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Human iron metabolism
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Diagram showing a generalized view of cellular iron homeostasis in humans. Iron import can occur via endocytosis of transferrin receptor 1 or via ferrous iron importers DMT1 and ZIP14, which require the activity of iron reductases such as STEAP2, SDR-2 and Dcytb. Intracellular iron can be stored in ferritin, used for protein biosynthesis, generate reactive oxygen species (ROS) and regulate transcription via iron-responsive element-binding proteins (IRP1/2). Export occurs through ferroportin, often aided by hephaestin (Hp) and/or ceruloplasmin (Cp), and repressed by hepcidin.
Human iron metabolism is the set of chemical reactions that maintain human homeostasis of iron at both the systemic and cellular level. The control of this necessary but potentially toxic metal is an important part of many aspects of human health and disease. Hematologists have been especially interested in systemic iron metabolism because iron is essential for red blood cells, where most of the human body's iron is contained. Understanding iron metabolism is also important for understanding diseases of iron overload, such as hereditary hemochromatosis, and iron deficiency, such as iron deficiency anemia.
Contents
[hide]
1 Importance of iron regulation
1.1 Cellular respiration
1.2 Oxygen transport
1.3 Toxicity
1.4 Bacterial protection
2 Body iron stores
3 Mechanisms of iron regulation
3.1 Systemic iron regulation
3.1.1 Dietary iron uptake
3.1.2 Iron recycling and loss
3.2 Cellular iron regulation
3.2.1 Iron import
3.2.2 The labile iron pool
3.2.3 The storage iron pool
3.2.4 Iron export
3.2.5 Translational control of cellular iron
4 Iron-related pathology
4.1 Iron deficiency
4.2 Iron overload
5 References
6 Further reading
7 External links
Importance of iron regulation[edit]
Structure of Heme b; "Fe" is the chemical symbol of iron, "II" indicates its oxidation state.
Iron is an essential bioelement for most forms of life, from bacteria to mammals. Its importance lies in its ability to mediate electron transfer. In the ferrous state, iron acts as an electron donor, while in the ferric state it acts as an acceptor. Thus, iron plays a vital role in the catalysis of enzymatic reactions that involve electron transfer (reduction and oxidation, redox). Proteins can contain iron as part of different cofactors, such as iron-sulfur clusters (Fe-S) and heme groups, both of which are assembled in mitochondria.
Cellular respiration[edit]
Main article: Cellular respiration
Human cells require iron in order to obtain energy as ATP from a multi-step process known as cellular respiration, more specifically from oxidative phosphorylation at the mitochondrial cristae. Iron is present in the iron-sulfur clusters and heme groups of the electron transport chain proteins that generate a proton gradient that allows ATP synthase to synthesize ATP (chemiosmosis).
Heme groups are part of hemoglobin, a protein found in red blood cells that serves to transport oxygen from the lungs to the tissues. Heme groups are also present in myoglobin to store and diffuse oxygen in muscle cells.
Oxygen transport[edit]
See also: Hemoglobin and myoglobin
The human body needs iron for oxygen transport. Oxygen (O2) is required for the functioning and survival of nearly all cell types. Oxygen is transported from the lungs to the rest of the body bound to the heme group of hemoglobin in erythrocytes. In muscles cells, iron binds myoglobin, which regulates its release.
Toxicity[edit]
Iron is also potentially toxic. Its ability to donate and accept electrons means that it can catalyze the conversion of hydrogen peroxide into free radicals. Free radicals can cause damage to a wide variety of cellular structures, and ultimately kill the cell.[1]
Iron bound to proteins or cofactors such as heme is safe. Also, there are virtually no truly free iron ions in the cell, since they readily form complexes with organic molecules. However, some of the intracellular iron is bound to low-affinity complexes, and is termed labile iron or "free" iron. Iron in such complexes can cause damage as described above.[2]
To prevent that kind of damage, all life forms that use iron bind the iron atoms to proteins. This binding allows cells to benefit from iron while also limiting its ability to do harm.[1][3] Typical intracellular labile iron concentrations in bacteria are 10-20 micromolar,[4] though they can be 10-fold higher in anaerobic environment,[5] where free radicals and reactive oxygen species are scarcer. In mammalian cells, intracellular labile iron concentrations are typically smaller than 1 micromolar, less than 5 percent of total cellular iron.[2]
Bacterial protection[edit]
Electron micrograph of E. coli. Most bacteria that cause human disease require iron to live and to multiply.
In response to a systemic bacterial infection, the immune system initiates a process known as iron withholding. If bacteria are to survive, then they must obtain iron from their environment. Disease-causing bacteria do this in many ways, including releasing iron-binding molecules called siderophores and then reabsorbing them to recover iron, or scavenging iron from hemoglobin and transferrin. The harder they have to work to get iron, the greater a metabolic price they must pay. That means that iron-deprived bacteria reproduce more slowly. So our control of iron levels appears to be an important defense against most bacterial infections; there are some exceptions however. TB causing bacterium can reside within macrophages which are an iron rich environment and Borrelia burgdorferi utilises manganese in place of iron. People with increased amounts of iron, like people with hemochromatosis, are more susceptible to some bacterial infection.[6]
Although this mechanism is an elegant response to short-term bacterial infection, it can cause problems when inflammation goes on for longer. Since the liver produces hepcidin in response to inflammatory cytokines, hepcidin levels can increase as the result of non-bacterial sources of inflammation, like viral infection, cancer, auto-immune diseases or other chronic diseases. When this occurs, the sequestration of iron appears to be the major cause of the syndrome of anemia of chronic disease, in which not enough iron is available to produce enough hemoglobin-containing red blood cells.[3]
Body iron stores[edit]
Illustration of blood cell production in the bone marrow. In iron deficiency, the bone marrow produces fewer blood cells, and as the deficiency gets worse, the cells become smaller.
Most well-nourished people in industrialized countries have 4 to 5 grams of iron in their bodies (∼38 mg iron/kg body weight for women and ∼50 mg iron/kg body for men).[7] Of this, about 6997250000000000000♠2.5 g is contained in the hemoglobin needed to carry oxygen through the blood, and most of the rest (approximately 2 grams in adult men, and somewhat less in women of childbearing age) is contained in ferritin complexes that are present in all cells, but most common in bone marrow, liver, and spleen. The liver's stores of ferritin are the primary physiologic source of reserve iron in the body. The reserves of iron in industrialized countries tend to be lower in children and women of child-bearing age than in men and in the elderly. Women who must use their stores to compensate for iron lost through menstruation, pregnancy or lactation have lower non-hemoglobin body stores, which may consist of 6996500000000000000♠500 mg, or even less.
Of the body's total iron content, about 6996399999999999999♠400 mg is devoted to cellular proteins that use iron for important cellular processes like storing oxygen (myoglobin) or performing energy-producing redox reactions (cytochromes). A relatively small amount (3–4 mg) circulates through the plasma, bound to transferrin.[8] Because of its toxicity, free soluble iron is kept in low concentration in the body.
