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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 the systemic and cellular level. Iron is both necessary to the body and potentially toxic, and controlling iron levels in the body is a critically 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
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,[citation needed] including calcium, phytates and tannins.[citation needed] Black tea steeped for long has high tannins.[citation needed]
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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Metabolism: Metal metabolism
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Help
Category:British reggae musical groups
From Wikipedia, the free encyclopedia
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Pages in category "British reggae musical groups"
The following 47 pages are in this category, out of 47 total. This list may not reflect recent changes (learn more).
A
Alpha & Omega (band)
Anweledig
Asher D and Daddy Freddy
Aswad (band)
B
Basque Dub Foundation
The Beat (British band)
Beshara (band)
Black Roots (band)
Black Slate
Black Star Liner
The Blackstones
The Brothers (band)
Brown Sugar (group)
The Bush Chemists
By the Rivers
C
China Black
The Cimarons
D
Dreadzone
Dub Syndicate
F
Faya (band)
G
Greyhound (band)
L
Latin Quarter (band)
Louchie Lou & Michie One
M
Mafia & Fluxy
The Marvels
Matumbi (band)
Misty in Roots
Mr Hudson and the Library
Mungo's Hi Fi
Musical Youth
N
New Age Steppers
P
Pama International
Poet and the Roots
R
Radical Dance Faction
Resonators (band)
The Ruts
S
Saxon Studio International
Singers & Players
The Skints
The Specials
Steel Pulse
Symarip
T
Tradition (band)
Twilight Circus Dub Sound System
U
UB40
V
Vibronics
Z
Zion Train
Retrieved from "https://en.wikipedia.org/w/index.php?title=Category:British_reggae_musical_groups&oldid=676859322"
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British musical groups by genre
Reggae musical groups by nationality
British reggae musicians
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Ijma
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Usul al-fiqh
Fiqh
Ijazah
Ijma
Ijtihad
Ikhtilaf
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Madhhab
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v
t
e
ʾIjmāʿ (Arabic: إجماع [ʔidʒmɑːʕ]) is an Arabic term referring to the consensus or agreement of the Muslim scholars basically on religious issues.[1]:472 Various schools of thought within Islamic jurisprudence may define this consensus to be that of the first generation of Muslims only; or the consensus of the first three generations of Muslims; or the consensus of the jurists and scholars of the Muslim world, or scholarly consensus; or the consensus of all the Muslim world, both scholars and laymen.
Contents
1 Usage
1.1 Sunni view
1.2 Shia view
1.3 Mu'tazilite view
2 See also
3 References
4 External links
Usage[edit]
Sunni view[edit]
The hadith of Muhammad which states that "My ummah will never agree upon an error"[2] is often cited as a proof for the validity of ijmā'. (While this hadith has only a limited number of transmissions bringing it to hadith collectors, and so is less reliable than would be preferred, Sunni scholars argue that they had come to a consensus that Muhammad had affirmed the Muslim communities infallibility so that the hadith was certain.)[3] Sunni Muslims regard ijmā' as the third fundamental source of Sharia law, just after the divine revelation of the Qur'an, and the prophetic practice known as Sunnah.
There are differing views over who is considered a part of this consensus, whether "the consensus is needed only among the scholars of a particular school, or legists, or legists of an early era, or the Companions, or scholars in general, or the entire Muslim community."[4][5] [6][7][8][9]
Malik ibn Anas held the view that the religiously binding consensus was only the consensus of Muhammad's companions and the direct successors of those companions in the city of Medina.[10]
According to Iraqi academic Majid Khadduri, Al-Shafi'i held the view that religiously binding consensus had to include all of the Muslim community in every part of the world, both the religiously learned and the layman.[11][12] Thus, if even one individual out of millions would hold a differing view, then consensus would not have been reached. In an attempt to define consensus in a form which was more likely to ever occur, Al-Ghazali expanding on al-Shafi'i's definition to define consensus as including all of the Muslim community in regard to religious principles and restricting the meaning to only the religiously learned in regard to finer details.[13]
Abu Hanifa, Ahmad bin Hanbal and Dawud al-Zahiri, on the other hand, considered this consensus to only include the companions of Muhammad, excluding all generations which followed them, in Medina and elsewhere.[14][15]
Views within Sunni Islam branched off even further in later generations, with Muhammad ibn Zakariya al-Razi defining even a simple majority view as constituting consensus and Ibn Taymiyyah restricting consensus to the view of the religiously learned only.[15] Muhammad ibn Jarir al-Tabari's position was not entirely clear, as modern scholarship has attributed to him both the view that consensus means a simple majority,[15] and that it means only the consensus of the companions of Muhammad.[16]
According to Ahmad Hasan, the majority view is split between two possibilities: that religiously binding consensus is the consensus of the entire Muslim community, or that religiously binding consensus is just the consensus of the religiously learned.[17] The names of two kinds of consensus are:
ijma al-ummah - a whole community consensus.
