme Iron

Found in:

• Red meat

• Poultry

• Fish

Absorption rate:

15-35%

Non-Heme Iron

Found in:

• Legumes

• Grains

• Vegetables

• Fortified foods

Absorption rate:

2-20%

Animal proteins also improve absorption of non-heme iron due to their cysteine content.

The Iron Transport System

A useful way to understand iron metabolism is to imagine a harbour.

Ferritin = The Storage Warehouse

Ferritin stores iron inside tissues.

The liver acts as the primary storage site.

Ferritin is often measured on blood tests because serum ferritin generally reflects overall iron reserves.

Transferrin = The Taxi Service

Iron cannot float freely through the bloodstream.

It must be carried by a specialised transport protein called transferrin.

Think of transferrin as a fleet of taxis carrying iron to:

• Bone marrow

• Muscles

• Liver

• Other tissues

Transferrin Saturation

This measures how full the taxis are.

Low transferrin saturation means there are lots of taxis driving around but very few passengers (iron molecules).

High transferrin saturation means the taxis are overloaded.

Hepcidin: The Master Controller of Iron

Perhaps the most important regulator of iron metabolism is a hormone called hepcidin.

Produced by the liver, hepcidin acts as the master controller of iron distribution.

Its primary job is regulating ferroportin.

Ferroportin

Ferroportin acts like the harbour gate.

It allows stored iron to leave:

• Enterocytes

• Macrophages

• Liver cells

and enter circulation.

When hepcidin rises, ferroportin is blocked.

The gates close.

Iron becomes trapped inside storage sites.

As a result:

• Ferritin may remain normal or elevated

• Transferrin saturation falls

• Functional iron availability drops

  
  

This creates a situation where iron exists within the body but cannot be utilised properly.

Iron Dysregulation and Chronic Inflammation

One of the most common reasons people develop functional iron deficiency is inflammation.

Inflammatory cytokines such as:

• IL-6

• IL-1

• IL-22

• Lipopolysaccharides (LPS)

stimulate hepcidin production.

The body deliberately hides iron away from microbes because bacteria require iron for growth.

This is an intelligent survival mechanism.

The downside is that chronic inflammation can leave the individual functionally iron deficient despite apparently adequate iron stores.

Common triggers include:

• Chronic infections

• Dysbiosis

• SIBO

• Autoimmune disease

• Obesity

• Inflammatory bowel disease

• Cancer

Iron Deficiency Anaemia

Iron deficiency anaemia develops when insufficient iron is available to support red blood cell production.

Common symptoms include:

• Fatigue

• Poor exercise tolerance

• Breathlessness

• Hair loss

• Restless legs

• Brain fog

• Poor concentration

• Dizziness

• Headaches

• Cold hands and feet

• Low mood

• Weakness

Physical signs may include:

• Glossitis (smooth tongue)

• Loss of papillae

• Angular stomatitis

• Spoon-shaped nails

• Pallor

Blood Test Patterns in Iron Deficiency Anaemia

Typical findings include:

• Low haemoglobin

• Low ferritin

• Low transferrin saturation

• High transferrin

• High TIBC

• Low MCH

• Low MCV

• Elevated RDW

A high RDW combined with a low MCV is strongly suggestive of iron deficiency.

Iron Deficiency Without Anaemia

This is frequently missed.

A person may have:

• Normal haemoglobin

• Normal red blood cell count

  
  

yet still experience symptoms due to depleted iron stores.

This is known as Iron Deficiency Without Anaemia (IDWA).

Common symptoms include:

• Hair shedding

• Fatigue

• Reduced exercise capacity

• Brain fog

• Restless legs

• Poor concentration

Ferritin becomes particularly important here.

Ferritin Thresholds

WHO definition: Ferritin <15 µg/L

Clinical practice: Ferritin <30 µg/L often indicates iron deficiency.

In inflammatory conditions, ferritin can become falsely elevated because ferritin is a positive acute-phase reactant.

In these individuals, ferritin may need to be interpreted using higher thresholds, often up to 100 µg/L alongside transferrin saturation.

When Iron Tablets Are Not the Answer

Before reaching for supplements, it is important to ask why iron is low.

Potential causes include:

Blood Loss

• Heavy menstrual bleeding

• Gastrointestinal bleeding

• NSAID use

• Ulcers

• Polyps

Poor Absorption

• Low stomach acid

• H. pylori

• Coeliac disease

• Inflammatory bowel disease

• Long-term PPI use

Increased Requirements

• Pregnancy

• Adolescence

• Endurance training

• Athletes

Chronic Inflammation

• Autoimmune disease

• Obesity

• Chronic infections

Dysbiosis and SIBO

Many pathogenic organisms compete aggressively for iron.

Gram-negative bacteria produce compounds called siderophores which can outcompete transferrin for available iron.

In these situations, addressing gut dysfunction may be more effective than simply increasing iron intake.

The H. pylori Connection

H. pylori is an often overlooked cause of iron deficiency.

It can:

• Reduce stomach acid production

• Impair iron absorption

• Contribute to chronic gastritis

• Increase risk of SIBO

  
  

Studies show eradication of H. pylori can normalise ferritin and blood count markers in some patients without the need for long-term iron supplementation.

Understanding Anaemia of Chronic Disease

This pattern looks very different from classic iron deficiency.

Typical findings include:

• Low serum iron

• Low transferrin

• Low transferrin saturation

• Normal or elevated ferritin

The key difference is that iron is present but trapped.

High hepcidin prevents iron mobilisation.

Giving large amounts of supplemental iron without addressing the inflammatory driver may not solve the problem.

Supporting Iron Status

The correct approach depends on the underlying cause.

Strategies may include:

• Improving stomach acid production

• Addressing H. pylori

• Investigating heavy menstrual bleeding

• Correcting B12 and folate deficiencies

• Reducing chronic inflammation

• Treating dysbiosis and SIBO

• Supporting sleep and oxygenation

• Investigating sleep apnoea where appropriate

Iron Supplement Considerations

Ferrous bisglycinate is often better tolerated than standard ferrous sulphate.

Iron is generally best taken:

• With vitamin C

• Away from calcium

• Away from magnesium

• Away from zinc

• Away from thyroid medication

Lactoferrin

Lactoferrin is particularly interesting because it:

• Improves iron utilisation

• Supports iron delivery to tissues

• Has antimicrobial properties

• May be beneficial where dysbiosis or chronic infection is present

The Bigger Picture

Iron deficiency is rarely just an iron problem.

It may reflect:

• Poor digestion

• Chronic inflammation

• Hidden blood loss

• Dysbiosis

• Autoimmune disease

• Hormonal imbalance

• Increased physiological demand

Understanding ferritin, transferrin saturation, hepcidin and inflammation provides a far more complete picture than looking at serum iron alone.

If you are tired, cold, breathless, struggling with hair loss or poor exercise tolerance despite being told your iron is “normal”, it may be worth looking beyond haemoglobin alone and exploring the wider picture of iron regulation.