The Two Forms of Dietary Iron
Dietary iron exists in two main chemical states: ferric (Fe³⁺) and ferrous (Fe²⁺). The vast majority of iron in plant-based foods (non-heme iron) is in the oxidized ferric state, while heme iron found in meat, poultry, and fish contains ferrous iron. A critical difference in the human body's handling of these two forms dictates their bioavailability and absorption efficiency.
Heme iron is absorbed intact as a whole compound and is far more readily absorbed, with an absorption rate of approximately 15% to 35%. Non-heme iron absorption, by contrast, is much less efficient and highly susceptible to dietary inhibitors and enhancers.
The Conversion of Ferric to Ferrous Iron
For the body to absorb non-heme iron, it must undergo a vital conversion process. The oxidized ferric (Fe³⁺) iron must be reduced to the more soluble and absorbable ferrous (Fe²⁺) form. This conversion occurs primarily in the duodenum and upper jejunum, the first parts of the small intestine.
The acidic environment of the stomach, produced by gastric acid, is the first step, as it helps release ferric iron from the food matrix. Once in the duodenum, a brush-border enzyme called duodenal cytochrome B (DcytB) reduces the ferric (Fe³⁺) ions to ferrous (Fe²⁺) ions. Only after this reduction can the ferrous iron be transported into the intestinal absorptive cells (enterocytes) via the divalent metal transporter 1 (DMT1).
Factors Affecting Ferric Iron Conversion
The efficiency of this conversion and subsequent absorption is heavily influenced by several factors:
Enhancers of Absorption
- Ascorbic Acid (Vitamin C): This is the most potent enhancer of non-heme iron absorption. It aids absorption by chelating ferric ions in the stomach and reducing them to the ferrous state, keeping them soluble and readily available for uptake.
- Meat, Fish, and Poultry (The 'Meat Factor'): Beyond providing readily absorbed heme iron, these animal tissues contain a 'meat factor' that enhances the absorption of non-heme iron from plant sources consumed in the same meal.
Inhibitors of Absorption
- Phytates: Found in whole grains, cereals, legumes, and nuts, phytates bind to iron, forming insoluble complexes that the body cannot absorb.
- Polyphenols: Present in tea, coffee, wine, vegetables, and fruit, polyphenols can significantly inhibit iron absorption by forming complexes with it.
- Calcium: High levels of calcium can interfere with the absorption of both heme and non-heme iron.
Ferric vs. Ferrous Iron Absorption: A Comparison
| Feature | Ferrous Iron (Fe²⁺) | Ferric Iron (Fe³⁺) | 
|---|---|---|
| Absorption Form | Actively absorbed by intestinal cells via DMT1. | Requires conversion to ferrous iron before absorption. | 
| Bioavailability | Higher bioavailability, especially in supplement form like ferrous sulfate. | Lower bioavailability; requires reduction and is hindered by dietary factors. | 
| Dietary Sources | Primarily in heme iron from animal products. | Abundant in non-heme iron from plant-based foods. | 
| Effect of Vitamin C | Absorption is enhanced but less dependent on it than ferric iron. | Conversion and absorption are heavily dependent on the presence of vitamin C. | 
| Gastrointestinal pH | Stays soluble over a wider pH range, increasing its chances of absorption. | Becomes insoluble and precipitates at neutral or alkaline pH found in the small intestine. | 
The Role of Supplements
Since ferric iron is poorly absorbed, most oral iron supplements use ferrous salts, such as ferrous sulfate, because they are more bioavailable and easily absorbed. Newer formulations, like ferric maltol, have also shown effectiveness, particularly for those with inflammatory conditions. The choice of supplement and the presence of enhancers or inhibitors can significantly impact its efficacy.
The Body's Regulation of Absorption
The body tightly regulates iron absorption to maintain homeostasis and prevent both deficiency and dangerous overload. A key regulator is the peptide hormone hepcidin, produced by the liver. When iron levels are high, hepcidin production increases, binding to ferroportin (the iron export protein) and causing its degradation. This prevents iron from entering the bloodstream and leads to its removal from the body when the intestinal cells are shed. Conversely, when iron stores are low, hepcidin levels drop, allowing more iron to be absorbed.
Conclusion
In summary, humans cannot directly absorb ferric iron effectively. The process is a two-step mechanism where ferric iron is first chemically reduced to the ferrous state in the duodenum before it can be taken up by intestinal cells. This conversion is influenced by dietary factors like vitamin C, which enhances absorption, and inhibitors such as phytates and polyphenols. The body’s regulatory systems, particularly hepcidin, further control the amount of iron absorbed based on its needs. While heme iron from animal sources bypasses this conversion, understanding the non-heme process is crucial for optimizing absorption from plant-based diets and supplements.
For more detailed information on the biochemical processes of iron absorption, see the resource at NCBI Bookshelf.