Iron deficiency first affects the storage iron in the body, and depletion of these stores is thought to be relatively non-symptomatic, although some vague and non-specific symptoms have been associated with it. Since iron is primarily required for hemoglobin, iron deficiency anemia is the primary clinical manifestation of iron deficiency. Iron-deficient people will suffer or die from organ damage well before cells run out of the iron needed for intracellular processes like electron transport.
Macrophages of the reticuloendothelial system store iron as part of the process of breaking down and processing hemoglobin from engulfed red blood cells. Iron is also stored as a pigment called hemosiderin which is an ill-defined deposit of protein and iron, created by macrophages where excess iron is present, either locally or systemically for example among people with iron overload due to frequent blood cell destruction and transfusions. If the systemic iron overload is corrected, over time the hemosiderin is slowly resorbed by macrophages.
Mechanisms of iron regulation[edit]
Human iron homeostasis is regulated at two different levels. Systemic iron levels are balanced by the controlled absorption of dietary iron by enterocytes, the cells that line the interior of the intestines, and the uncontrolled loss of iron from epithelial sloughing, sweat, injuries and blood loss. In addition, systemic iron is continuously recycled. Cellular iron levels are controlled differently by different cell types due to the expression of particular iron regulatory and transport proteins.
Systemic iron regulation[edit]
Humans use 6995199999999999999♠20 mg of iron each day for the production of new red blood cells, much of which is recycled from old red blood cells.
Dietary iron uptake[edit]
The absorption of dietary iron is a variable and dynamic process. The amount of iron absorbed compared to the amount ingested is typically low, but may range from 5% to as much as 35% depending on circumstances and type of iron. The efficiency with which iron is absorbed varies depending on the source. Generally the best-absorbed forms of iron come from animal products. Absorption of dietary iron in iron salt form (as in most supplements) varies somewhat according to the body’s need for iron, and is usually between 10% and 20% of iron intake. Absorption of iron from animal products, and some plant products, is in the form of heme iron, and is more efficient, allowing absorption of from 15% to 35% of intake. Heme iron in animals is from blood and heme-containing proteins in meat and mitochondria, whereas in plants, heme iron is present in mitochondria in all cells that use oxygen for respiration.
Like most mineral nutrients, the majority of the iron absorbed from digested food or supplements is absorbed in the duodenum by enterocytes of the duodenal lining. These cells have special molecules that allow them to move iron into the body. To be absorbed, dietary iron can be absorbed as part of a protein such as heme protein or iron must be in its ferrous Fe2+ form. A ferric reductase enzyme on the enterocytes’ brush border, duodenal cytochrome B (Dcytb), reduces ferric Fe3+ to Fe2+.[9] A protein called divalent metal transporter 1 (DMT1), which can transport several divalent metals across the plasma membrane, then transports iron across the enterocyte’s cell membrane into the cell.
These intestinal lining cells can then either store the iron as ferritin, which is accomplished by Fe3+ binding to apoferritin (in which case the iron will leave the body when the cell dies and is sloughed off into feces), or the cell can release it into the body via the only known iron exporter in mammals, ferroportin. Hephaestin, a ferroxidase that can oxidize Fe2+ to Fe3+ and is found mainly in the small intestine, helps ferroportin transfer iron across the basolateral end of the intestine cells. In contrast, ferroportin is post-translationally repressed by hepcidin, a 25-amino acid peptide hormone. The body regulates iron levels by regulating each of these steps. For instance, enterocytes synthesize more Dcytb, DMT1 and ferroportin in response to iron deficiency anemia.[10] Iron absorption from diet is enhanced in the presence of vitamin C and diminished by excess calcium, zinc, or manganese.[11][citation needed]
The human body’s rate of iron absorption appears to respond to a variety of interdependent factors, including total iron stores, the extent to which the bone marrow is producing new red blood cells, the concentration of hemoglobin in the blood, and the oxygen content of the blood. The body also absorbs less iron during times of inflammation, in order to deprive bacteria of iron. Recent discoveries demonstrate that hepcidin regulation of ferroportin is responsible for the syndrome of anemia of chronic disease.
Iron recycling and loss[edit]
Most of the iron in the body is hoarded and recycled by the reticuloendothelial system, which breaks down aged red blood cells. In contrast to iron uptake and recycling, there is no physiologic regulatory mechanism for excreting iron. People lose a small but steady amount by gastrointestinal blood loss, sweating and by shedding cells of the skin and the mucosal lining of the gastrointestinal tract. The total amount of loss for healthy people in the developed world amounts to an estimated average of 6994100000000000000♠1 mg a day for men, and 1.5–2 mg a day for women with regular menstrual periods.[citation needed] People with gastrointestinal parasitic infections, more commonly found in developing countries, often lose more.[1] Those who cannot regulate absorption well enough get disorders of iron overload. In these diseases, the toxicity of iron starts overwhelming the body's ability to bind and store it.[12]
Cellular iron regulation[edit]
Iron import[edit]
Most cell types take up iron primarily through receptor-mediated endocytosis via transferrin receptor 1 (TFR1), transferrin receptor 2 (TFR2) and GAPDH. TFR1 has a 30-fold higher affinity for transferrin-bound iron than TFR2 and thus is the main player in this process.[13][14] The higher order multifunctional glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) also acts as a transferrin receptor.[15][16] Transferrin-bound ferric iron is recognized by these transferrin receptors, triggering a conformational change that causes endocytosis. Iron then enters the cytoplasm from the endosome via importer DMT1 after being reduced to its ferrous state by a STEAP family reductase.[17]
Alternatively, iron can enter the cell directly via plasma membrane divalent cation importers such as DMT1 and ZIP14 (Zrt-Irt-like protein 14).[18] Again, iron enters the cytoplasm in the ferrous state after being reduced in the extracellular space by a reductase such as STEAP2, STEAP3 (in erythrocytes), Dcytb (in enterocytes) and SDR2.[17]
The labile iron pool[edit]
In the cytoplasm, ferrous iron is found in a soluble, chelatable state which constitutes the labile iron pool (~0.001 mM).[19] In this pool, iron is thought to be bound to low-mass compounds such as peptides, carboxylates and phosphates, although some might be in a free, hydrated form (aqua ions).[19] Alternatively, iron ions might be bound to specialized proteins known as metallochaperones.[20] Specifically, poly-r(C)-binding proteins (PCBPs) appear to mediate transfer of free iron to ferritin (for storage) and non-heme iron enzymes (for use in catalysis).[18][21] The labile iron pool is potentially toxic due to iron's ability to generate reactive oxygen species. Iron from this pool can be taken up by mitochondria via mitoferrin to synthesize Fe-S clusters and heme groups.[17]
The storage iron pool[edit]
Iron can be stored in ferritin as ferric iron due to the ferroxidase activity of the ferritin heavy chain.[22] Dysfunctional ferritin may accumulate as hemosiderin, which can be problematic in cases of iron overload.[23] The ferritin storage iron pool is much larger than the labile iron pool, ranging in concentration from 0.7 mM to 3.6 mM.[19]