ijma al-aimmah - a consensus by religious authorities.[18]
Shia view[edit]
Initially, for Shia the authority of the Imams rendered the consensus as irrelevant. With the development of sectarian communities of Imami Shīa Islam, the question of guidance and interpretation between different ulamas became an issue, however the importance of ijmā never reached the level and certainty it had in Sunni Islam. Later, since Safavid and with the establishment of Usuli school at the turn the 19th century the authority of living mujtahid is accepted, however it dies with him. For Shia, the status of ijmā is ambiguous.[19]
Mu'tazilite view[edit]
The ancient Mu'tazilite sect did not consider consensus to be a valid source of law, primarily due to their rationalist criticism of the first generation of Muslims, whom the Mu'tazila viewed as possessing defective personalities and intellects.[20] Shi'ite theologians Al-Shaykh Al-Mufid and Sharif al-Murtaza held the Mu'tazilite theologian Nazzam's book Kitab al-Nakth, in which his student Al-Jahiz reports that he denied the validity of consensus for this reason, in high esteem.[21] Modern scholarship has suggested that this interest was motivated by the desire of Shi'ite theologians to impugn the character of the first three leaders of the Rashidun Caliphate, Abu Bakr, Umar and Uthman.[20]
See also[edit]
hidePart of a series on:
Islamism
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References[edit]
Jump up ^ Mohammad Taqi al-Modarresi (26 March 2016). The Laws of Islam (PDF). Enlight Press. ISBN 978-0994240989. Retrieved 23 December 2017.
Jump up ^ Narrated by al-Tirmidhi (4:2167), ibn Majah (2:1303), Abu Dawood, and others with slightly different wordings.
Jump up ^ Brown, Jonathan A.C. (2014). Misquoting Muhammad: The Challenge and Choices of Interpreting the Prophet's Legacy. Oneworld Publications. p. 56. ISBN 978-1780744209. Retrieved 4 June 2018.
Jump up ^ Forte, David F. (1978). "Islamic Law; the impact of Joseph Schacht" (PDF). Los Angeles International and Comparative Law Review. 1: 7. Retrieved 19 April 2018.
Jump up ^ See F. Ziadeh, Lawyers and the rule of law, and liberalism in modern Egypt 146-47 (1968) supra note 4, at 118
Jump up ^ see generally: K. Faruki, ISLAMIC JURISPRUDENCE 68 (1962)
Jump up ^ D. Mullah & M. Hidadjatullah, Principles of Mahomedan Law xxii (16th ed. 1968)
Jump up ^ Aqil Ahmad, A Text Book of Mohammadan Law 15 (4th rev. ed. 1966), supra note 22, at 17
Jump up ^ Aziz Ahmad, Islamic Law in Theory and Practice 2 (1956), Supra note 20, at 43
Jump up ^ Muhammad Muslehuddin, "Philosophy of Islamic Law and Orientalists," Kazi Publications, 1985, p. 146
Jump up ^ Majid Khadduri, Introduction to Al-Shafi'i's al-Risala, pg.33
Jump up ^ Mansoor Moaddel, Islamic Modernism, Nationalism, and Fundamentalism: Episode and Discourse, pg. 32. Chicago: University of Chicago Press, 2005.
Jump up ^ Majid Khadduri, Introduction to Al-Shafi'i's al-Risala, pg.38-39
Jump up ^ Muhammad Muslehuddin, "Philosophy of Islamic Law and Orientalists," Kazi Publications, 1985, p. 81
^ Jump up to: a b c Dr. Mohammad Omar Farooq, "The Doctrine of Ijma: Is there a consensus?," June 2006
Jump up ^ Devin J. Stewart, "Muhammad b. Jarir al-Tabari's al-Bayan 'an Usul al-Ahkam and the Genre of Usul al-Fiqh in Ninth Century Baghdad," pg. 339. Taken from Abbasid Studies: Occasional Papers of the School of Abbasid Studies, Cambridge, 6–10 January 2002. Edited by James Montgomery. Leuven: Peeters Publishers and the Department of Oriental Studies, 2004.
