<unk>  deficiency<unk>  is an important topic in prenatal care because women can sometimes become<unk> -deficient from the increased<unk>  demands of pregnancy. Functional or actual<unk>  deficiency can result from a variety of causes. These causes can be grouped into several categories: * Increased demand for<unk> , which the diet cannot accommodate. * Increased loss of<unk>  (usually through loss of blood). * Nutritional deficiency. This can result due to a lack of dietary<unk>  or consumption of foods that inhibit<unk>  absorption. Absorption inhibition has been observed caused by phytates in bran, calcium from supplements or dairy products, and tannins from tea, although in all three of these studies the effect was small and the authors of the studies cited regarding bran and tea note that the effect will probably only have a noticeable impact when most<unk>  is obtained from vegetable sources. * Acid-reducing medications: Acid-reducing medications reduce the absorption of dietary<unk> . These medications are commonly used for gastritis, reflux disease, and ulcers. Proton pump inhibitors (PPIs), H2 antihistamines, and antacids will reduce<unk>  metabolism. * Damage to the intestinal lining. Examples of causes of this kind of damage include surgery involving the duodenum or diseases like Crohn's or celiac sprue which severely reduce the surface area available for absorption. Helicobacter pylori infections also reduce the availability of<unk> . * Inflammation leading to hepcidin-induced restriction on<unk>  release from enterocytes (see above). * Is also a common occurrence in pregnant women, and in growing adolescents due to poor diets. * Acute blood loss or acute liver cirrhosis creates a lack of transferrin therefore causing<unk>  to be secreted from the body.<unk>  overload The body is able to substantially reduce the amount of<unk>  it absorbs across the mucosa. It does not seem to be able to entirely shut down the<unk>  transport process. Also, in situations where excess<unk>  damages the intestinal lining itself (for instance, when children eat a large quantity of<unk>  tablets produced for adult consumption), even more<unk>  can enter the bloodstream and cause a potentially deadly syndrome of<unk>  overload. Large amounts of free<unk>  in the circulation will cause damage to critical cells in the liver, the heart and other metabolically active organs.<unk>  toxicity results when the amount of circulating<unk>  exceeds the amount of transferrin available to bind it, but the body is able to vigorously regulate its<unk>  uptake. Thus,<unk>  toxicity from ingestion is usually the result of extraordinary circumstances like<unk>  tablet over-consumption rather than variations in diet. The type of acute toxicity from<unk>  ingestion causes severe mucosal damage in the gastrointestinal tract, among other problems. Excess<unk>  has been linked to higher rates of disease and mortality. For example, breast cancer patients with low ferroportin expression (leading to higher concentrations of intracellular<unk>  survive for a shorter period of time on average, while high ferroportin expression predicts 90% 10-year survival in breast cancer patients. Similarly, genetic variations in<unk>  transporter genes known to increase serum<unk>  levels also reduce lifespan and the average number of years spent in good health. It has been suggested that mutations that increase<unk>  absorption, such as the ones responsible for hemochromatosis (see below), were selected for during Neolithic times as they provided a selective advantage against<unk> -deficiency anemia. The increase in systemic<unk>  levels becomes pathological in old age, which supports the notion that antagonistic pleiotropy or "hyperfunction" drives human aging. Chronic<unk>  toxicity is usually the result of more chronic<unk>  overload syndromes associated with genetic diseases, repeated transfusions or other causes. In such cases the<unk>  stores of an adult may reach 50 grams (10 times normal total body<unk>  or more. The most common diseases of<unk>  overload are hereditary hemochromatosis (HH), caused by mutations in the HFE gene, and the more severe disease juvenile hemochromatosis (JH), caused by mutations in either hemojuvelin (HJV) or hepcidin (HAMP). The exact mechanisms of most of the various forms of adult hemochromatosis, which make up most of the genetic<unk>  overload disorders, remain unsolved. So, while researchers have been able to identify genetic mutations causing several adult variants of hemochromatosis, they now must turn their attention to the normal function of these mutated genes.
Human iron metabolism
Human blood group systems
Selenium in biology
Fatty acid ratio in food
Ethanol metabolism
Composition of the human body
Purine metabolism
Pregnancy specific biological substances