Iron export[edit]
Iron export occurs in a variety of cell types, including neurons, erythrocytes, macrophages and enterocytes. The latter two are especially important since systemic iron levels depend upon them. There is only one known iron exporter, ferroportin.[24] It transports ferrous iron out of the cell, generally aided by ceruloplasmin and/or hephaestin (mostly in enterocytes), which oxidize iron to its ferric state so it can bind ferritin in the extracellular medium.[17] Hepcidin causes the internalization of ferroportin, decreasing iron export. Besides, hepcidin seems to downregulate both TFR1 and DMT1 through an unknown mechanism.[25] Another player assisting ferroportin in effecting cellular iron export is GAPDH.[26] A specific post translationally modified isoform of GAPDH is recruited to the surface of iron loaded cells where it recruits apo-transferrin in close proximity to ferroportin so as to rapidly chelate the iron extruded.[27]
The expression of hepcidin, which only occurs in certain cell types such as hepatocytes, is tightly controlled at the transcriptional level and it represents the link between cellular and systemic iron homeostasis due to hepcidin's role as "gatekeeper" of iron release from enterocytes into the rest of the body.[17] Erythroblasts produce erythroferrone, a hormone which inhibits hepcidin and so increases the availability of iron needed for hemoglobin synthesis.[28]
Translational control of cellular iron[edit]
Although some control exists at the transcriptional level, the regulation of cellular iron levels is ultimately controlled at the translational level by iron-responsive element-binding proteins IRP1 and especially IRP2.[29] When iron levels are low, these proteins are able to bind to iron-responsive elements (IREs). IREs are stem loop structures in the untranslated regions (UTRs) of mRNA.[17]
Both ferritin and ferroportin contain an IRE in their 5' UTRs, so that under iron deficiency their translation is repressed by IRP2, preventing the unnecessary synthesis of storage protein and the detrimental export of iron. In contrast, TFR1 and some DMT1 variants contain 3' UTR IREs, which bind IRP2 under iron deficiency, stabilizing the mRNA, which guarantees the synthesis of iron importers.[17]
Iron-related pathology[edit]
Main article: Iron metabolism disorder
Iron deficiency[edit]
Main article: Iron deficiency
Iron is an important topic in prenatal care because women can sometimes become iron-deficient from the increased iron demands of pregnancy.
Functional or actual iron deficiency can result from a variety of causes. These causes can be grouped into several categories:
Increased demand for iron, which the diet cannot accommodate.
Increased loss of iron (usually through loss of blood).
Nutritional deficiency. This can result due to a lack of dietary iron or consumption of foods that inhibit iron absorption, including calcium, phytates and tannins. Black tea steeped for long has high tannins.
Inability to absorb iron: A common cause of iron deficiency is the widespread use of acid reducing medications, the strongest of which are proton pump inhibitors (PPIs) such as omeprazole.[citation needed]
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.
Inflammation leading to hepcidin-induced restriction on iron release from enterocytes (see above).
Iron overload[edit]
Main article: Iron overload
The body is able to substantially reduce the amount of iron it absorbs across the mucosa. It does not seem to be able to entirely shut down the iron transport process. Also, in situations where excess iron damages the intestinal lining itself (for instance, when children eat a large quantity of iron tablets produced for adult consumption), even more iron can enter the bloodstream and cause a potentially deadly syndrome of iron overload. Large amounts of free iron in the circulation will cause damage to critical cells in the liver, the heart and other metabolically active organs.
Iron toxicity results when the amount of circulating iron exceeds the amount of transferrin available to bind it, but the body is able to vigorously regulate its iron uptake. Thus, iron toxicity from ingestion is usually the result of extraordinary circumstances like iron tablet over-consumption[1][30] rather than variations in diet. The type of acute toxicity from iron ingestion causes severe mucosal damage in the gastrointestinal tract, among other problems.
Chronic iron toxicity is usually the result of more chronic iron overload syndromes associated with genetic diseases, repeated transfusions or other causes. In such cases the iron stores of an adult may reach 50 grams (10 times normal total body iron) or more. Classic examples of genetic iron overload includes hereditary hemochromatosis (HH) and the more severe disease juvenile hemochromatosis (JH) caused by mutations in either the gene RGMc gene, a member of a three gene repulsive guidance molecule family,[31] (also called hemojuvelin (HJV), and HFE2), Hemojuvelin, or the HAMP gene that encodes (an iron regulatory peptide). The exact mechanisms of most of the various forms of adult hemochromatosis, which make up most of the genetic iron 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.
References[edit]
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Further reading[edit]
Andrews S, Norton I, Salunkhe AS, Goodluck H, Aly WS, Mourad-Agha H, Cornelis P (2013). "Chapter 7, Control of Iron Metabolism in Bacteria". In Banci L. Metallomics and the Cell. Metal Ions in Life Sciences. 12. Springer. doi:10.1007/978-94-007-5561-1_7. ISBN 978-94-007-5560-4. electronic-book ISBN 978-94-007-5561-1 ISSN 1559-0836 electronic-ISSN 1868-0402
Andrews NC (May 2004). "Anemia of inflammation: the cytokine-hepcidin link". The Journal of Clinical Investigation. 113 (9): 1251–3. doi:10.1172/JCI21441. PMC 398435  . PMID 15124013.
Camaschella C (Dec 2005). "Understanding iron homeostasis through genetic analysis of hemochromatosis and related disorders". Blood. 106 (12): 3710–7. doi:10.1182/blood-2005-05-1857. PMID 16030190.
Frazer DM, Anderson GJ (Oct 2005). "Iron imports. I. Intestinal iron absorption and its regulation". American Journal of Physiology. Gastrointestinal and Liver Physiology. 289 (4): G631–5. doi:10.1152/ajpgi.00220.2005. PMID 16160078.
Insel P, Ross D, McMahon K, Bernstein M (2011). "Iron". Nutrition (4th ed.). Sudbury, Massachusetts: Jones and Bartlett Publishers. pp. 510–514. ISBN 978-0-7637-7663-3. Retrieved June 25, 2012. See esp. pp. 513-514 CS1 maint: Uses authors parameter (link)
Lammi-Keef CJ, Couch SC, Philipson EH, eds. (2008). "Dietary diversification and modification of iron". Handbook of Nutrition and Pregnancy. Nutrition & Health. Totowa, New Jersey: Humana Press. pp. 350–351. doi:10.1007/978-1-59745-112-3. ISBN 978-1-59745-112-3. Retrieved June 25, 2012. CS1 maint: Uses editors parameter (link)
Panel on Micronutrients; Subcommittees on Upper Reference Levels of Nutrients and of Interpretation and Uses of Dietary Reference Intakes; the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes (2001). "Iron". Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, D.C: Food and Nutrition Board, Institute of Medicine. pp. 290–393. ISBN 978-0-309-07279-3. Retrieved June 25, 2012.
Reilly C (2004). "Iron". The Nutritional Trace Metals. Oxford, UK & Ames, Iowa: Blackwell Publishing. pp. 35–81. ISBN 1-4051-1040-6. Retrieved June 25, 2012.
External links[edit]
A comprehensive NIH factsheet on iron and nutrition
Iron Disorders Institute: A nonprofit group concerned with iron disorders; site has helpful links and information on iron-related medical disorders.
An interactive medical learning portal on iron metabolism
Information about iron outside the body
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Pentose phosphate pathway
Fructolysis
Galactolysis
Glycosylation
N-linked
O-linked