Jump up ^ Ahmad Hasan, "The Doctrine of Ijma': A Study of the Juridical Principle of Consensus," New Delhi, India: Kitab Bhaban, 2003, pg.81
Jump up ^ Corinna Standke (30 August 2008). Sharia - The Islamic Law. GRIN Verlag. pp. 4–5. ISBN 978-3-640-14967-4. Retrieved 9 June 2012.
Jump up ^ Sami Zubaida (8 July 2005). Law And Power In The Islamic World. I.B.Tauris. p. 14. ISBN 978-1-85043-934-9. Retrieved 9 June 2012.
^ Jump up to: a b Devin Stewart, "Muhammad b. Dawud al-Zahiri's Manual of Jurisprudence." Taken from Studies in Islamic Law and Society Volume 15: Studies in Islamic Legal Theory. Edited by Bernard G. Weiss. Pg. 107. Leiden: 2002. Brill Publishers.
Jump up ^ Josef van Ess, Das Kitab al-nakt des Nazzam und seine Rezeption im Kitab al-Futya des Gahiz. Gottingen: Vandenhoeck & Reprecht, 1971.
External links[edit]
The Doctrine of Ijma': Is there a consensus? by Dr. Mohammad Omar Farooq
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Framingham Risk Score
From Wikipedia, the free encyclopedia
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The Framingham Risk Score is a gender-specific algorithm used to estimate the 10-year cardiovascular risk of an individual. The Framingham Risk Score was first developed based on data obtained from the Framingham Heart Study, to estimate the 10-year risk of developing coronary heart disease.[1] In order to assess the 10-year cardiovascular disease risk, cerebrovascular events, peripheral artery disease and heart failure were subsequently added as disease outcomes for the 2008 Framingham Risk Score, on top of coronary heart disease.[2]
Contents
[hide]
1 Cardiovascular Risk Scoring systems
2 Usefulness
3 Issues Raised by Cardiovascular Risk Prediction
4 Background
5 Validation
6 Limitations
7 Versions
7.1 Differences between the versions
8 CHD Risk Equivalent
9 Analysis of the US population with the Framingham/ATP III criteria
10 Scoring
10.1 Framingham Risk Score for Women
10.2 Framingham Risk Score for Men
11 Further risk score profiles based on the Framingham Heart Study
12 See also
13 References
Cardiovascular Risk Scoring systems[edit]
The Framingham Risk Score is one of a number of scoring systems used to determine an individual's chances of developing cardiovascular disease. A number of these scoring systems are available online.[3][4] Cardiovascular risk scoring systems give an estimate of the probability that a person will develop cardiovascular disease within a specified amount of time, usually 10 to 30 years.[5] Because they give an indication of the risk of developing cardiovascular disease, they also indicate who is most likely to benefit from prevention. For this reason, cardiovascular risk scores are used to determine who should be offered preventive drugs such as drugs to lower blood pressure and drugs to lower cholesterol levels. For example, nearly 30% of coronary heart disease (CHD) events in both men and women were singularly attributable to blood pressure levels that exceeded high normal (≥130/85), showing that blood pressure management and monitoring is paramount both to cardiovascular health and prediction of outcomes.[6]
Usefulness[edit]
Because risk scores such as the Framingham Risk Score give an indication of the likely benefits of prevention, they are useful for both the individual patient and for the clinician in helping decide whether lifestyle modification and preventive medical treatment, and for patient education, by identifying men and women at increased risk for future cardiovascular events.[7] Coronary heart disease (CHD) risk at 10 years in percent can be calculated with the help of the Framingham Risk Score. Individuals with low risk have 10% or less CHD risk at 10 years, with intermediate risk 10-20%, and with high risk 20% or more. However it should be remembered that these categorisations are arbitrary.
