Accidental overdose due to consumption of iron-containing products is the leading cause of iron poisoning in children under 6. The oral lethal dose of elemental iron is about 200–250 mg per kilogram of body weight but significantly less has proven fatal.
Taking iron supplements can cause some adverse effects, which may include gastrointestinal irritation, nausea, vomiting, diarrhea, and constipation. Stools May sometimes appear darker than usual. Liquids containing iron may stain the teeth temporarily but this can be counteracted by adding water to the liquid. Eating before taking iron supplements may reduce gastrointestinal symptoms (26).
Diseases related to excess iron intake.
Many studies have demonstrated that people with cirrhosis of the liver due to iron overload (e.g., 'hemochromatosis') brought about by hereditary conditions of have a significantly higher risk of liver cancer. There is no clear link, however, between iron intake and cancer risk in people without hemochromatosis (11).
Although the results were inconsistent, the risk of colorectal cancer and the incidence of precancerous polyps ('adenomas') were linked to indicators of increased iron status in a few epidemiological studies.
Iron consumption from food or supplements shows a more consistent link to colorectal cancer incidence than indicators of iron status or iron stores (31, 32). An increased risk of colorectal cancer has long been linked to excessive consumption of red meat, but this is not necessarily due to the resulting increase in iron intake – the cause could well be increased secretion of bile or exposure to carcinogens produced by cooking meat, for example (33). Especially combined with a high-fat diet, exposing colon cells to harmful reactive oxygen species that stem from iron-catalyzed reactions could be an explanation for increased colon cancer risk that occurs due to increased iron in the colon, rather than increased body iron stores.
Nevertheless, the relationship between dietary iron intake, iron stores, and the risk of colon cancer is still not clear.
Epidemiological studies of nutritional iron status and cardiovascular diseases in humans have not produced conclusive data, even though the role of iron-induced oxidative stress in atherosclerosis and heart attacks ('myocardial infarction') (27) has been indicated in animal studies.
No good evidence for a conclusive link between several different indicators of iron status and CHD was gleaned from a systematic review of 12 prospective cohort studies, in which there were 7,800 cases of coronary heart disease (CHD) (28). Increased dietary heme iron was found to be linked to increased incidence of heart attack in two large-scale prospective studies, but total dietary iron was not (29, 30).
It would be sensible for people not at risk of iron deficiency (e.g., adult men and postmenopausal women) to avoid excess iron consumption, even though the association between iron stores and CHD is in need of further investigation.
Oxidative stress can be caused by accumulation of excess iron, and this can lead to damage to nerve cells in the brain and contribute to several neurodegenerative diseases such as Alzheimer's and Parkinson's (34). The harmful accumulation of iron in the brain would seem to be a result of a failure in the iron regulation process in cells rather than increased dietary iron.
However, the mechanisms responsible for this failure are as yet unknown (35).
Despite normal intake, a few genetic disorders may result in disease-causing iron accumulation in the body. Iron deposition in the liver and other tissues is a characteristic of 'Hereditary hemochromatosis'. This occurs due to a slight increase in intestinal iron absorption over several years (36, 37) and can lead to cirrhosis of the liver if left untreated. Other consequences include diabetes, heart muscle damage, and arthritis.
A prerequisite for 'Sub-Saharan African hemochromatosis' would seem to be high iron intake in conjunction with an as yet unidentified genetic factor, in contrast to hereditary hemochromatosis (1, 38, 39).
People with serious hereditary 'anemias' that are not a result of iron deficiency may also be prone to iron overload. The body's continuous production of red blood cells may be at the root of excessive absorption of dietary iron (1).
Tolerable upper intake level
The European Food Safety Authority has decided that the available data are not sufficient to establish an upper level for iron from dietary sources (23).
|Age Group||UL (mg/day)|
|Infants 0-12 months||not possible to establish*|
|Children 1-13 years||40|
|Adolescents 14-18 years||45|
|Adults 19 years and older||45|
* The UL applies also to pregnant and breast-feeding women.
The UL is not meant to apply to individuals being treated with iron under close medical supervision.
Individuals with hereditary conditions of iron overload (e.g. 'hemochromatosis'), as well as individuals with alcoholic cirrhosis and other liver diseases, may experience adverse effects at iron intake levels below the UL (11).
Because of the potential for interactions, dietary supplements should not be taken with medication without first talking to an experienced healthcare provider.