Nonhuman
Photosynthesis
Anoxygenic photosynthesis
Chemosynthesis
Carbon fixation
Xylose metabolism
Radiotrophism
Lipid metabolism
(lipolysis, lipogenesis)
Fatty acid metabolism
Fatty acid degradation (Beta oxidation)
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Steroid metabolism
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Eicosanoid metabolism
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Amino acid
Amino acid synthesis
Urea cycle
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metabolism
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Pyrimidine metabolism
Other
Metal metabolism
Iron metabolism
Ethanol metabolism
[show]
v
t
e
Metabolism: Metal metabolism
Transition metal
Iron metabolism
Absorption in
Duodenum
Iron(II) oxide:
DMT1 (SLC11A2)
Ferritin
Hephaestin/Ferroportin (SLC11A3/SLC40A1)
Transferrin to Transferrin receptor
TFR1
TFR2
Iron(III) oxide:
Duodenal cytochrome B
Integrin
Calreticulin/mobilferrin
Ferritin
Other
Iron-binding proteins:
Ferritin
Hepcidin/HAMP
Hemojuvelin
Iron-responsive element-binding protein
Aconitase
Ceruloplasmin
HFE
Hemosiderin
Lactoferrin
Copper metabolism
ATP7A
ATP7B
Ceruloplasmin
SLC31A1
ATOX1
Zinc metabolism
TMC6
TMC8
SLC30A1
SLC39A4
Electrolyte
Sodium metabolism
Na+/K+-ATPase
Phosphate metabolism
Phosphoric acids and phosphates
Magnesium metabolism
Magnesium transporter
Calcium metabolism
Calcium-sensing receptor
Calcium-binding protein
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Categories:
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text:
United States presidential line of succession
From Wikipedia, the free encyclopedia
Jump to: navigation, search
The United States presidential line of succession is the order in which persons may become or act as President of the United States if the incumbent President becomes incapacitated, dies, resigns, or is removed from office (by impeachment by the House of Representatives and subsequent conviction by the Senate). The line of succession is set by the United States Constitution and the Presidential Succession Act of 1947[1] as subsequently amended to include newly created cabinet offices. The succession follows the order of Vice President, Speaker of the House of Representatives, President pro tempore of the Senate, and then the heads of federal executive departments who form the Cabinet of the United States. The Cabinet currently has fifteen members, beginning with the Secretary of State, and followed by the rest in the order of their positions' creation. Those heads of department who are ineligible to act as President are also ineligible to succeed the President by succession, for example most commonly if they are not a natural-born U.S. citizen.
Several constitutional law experts have raised questions as to the constitutionality of the provisions that the Speaker of the House and the President pro tempore of the Senate succeed to the presidency,[2] and in 2003 the Continuity of Government Commission raised a number of other issues with the current line of succession.[3]
Contents
[hide]
1 Current order
2 Eligibility
2.1 Eligibility requirements
2.2 Acting officers
3 Motivation for changes to the succession in 1945
4 Constitutional provisions
5 Acting President and President
6 History of succession law set by Congress
6.1 Presidential Succession Act 1792
6.2 Presidential Succession Act 1886
6.3 Presidential Succession Act 1947
6.4 Postmaster General removed 1971
6.5 Secretary of Homeland Security added 2006
7 Successions beyond Vice President
8 Constitutional concerns
9 See also
10 References
11 Further reading
12 External links
Current order[edit]
The current presidential order of succession is as follows:[4]
Key
Eligible Democrat (D)
Eligible Republican (R)
Eligible Independent (I)
Eligible unknown
Not eligible
No.
Office
Current officer
1
Vice President Mike Pence (R)
2
Speaker of the House of Representatives Paul Ryan (R)
3
President pro tempore of the Senate Orrin Hatch (R)
4
Secretary of State Rex Tillerson (R)
5
Secretary of the Treasury Steven Mnuchin (R)
6
Secretary of Defense James Mattis (I)
7
Attorney General Jeff Sessions (R)
8
Secretary of the Interior Ryan Zinke (R)
9
Secretary of Agriculture Sonny Perdue (R)
10
Secretary of Commerce Wilbur Ross (R)
11
Secretary of Labor Alex Acosta (R)
12
Secretary of Health and Human Services Eric Hargan (R)[a]
Acting
13
Secretary of Housing and Urban Development Ben Carson (R)
–
Secretary of Transportation Elaine Chao (R)[b]
14
Secretary of Energy Rick Perry (R)
15
Secretary of Education Betsy DeVos (R)
16
Secretary of Veterans Affairs David Shulkin (I)
17
Secretary of Homeland Security Elaine Duke (I)[a]
Acting
^ Jump up to: a b This listing assumes that acting officers whose prior appointment required Senate confirmation are eligible for the line of succession. See Acting officers below.
Jump up ^ Not a natural-born citizen (acquired U.S. citizenship by naturalization) and thus ineligible for the Presidency.
Cabinet officers are in line according to the chronological order of their department's creation or the department of which their department is the successor (the Department of Defense being successor to the Department of War, and the Department of Health and Human Services being successor to the Department of Health, Education and Welfare).[a]
Eligibility[edit]
Eligibility requirements[edit]
To be eligible to serve as President, a person must be a natural-born U.S. citizen, at least 35 years of age, and a resident within the United States for at least 14 years. These eligibility requirements are specified both in the U.S. Constitution, Article II, Section 1, Clause 5, and in the Presidential Succession Act of 1947 (3 U.S.C. § 19(e)).
Acting officers[edit]
Acting officers may be eligible. In 2009, the Continuity of Government Commission, a private non-partisan think tank, reported,
The language in the current Presidential Succession Act is less clear than that of the 1886 Act with respect to Senate confirmation. The 1886 Act refers to "such officers as shall have been appointed by the advice and consent of the Senate to the office therein named..." The current act merely refers to "officers appointed, by and with the advice and consent of the Senate." Read literally, this means that the current act allows for acting secretaries to be in the line of succession as long as they are confirmed by the Senate for a post (even for example, the second or third in command within a department). It is common for a second in command to become acting secretary when the secretary leaves office. Though there is some dispute over this provision, the language clearly permits acting secretaries to be placed in the line of succession. (We have spoken to acting secretaries who told us they had been placed in the line of succession.)[5]
Motivation for changes to the succession in 1945[edit]
Two months after succeeding Franklin D. Roosevelt, President Harry S. Truman proposed that the Speaker of the House and the President pro tempore of the Senate be granted priority in the line of succession over the Cabinet so as to ensure the President would not be able to appoint his successor to the Presidency.[6]
The Secretary of State and the other Cabinet officials are appointed by the President, while the Speaker of the House and the President pro tempore of the Senate are elected officials. The Speaker is chosen by the U.S. House of Representatives, and every Speaker has been a member of that body for the duration of their term as Speaker, though this is not technically a requirement; the President pro tempore is chosen by the U.S. Senate and customarily the Senator of the majority party with the longest record of continuous service fills this position. The Congress approved this change and inserted the Speaker and President pro tempore in line, ahead of the members of the Cabinet in the order in which their positions were established.