A more useful metric is to consider the effects of treatment. If a group of 100 persons all have a 20% ten-year risk of cardiovascular disease it means that we should expect that 20 of these 100 individuals will develop cardiovascular disease (coronary heart disease or stroke) in the next 10 years and eighty of them will not develop cardiovascular disease in the next 10 years. If they were to take a combination of treatments (for example drugs to lower cholesterol levels plus drugs to lower blood pressure) that reduced their risk of cardiovascular disease by half it means that 10 of these 100 individuals should be expected to develop cardiovascular disease in the next 10 years and 90 of them should not be expected to develop cardiovascular disease. If that was the case then 10 of these individuals would have avoided cardiovascular disease by taking treatment for 10 years; 10 would get cardiovascular disease whether or not they took treatment; and 80 would not have got cardiovascular disease whether or not they took treatment.
Despite their widespread popularity, randomised trials assessing the impact of using cardiovascular disease risk scores show limited impact on patient outcomes. Although there is good evidence that targeting individuals with high total CVD risk is the most efficient way to reduce CVD-related morbidity and mortality, to date trials assessing the usefulness of risk scores at helping clinicians target high risk patients show limited benefit.[8]
Issues Raised by Cardiovascular Risk Prediction[edit]
It is important to recognize that the strongest predictor of cardiovascular risk in any risk equation is age. Almost all persons aged 70 and over are at >20% ten year cardiovascular risk and almost nobody aged under 40 is at >20% ten year cardiovascular risk. Since those who benefit most from treatment are those at highest risk, this means that treatment of patients with raised blood pressure and raised cholesterol levels in their thirties benefits very few. Whereas treatment of patients with "normal" blood pressure and "normal" cholesterol levels in their seventies benefits many. This casts doubt on the wisdom of categorizing individuals as having high blood pressure or raised cholesterol and treating these individual risk factors without a consideration of both their overall risk of cardiovascular disease and of the probability that they will benefit.
Background[edit]
Cardiovascular disease is common in the general population, affecting the majority of adults. It includes: 1) Coronary heart disease (CHD): Myocardial infarction (MI), angina pectoris, heart failure (HF), and coronary death. 2) Cerebrovascular disease, stroke and transient ischemic attack (TIA). 3) Peripheral arterial disease, intermittent claudication and significant limb ischemia. 4) Aortic disease: Aortic atherosclerosis, thoracic aortic aneurysm, and abdominal aortic aneurysm.
An individual’s risk for future cardiovascular events is modifiable, by lifestyle changes and preventive medical treatment. Lifestyle changes can include stopping smoking, healthy diet, regular exercise, etc. Preventive medical treatment can include a statin, mini dose aspirin, treatment for hypertension, etc. It is important to be able to predict the risk of an individual patient, in order to decide when to initiate lifestyle modification and preventive medical treatment.
Multiple risk models for the prediction of cardiovascular risk of individual patients have been developed. One such key risk model is the Framingham Risk Score.
The Framingham Risk Score is based on findings from the Framingham Heart Study.
Validation[edit]
The Framingham Risk Score has been validated in the USA, both in men and women, both in European Americans and African Americans.[9] While several studies have claimed to improve on the FRS, there is little evidence for any improved prediction beyond the Framingham risk score [10]
Limitations[edit]
There are two limitations.
The Framingham Risk Score predicts only future coronary heart disease (CHD) events, however, it does not predict future total cardiovascular events, meaning that it does not predict risk for stroke, transient ischemic attack (TIA), and heart failure. These also important patient outcomes were included in the 2008 Framingham General Cardiovascular Risk Score.[11] The predicted risk for an individual usually is higher with the 2008 Framingham General Cardiovascular Risk Score than with the 2002 Framingham Risk Score.
The Framingham Risk Score could overestimate (or underestimate) risk in populations other than the US population,[12][13] and within the USA in populations other than European Americans and African Americans, e.g. Hispanic Americans and Native Americans.[14] It is not yet clear if this limitation is real, or appears to be real because of differences in methodology, etc. As a result, other countries may prefer to use another risk score, e.g. SCORE (HeartScore is the interactive version of SCORE - Systematic COronary Risk Evaluation),[15] which has been recommended by the European Society of Cardiology in 2007.[16]
If possible, a cardiology professional should select the risk prediction model which is most appropriate for an individual patient and should remember that this is only an estimate.
Versions[edit]
The current version of the Framingham Risk Score was published in 2008. The publishing body is the ATP III, i.e. the «Adult Treatment Panel III», an expert panel of the National Heart, Lung, and Blood Institute, which is part of the National Institutes of Health (NIH), USA.