In his speech supporting the changes, Truman noted that the House of Representatives is more likely to be in political agreement with the President and Vice President than the Senate. The succession of a Republican to a Democratic Presidency would further complicate an already unstable political situation. However, when the changes to the succession were signed into law, they placed Republican House Speaker Joseph W. Martin first in the line of succession after the Vice President.[7]
Some of Truman's critics said that his ordering of the Speaker before the President pro tempore was motivated by his dislike of the then-current holder of the latter rank, Senator Kenneth McKellar.[8] Further motivation may have been provided by Truman's preference for House Speaker Sam Rayburn to be next in the line of succession, rather than Secretary of State Edward R. Stettinius, Jr.[7]
Constitutional provisions[edit]
The line of succession is mentioned in three places in the Constitution:
Article II, Section 1, Clause 6 makes the Vice President first in the line of succession and allows the Congress to provide by law for cases in which neither the President nor Vice President can serve. The current such law governing succession is the Presidential Succession Act of 1947 (3 U.S.C. § 19).
Section 3 of the 20th Amendment provides that if the President-elect dies before his term begins, the Vice President-elect becomes President on Inauguration Day and serves for the full term to which the President-elect was elected. The section also provides that if, on Inauguration Day, a president has not been chosen or the President-elect does not qualify for the presidency, the Vice President-elect acts as president until a president is chosen or the President-elect qualifies. Finally, Section 3 allows the Congress to provide by law for cases in which neither a President-elect nor a Vice President-elect is eligible or available to serve.
The 25th Amendment, ratified in 1967, clarified Article II, Section 1: that the Vice President is the direct successor of the President. He or she becomes President if the President dies, resigns or is removed from office. The amendment also provides for the situation where the President is temporarily disabled, such as if the President has a surgical procedure or becomes mentally unfit.
The amendment also provides for Vice Presidential succession, by requiring Vice Presidential vacancies to be filled by the President and confirmed by both houses of the Congress. Previously, whenever a Vice President had succeeded to the Presidency or had otherwise left the office empty (through death, resignation, or removal from office), the Vice Presidency remained vacant until the next Presidential and Vice Presidential terms began.
Acting President and President[edit]
Main article: Acting President of the United States
New President Lyndon Johnson was sworn in aboard Air Force One, following the assassination of John F. Kennedy in 1963.
Article II, Section 1 of the United States Constitution provides that:
In case of the removal of the President from office, or of his death, resignation, or inability to discharge the powers and duties of the said office, the same shall devolve on the Vice President ... until the disability be removed, or a President elected.
This originally left open the question whether "the same" refers to "the said office" or only "the powers and duties of the said office." Some historians, including Edward Corwin[9] and John D. Feerick,[9] have argued that the framers' intention was that the Vice President would remain Vice President while executing the powers and duties of the Presidency; however, there is also much evidence to the contrary, the most compelling of which is Article I, section 3, of the Constitution itself, the relevant text of which reads:
The Vice President of the United States shall be President of the Senate, but shall have no vote, unless they be equally divided.
The Senate shall chuse [sic] their other officers, and also a President pro tempore, in the absence of the Vice President, or when he shall exercise the office of President of the United States.
This text appears to answer the hypothetical question of whether the office or merely the powers of the Presidency devolved upon the Vice President on his succession. Thus, the 25th Amendment merely restates and reaffirms the validity of existing precedent, apart from adding new protocols for Presidential disability.[original research?] Not everyone agreed with this interpretation when it was first actually tested, and it was left to Vice President John Tyler, the first presidential successor in U.S. history, to establish the precedent that was respected in the absence of the 25th Amendment.
In 1841, John Tyler became the first person to succeed to the presidency.
Upon the death of President William Henry Harrison in 1841 and after a brief hesitation, Tyler took the position that he was the President and not merely acting President upon taking the presidential oath of office. However, some contempories—including John Quincy Adams,[9][10] Henry Clay[11] and other members of Congress[10][11] Whig party leaders[11] and even Tyler's own cabinet[10][11]—believed that he was only acting as President and did not have the office itself.
Nonetheless, Tyler adhered to his position, even returning, unopened, mail addressed to the "Acting President of the United States" sent by his detractors.[12] Tyler's view ultimately prevailed when the Senate voted to accept the title "President,"[11] and this precedent was followed thereafter. The question was finally resolved by Section 1 of the 25th Amendment, which specifies that "In case of the removal of the President from office or of his death or resignation, the Vice President shall become President." The Amendment does not specify whether officers other than the Vice President can become President rather than Acting President in the same set of circumstances. The Presidential Succession Act refers only to other officers acting as President rather than becoming President.
History of succession law set by Congress[edit]
Presidential Succession Act 1792[edit]
Main article: Presidential Succession Act
Wikisource has original text related to this article:
Presidential Succession Act 1792
The Presidential Succession Act of 1792 was the first succession law passed by Congress. The act was contentious because the Federalists did not want the then Secretary of State, Thomas Jefferson, who had become the leader of the Democratic-Republicans, to follow the Vice President in the succession. There were also separation of powers concerns over including the Chief Justice of the United States in the line. The compromise they worked out established the President pro tempore of the Senate as next in line after the Vice President, followed by the Speaker of the House of Representatives.
In either case, these officers were to "act as President of the United States until the disability be removed or a president be elected." The Act called for a special election to be held in November of the year in which dual vacancies occurred (unless the vacancies occurred after the first Wednesday in October, in which case the election would occur the following year; or unless the vacancies occurred within the last year of the presidential term, in which case the next election would take place as regularly scheduled). The people elected President and Vice President in such a special election would have served a full four-year term beginning on March 4 of the next year, but no such election ever took place.
Presidential Succession Act 1886[edit]
Wikisource has original text related to this article:
Presidential Succession Act 1886
In 1881, after the death of President Garfield, and in 1885, after the death of Vice President Hendricks, there had been no President pro tempore in office, and as the new House of Representatives had yet to convene, no Speaker either,[13] leaving no one at all in the line of succession after the vice president. When Congress convened in December 1885, President Cleveland asked for a revision of the 1792 act, which was passed in 1886. Congress replaced the President pro tempore and Speaker with officers of the President's Cabinet with the Secretary of State first in line. In the first 100 years of the United States, six former Secretaries of State had gone on to be elected President, while only two congressional leaders had advanced to that office. As a result, changing the order of the line of succession seemed reasonable.[citation needed]
Presidential Succession Act 1947[edit]
Wikisource has original text related to this article:
Presidential Succession Act 1947
The Presidential Succession Act of 1947, signed into law by President Harry S. Truman, added the Speaker of the House and President pro tempore back in the line, but switched the two from the 1792 order. It remains the sequence used today[update]. Since the reorganization of the military in 1947 had merged the War Department (which governed the Army) with the Department of the Navy into the Department of Defense, the Secretary of Defense took the place in the order of succession previously held by the Secretary of War. The office of Secretary of the Navy, which had existed as a Cabinet-level position since 1798, had become subordinate to the Secretary of Defense in the military reorganization, and so was dropped from the line of succession in the 1947 Succession Act.
Postmaster General removed 1971[edit]
Until 1971, the Postmaster General, the head of the Post Office Department, was a member of the Cabinet, initially the last in the presidential line of succession before new officers were added. Once the Post Office Department was re-organized into the United States Postal Service, a special agency independent of the executive branch, the Postmaster General ceased to be a member of the Cabinet and was thus removed from the line of succession.[14]
Secretary of Homeland Security added 2006[edit]
The United States Department of Homeland Security was created in 2002. On March 9, 2006, pursuant to the renewal of the Patriot Act as Pub.L. 109–177, the Secretary of Homeland Security was added to the line of succession. The order of Cabinet members in the line has always been the same as the order in which their respective departments were established. Despite custom, many in Congress had wanted the Secretary to be placed at number eight on the list – below the Attorney General, above the Secretary of the Interior, and in the position held by the Secretary of the Navy prior to the creation of the Secretary of Defense – because the Secretary, already in charge of disaster relief and security, would presumably be more prepared to take over the presidency than some of the other Cabinet secretaries.[citation needed] Despite this, the 2006 law explicitly specifies that the "Secretary of Homeland Security" follows the "Secretary of Veterans Affairs" in the succession, effectively at the end of the list.[15]
Successions beyond Vice President[edit]
David Rice Atchison's tombstone (Plattsburg, Missouri), including the claim "President of the United States for One Day"
While nine Vice Presidents have succeeded to the office upon the death or resignation of the President, and two Vice Presidents have temporarily served as acting President, no other officer has ever been called upon to act as President. On March 4, 1849, President Zachary Taylor's term began, but he declined to be sworn in on a Sunday, citing religious beliefs, and the Vice President was not sworn either. As the last President pro tempore of the Senate, David Rice Atchison was thought by some to be next in line after the Vice President, and his tombstone claims that he was US President for the day. However, Atchison took no oath of office to the presidency either, and his term as Senate President pro tempore had by then expired.[16][17]
In 1865, when Andrew Johnson assumed the Presidency on the death of Abraham Lincoln, the office of Vice President became vacant. At that time, the Senate President pro tempore was next in line to the presidency. In 1868, Johnson was impeached by the House of Representatives and subjected to trial in the Senate, and if he had been convicted and thereby removed from office, Senate President pro tempore Benjamin Wade would have become acting President. This posed a conflict of interest, as Wade's "guilty" vote could have been decisive in removing Johnson from office and giving himself presidential powers and duties. (Johnson was acquitted by a one-vote margin.)
In his book The Shadow Presidents, which he published in 1979, Michael Medved describes a situation that arose prior to the 1916 election, when the First World War was raging in Europe. In view of the contemporary international turmoil, President Woodrow Wilson thought that if he lost the election it would be better for his opponent to begin his administration straight away, instead of waiting through the lame duck period, which at that time had a duration of almost four months. President Wilson and his aides formed a plan to exploit the rule of succession so that his rival Charles Evans Hughes could take over the Presidency as soon as the result of the election was clear. The plan was that Wilson would appoint Hughes to the post of Secretary of State. Wilson and his Vice President Thomas R. Marshall would then resign, and as the Secretary of State was at that time designated next in line of succession, Hughes would become President immediately. As it happened, President Wilson won re-election, so the plan was never put into action.[18]
New President Gerald Ford is sworn in following the resignation of Richard Nixon on August 9, 1974.
Since the 25th Amendment's ratification, its Second Section, which addresses Vice Presidential succession as noted above, has been invoked twice.
During the 1973 Vice Presidential vacancy, House Speaker Carl Albert was first in line. As the Watergate scandal made President Nixon's removal or resignation possible, Albert would have become Acting President and—under Title 3, Section 19(c) of the U.S. Code—would have been able to "act as President until the expiration of the then current Presidential term" on January 20, 1977. Albert openly questioned whether it was appropriate for him, a Democrat, to assume the powers and duties of the presidency when there was a public mandate for the Presidency to be held by a Republican. Albert announced that should he need to assume the Presidential powers and duties, he would do so only as a caretaker. However, with the nomination and confirmation of Gerald Ford to the Vice Presidency, which marked the first time the Second Section of the Twenty-fifth Amendment was invoked, these series of events were never tested. Albert again became first-in-line during the first four months of Ford's Presidency, before the confirmation of Vice President Nelson Rockefeller,[citation needed] which marked the second time Section 2 of the Twenty-fifth Amendment was invoked.
In 1981, when President Ronald Reagan was shot, Vice President George H. W. Bush was traveling in Texas. Secretary of State Alexander Haig responded to a reporter's question regarding who was running the government by stating:
Constitutionally, gentlemen, you have the President, the Vice President and the Secretary of State in that order, and should the President decide he wants to transfer the helm to the Vice President, he will do so. He has not done that. As of now, I am in control here, in the White House, pending return of the Vice President and in close touch with him. If something came up, I would check with him, of course.[19]