The prior version was published in 2002 [17]
The original Framingham Risk Score had been published in 1998.[18]
Differences between the versions[edit]
The first Framingham Risk Score included age, sex, LDL cholesterol, HDL cholesterol, blood pressure (and also whether the patient is treated or not for his/her hypertension), diabetes, and smoking. It estimated the 10-year risk for coronary heart disease (CHD). It performed well, and correctly predicted 10-year risk for CHD in American men and women of European and African descent.
The updated version was modified to include dyslipidemia, age range, hypertension treatment, smoking, and total cholesterol, and it excluded diabetes, because Type 2 diabetes meanwhile was considered to be a CHD Risk Equivalent, having the same 10-year risk as individuals with prior CHD. Patients with Type 1 diabetes were considered separately with slightly less aggressive goals; while at increased risk, no study had shown them to be at equivalent risk for CHD as those with previously diagnosed coronary disease or Type 2 diabetes.[17]
CHD Risk Equivalent[edit]
Some patients without known CHD have risk of cardiovascular events that is comparable to that of patients with established CHD. Cardiology professionals refer to such patients as having a CHD risk equivalent. These patients should be managed as patients with known CHD.
CHD risk equivalents are patients with a 10-year risk for MI or coronary death >20%. CHD risk equivalents are primarily other clinical forms of atherosclerotic disease. The National Cholesterol Education Program NCEP's ATP III guidelines also list diabetes as a CHD risk equivalent since it also has a 10-year risk for CHD around 20%. NCEP ATP III CHD risk equivalents are:
clinical coronary heart disease (CHD)
symptomatic carotid artery disease (CAD)
peripheral arterial disease (PAD)
abdominal aortic aneurysm (AAA)
diabetes mellitus
Chronic Kidney Disease
Analysis of the US population with the Framingham/ATP III criteria[edit]
The Framingham/ATP III criteria were used to estimate CHD risk in the USA. Data from 11,611 patients from a very large study, the NHANES III, were used. The patients were 20 to 79 years of age, and had no self reported CHD, stroke, peripheral arterial disease, or diabetes.
The results: 82% of patients had low risk (10% or less CHD risk at 10 years). 16% had intermediate risk (10-20%). 3% had high risk (20% or more).[19]
High risk was most commonly found in patients with advanced age, and was more common in men than women. High risk patients are sometimes become unknown with certain signs and symptoms of cardiac failure
Scoring[edit]
Framingham Risk Score for Women[edit]
Age: 20–34 years: Minus 7 points. 35–39 years: Minus 3 points. 40–44 years: 0 points. 45–49 years: 3 points. 50–54 years: 6 points. 55–59 years: 8 points. 60–64 years: 10 points. 65–69 years: 12 points. 70–74 years: 14 points. 75–79 years: 16 points.
Total cholesterol, mg/dL: Age 20–39 years: Under 160: 0 points. 160-199: 4 points. 200-239: 8 points. 240-279: 11 points. 280 or higher: 13 points. • Age 40–49 years: Under 160: 0 points. 160-199: 3 points. 200-239: 6 points. 240-279: 8 points. 280 or higher: 10 points. • Age 50–59 years: Under 160: 0 points. 160-199: 2 points. 200-239: 4 points. 240-279: 5 points. 280 or higher: 7 points. • Age 60–69 years: Under 160: 0 points. 160-199: 1 point. 200-239: 2 points. 240-279: 3 points. 280 or higher: 4 points. • Age 70–79 years: Under 160: 0 points. 160-199: 1 point. 200-239: 1 point. 240-279: 2 points. 280 or higher: 2 points.
If cigarette smoker: Age 20–39 years: 9 points. • Age 40–49 years: 7 points. • Age 50–59 years: 4 points. • Age 60–69 years: 2 points. • Age 70–79 years: 1 point.
All non smokers: 0 points.
HDL cholesterol, mg/dL: 60 or higher: Minus 1 point. 50-59: 0 points. 40-49: 1 point. Under 40: 2 points.
Systolic blood pressure, mm Hg: Untreated: Under 120: 0 points. 120-129: 1 point. 130-139: 2 points. 140-159: 3 points. 160 or higher: 4 points. • Treated: Under 120: 0 points. 120-129: 3 points. 130-139: 4 points. 140-159: 5 points. 160 or higher: 6 points.
10-year risk in %: Points total: Under 9 points: <1%. 9-12 points: 1%. 13-14 points: 2%. 15 points: 3%. 16 points: 4%. 17 points: 5%. 18 points: 6%. 19 points: 8%. 20 points: 11%. 21=14%, 22=17%, 23=22%, 24=27%, >25= Over 30%
Framingham Risk Score for Men[edit]
Age: 20–34 years: Minus 9 points. 35–39 years: Minus 4 points. 40–44 years: 0 points. 45–49 years: 3 points. 50–54 years: 6 points. 55–59 years: 8 points. 60–64 years: 10 points. 65–69 years: 11 points. 70–74 years: 12 points. 75–79 years: 13 points.
Total cholesterol, mg/dL: Age 20–39 years: Under 160: 0 points. 160-199: 4 points. 200-239: 7 points. 240-279: 9 points. 280 or higher: 11 points. • Age 40–49 years: Under 160: 0 points. 160-199: 3 points. 200-239: 5 points. 240-279: 6 points. 280 or higher: 8 points. • Age 50–59 years: Under 160: 0 points. 160-199: 2 points. 200-239: 3 points. 240-279: 4 points. 280 or higher: 5 points. • Age 60–69 years: Under 160: 0 points. 160-199: 1 point. 200-239: 1 point. 240-279: 2 points. 280 or higher: 3 points. • Age 70–79 years: Under 160: 0 points. 160-199: 0 points. 200-239: 0 points. 240-279: 1 point. 280 or higher: 1 point.
If cigarette smoker: Age 20–39 years: 8 points. • Age 40–49 years: 5 points. • Age 50–59 years: 3 points. • Age 60–69 years: 1 point. • Age 70–79 years: 1 point.
All non smokers: 0 points.
HDL cholesterol, mg/dL: 60 or higher: Minus 1 point. 50-59: 0 points. 40-49: 1 point. Under 40: 2 points.
Systolic blood pressure, mm Hg: Untreated: Under 120: 0 points. 120-129: 0 points. 130-139: 1 point. 140-159: 1 point. 160 or higher: 2 points. • Treated: Under 120: 0 points. 120-129: 1 point. 130-139: 2 points. 140-159: 2 points. 160 or higher: 3 points.
10-year risk in %: Points total: 0 point: <1%. 1-4 points: 1%. 5-6 points: 2%. 7 points: 3%. 8 points: 4%. 9 points: 5%. 10 points: 6%. 11 points: 8%. 12 points: 10%. 13 points: 12%. 14 points: 16%. 15 points: 20%. 16 points: 25%. 17 points or more: Over 30%.[20]
Further risk score profiles based on the Framingham Heart Study[edit]
Not only coronary heart disease (CHD) events, but also further risks can be predicted. Risk prediction models for cardiovascular disease outcomes other than CHD events have also been developed by the Framingham Heart Study researchers. Amongst others, a risk score for 10-year risk for atrial fibrillation has been developed.[21][22]
A calculator for 10-year risk for atrial fibrillation is available on the Framingham Heart Study website: http://www.framinghamheartstudy.org/risk-functions/atrial-fibrillation/10-year-risk.php#
See also[edit]
QRISK
Coronary artery disease
Framingham Risk Score Calculator for Coronary Heart Disease - Cholesterol in mg/dL
Framingham Coronary Heart Disease Risk Score - Cholesterol in mg/dL or mmol/L
EuroHeart Project
References[edit]
Jump up ^ P.W., Wilson; D'Agostino, R.B.; Levy, D.; Belanger, A.M.; Silbershatz, H.; Kannel, W.B. (12 May 1998). "Prediction of coronary heart disease using risk factor categories.". Circulation. 97 (18): 1837–1847. PMID 9603539. doi:10.1161/01.CIR.97.18.1837. Retrieved 7 May 2013.
Jump up ^ D'Agostino, R.B.; Vasan, R.S.; Pencina, M.J.; Wolf, P.A.; Cobain, M.; Massaro, J.M.; Kannel, W.B. (22 January 2008). "General cardiovascular risk profile for use in primary care: the Framingham Heart Study". Circulation. 117 (6): 743–753. doi:10.1161/circulationaha.107.699579.