A bitter dispute ensued over the meaning of Haig's remarks. Most people believed that Haig was referring to the line of succession and erroneously claimed to have temporary Presidential authority, due to his implied reference to the Constitution. Haig and his supporters, noting his familiarity with the line of succession from his time as White House Chief of Staff during Richard Nixon's resignation, said he only meant that he was the highest-ranking officer of the Executive branch on-site, managing things temporarily until the Vice President returned to Washington.[citation needed]
Constitutional concerns[edit]
Several constitutional law experts have raised questions as to the constitutionality of the provisions that the Speaker of the House and the President pro tempore of the Senate succeed to the presidency.[20] James Madison, one of the authors of the Constitution, raised similar constitutional questions about the Presidential Succession Act of 1792 in a 1792 letter to Edmund Pendleton.[21] Two of these issues can be summarized:
The term "Officer" in the relevant clause of the Constitution is most plausibly interpreted to mean an "Officer of the United States", who must be a member of the Executive or Judicial Branch. The Speaker and the President pro tempore are not officers in this sense.
Under the principle of separation of powers, the Constitution specifically disallows legislative officials from also serving in the executive branch. For the Speaker or the Senate President pro tempore to become Acting President, they must resign their position, at which point they are no longer in the line of succession. This is seen by some to form a constitutional paradox. However, the current Act specifies that the Speaker becomes President "upon his resignation as Speaker" and as a member of Congress,[22] allowing for a seamless transition.
In 2003 the Continuity of Government Commission suggested that the current law has "at least seven significant issues ... that warrant attention", specifically:[23]
The reality that all figures in the current line of succession work and reside in the vicinity of Washington, D.C. In the event of a nuclear, chemical, or biological attack, it is possible that everyone on the list would be killed or incapacitated.
Doubt (such as those expressed above by James Madison) that congressional leaders are eligible to act as President.
A concern about the wisdom of including the President pro tempore in the line of succession as the "largely honorific post traditionally held by the longest-serving Senator of the majority party". For example, from January 20, 2001, to June 6, 2001, the President pro tempore was then-98-year-old Strom Thurmond of South Carolina.
A concern that the current line of succession can force the presidency to abruptly switch parties mid-term, as the President, Speaker, and the President pro tempore are not necessarily of the same party as each other.
A concern that the succession line is ordered by the dates of creation of the various executive departments, without regard to the skills or capacities of the persons serving as their Secretary.
The fact that, should a Cabinet member begin to act as President, the law allows the House to elect a new Speaker (or the Senate, a new President pro tempore), who could in effect remove the Cabinet member and assume the office themselves at any time.
The absence of a provision where a President is disabled and the vice presidency is vacant (for example, if an assassination attempt simultaneously wounded the President and killed the Vice President).
See also[edit]
Central Locator System
Designated survivor
List of United States presidential assassination attempts and plots
United States presidential line of succession in fiction
References[edit]
Jump up ^ 3 U.S.C. § 19
Jump up ^ "Is the Presidential Succession Law Constitutional?", Akhil Reed Amar, Stanford Law Review, November 1995.
Jump up ^ First Report p. 4, continuityofgovernment.org Retrieved December 28, 2010 via Internet Archive to repair dead link
Jump up ^ Wilson, Reid (October 20, 2013). "The Presidential order of succession". The Washington Post. ISSN 0190-8286. Retrieved November 10, 2015.
Jump up ^ "The Continuity of the Presidency," Continuity of Government Commission, June 2009, p. 34. (Archived by WebCite at [1] Accessed: 2012-05-23)
Jump up ^ "Special Message to the Congress on the Succession to the Presidency. June 19, 1945" by President Harry S. Truman; from the American Presidency Project archives
^ Jump up to: a b Wildavsky, Aaron B. (2003). Horowitz, Irving, ed. The revolt against the masses and other essays on politics and public policy (Google Books). Transaction Publishers. p. 122. ISBN 978-0-7658-0960-5. Retrieved July 24, 2009.
Jump up ^ "kipnotes.com - Nachrichten zum trading -". kipnotes.com - Nachrichten zum trading.
^ Jump up to: a b c Schlesinger, Arthur M., Jr. (Autumn 1974). "On the Presidential Succession". Political Science Quarterly. 89 (3): 475, 495–496. JSTOR 2148451.
^ Jump up to: a b c Rankin, Robert S. (Feb 1946). "Presidential Succession in the United States". The Journal of Politics. 8 (1): 44–56. JSTOR 2125607. doi:10.2307/2125607.
^ Jump up to: a b c d e Abbott, Philip (Dec 2005). "Accidental Presidents: Death, Assassination, Resignation, and Democratic Succession". Presidential Studies Quarterly. 35 (4): 627, 638. JSTOR 27552721. doi:10.1111/j.1741-5705.2005.00269.x.
Jump up ^ Crapol, Edward P. (2006). John Tyler: the accidental president. UNC Press Books. p. 10. ISBN 978-0-8078-3041-3. OCLC 469686610.
Jump up ^ Lewis, Charlton Thomas; Willsey, Joseph H. (1895). Harper's Book of Facts: a Classified History of the World; Embracing Science, Literature, and Art. New York: Harper & Brothers. p. 884. LCCN 01020386. Retrieved April 24, 2011.
Jump up ^ "U.S. Postmasters General". postalmuseum.si.edu. Retrieved November 10, 2015.
Jump up ^ US Congress (2005). USA PATRIOT Improvement and Reauthorization Act OF 2005. 109th Congress Public Law 177. Retrieved on October 29, 2015 from http://www.gpo.gov/fdsys/pkg/PLAW-109publ177/html/PLAW-109publ177.htm.
Jump up ^ "1801: President for a Day -- March 4, 1849". May 29, 2014.
Jump up ^ David Mikkelson (October 8, 2007). "President for a Day". snopes.
Jump up ^ Medved, Michael (1979). The Shadow Presidents: The Secret History of the Chief Executives and Their Top Aides. New York, U.S.A.: Times Books. p. 149. ISBN 0-8129-0816-3.
Jump up ^ "Alexander Haig", Time, April 2, 1984
Jump up ^ "Is the Presidential Succession Law Constitutional?", Akhil Reed Amar, Stanford Law Review, November 1995.
Jump up ^ "Article 2, Section 1, Clause 6: James Madison to Edmund Pendleton".
Jump up ^ Wikisource:Presidential Succession Act 1947
Jump up ^ First Report p. 4, continuityofgovernment.org Retrieved December 28, 2010 via Internet Archive to repair dead link
Further reading[edit]
Ask Gleaves: Presidential Succession from the website of Grand Valley State University
3 U.S.C. § 19 – "Vacancy in offices of both President and Vice President; officers eligible to act"
Presidential Succession Act of 1792, 1 Stat. 239 (from the American Memory website of the Library of Congress
"Presidential Line of Succession Examined", a September 20, 2003 article from the Milwaukee Journal Sentinel
"WI Presidential Succession Act of 1947 held unconstitutional", David Tenner, Usenet group: soc.history.what-if, January 14, 2003.
Fools, Drunkards, & Presidential Succession from the Federalist Society website
Testimony of M. Miller Baker from the U.S. Senate website
External links[edit]
The Presidency: Preserving Our Institutions Second report of the Continuity of Government Commission, June 2009 (includes the text of the Presidential Succession Acts of 1792, 1886 and 1947)
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Jump up ^ Never confirmed by and with the advice and consent of the Senate and thus ineligible for the presidential line of succession.
Jump up ^ Although Elaine Chao is the current Secretary of Transportation, she is not a natural-born citizen (acquired U.S. citizenship by naturalization) and thus ineligible for the Presidency.
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values: خط الخلافة الرئاسية في الولايات المتحدة – Arabic

values: Наследаванне прэзідэнцкіх паўнамоцтваў у ЗША – Belarusian

values: Поредност на заместниците на президента на САЩ – Bulgarian

values: Nástupnictví na úřad prezidenta Spojených států amerických – Czech

values: Nachfolge des Präsidenten der Vereinigten Staaten – German

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values: Ameerika Ühendriikide presidendijärjekord – Estonian

values: خط جانشینی ریاست جمهوری ایالات متحده آمریکا – Persian

values: Ordre de succession présidentielle des États-Unis – French

values: 미국 대통령 계승순위 – Korean

values: Linea di successione presidenziale negli Stati Uniti d'America – Italian

values: סדר הירושה של נשיא ארצות הברית – Hebrew

values: アメリカ合衆国大統領の継承順位 – Japanese

values: Linia sukcesji prezydenckiej (Stany Zjednoczone) – Polish

values: Linha de sucessão presidencial dos Estados Unidos – Portuguese

values: Actuala listă a liniei de succesiune prezidențiale SUA, 2006 – Romanian

values: Наследование президентских полномочий в США – Russian

values: U.S. Presidential line of succession – Simple English

values: Successionsordningen för USA:s president – Swedish

values: ลำดับการสืบทอดตำแหน่งประธานาธิบดีสหรัฐอเมริกา – Thai

values: Amerika Birleşik Devletleri başkanlık yerini alma sırası – Turkish

values: Лінія наступності президентських повноважень у США – Ukrainian

values: Thứ tự kế vị Tổng thống Hoa Kỳ – Vietnamese

values: 美國總統繼任順序 – Chinese

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