Jump up ^ Collins, Dylan; Lee, Joseph; Bobrovitz, Niklas; Koshiaris, Constantinos; Ward, Alison; Heneghan, Carl (2016-10-14). "Simple and adaptable R implementation of WHO/ISH cardiovascular risk charts for all epidemiological subregions of the world". F1000Research. 5. doi:10.12688/f1000research.9742.1.
Jump up ^ "Cardiovascular Risk Calculator and Chart v3.0". Cvrisk.mvm.ed.ac.uk. 2010-05-19. Retrieved 2013-09-14.
Jump up ^ "Risk Scoring Systems". Framingham Heart Study. Retrieved 7 May 2013.
Jump up ^ Wilson, PW; D'Agostino, RB; Levy, D; Belanger, AM; Silbershatz, H; Kannel, WB (1998). "Prediction of coronary heart disease using risk factor categories.". Circulation. 97 (18): 1837–47. PMID 9603539. doi:10.1161/01.cir.97.18.1837.
Jump up ^ Estimation of cardiovascular risk in an individual patient without known cardiovascular disease. Wilson PWF. In: UpToDate [Textbook of Medicine]. Basow, DS (Ed). Massachusetts Medical Society, and Wolters Kluwer publishers, The Netherlands. 2010.
Jump up ^ Collins, Dylan Raymond James; Tompson, Alice; Onakpoya, Igho; Roberts, Nia; Ward, Alison; Heneghan, Carl (2017). "Global cardiovascular risk assessment in the primary prevention of cardiovascular disease in adults: systematic review of systematic reviews". BMJ Open. PMID 28341688. doi:10.1136/bmjopen-2016-013650.
Jump up ^ Validation of the Framingham coronary heart disease prediction scores: results of a multiple ethnic groups investigation. D'Agostino RB Sr, Grundy S, Sullivan LM, Wilson P. JAMA. 2001 Jul 11;286(2):180-7.
Jump up ^ Tzoulaki, I.; Liberopoulos, G.; Ioannidis, JP. (Dec 2009). "Assessment of claims of improved prediction beyond the Framingham risk score.". JAMA. 302 (21): 2345–52. PMID 19952321. doi:10.1001/jama.2009.1757.
Jump up ^ D'Agostino RB Sr; Vasan RS; Pencina MJ; Wolf PA; Cobain M; Massaro JM; Kannel WB (Feb 2008). "General cardiovascular risk profile for use in primary care: the Framingham Heart Study". Circulation. 117 (6): 743–53. doi:10.1161/circulationaha.107.699579.
Jump up ^ Brindle P, Emberson J, Lampe F, Walker M, Whincup P, Fahey T, Ebrahim S (Nov 2003). "Predictive accuracy of the Framingham coronary risk score in British men: prospective cohort study". BMJ. 327 (7426): 1267. PMC 286248  . PMID 14644971. doi:10.1136/bmj.327.7426.1267.
Jump up ^ Liu J; Hong Y; D'Agostino RB Sr; Wu Z; Wang W; Sun J; Wilson PW; Kannel WB; Zhao D (Jun 2004). "Predictive value for the Chinese population of the Framingham CHD risk assessment tool compared with the Chinese Multi-Provincial Cohort Study". JAMA. 291 (21): 2591–9. doi:10.1001/jama.291.21.2591.
Jump up ^ Sacco RL, Khatri M, Rundek T, Xu Q, Gardener H, Boden-Albala B, Di Tullio MR, Homma S, Elkind MS, Paik MC (Dec 2009). "Improving global vascular risk prediction with behavioral and anthropometric factors. The multiethnic NOMAS (Northern Manhattan Cohort Study)". J Am Coll Cardiol. 54 (24): 2303–11. doi:10.1016/j.jacc.2009.07.047.
Jump up ^ Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project European Heart Journal 2003;24:987-1003
Jump up ^ Conroy RM, Pyorala K, Fitzgerald AP, Sans S, Menotti A, De Backer G, De Bacquer D, Ducimetiere P, Jousilahti P, Keil U, Njolstad I, Oganov RG, Thomsen T, Tunstall-Pedoe H, Tverdal A, Wedel H, Whincup P, Wilhelmsen L, Graham IM (Jun 2003). "Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project". Eur Heart J. 24 (11): 987–1003. doi:10.1016/s0195-668x(03)00114-3.
^ Jump up to: a b Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002 Dec 17;106(25):3143-421.
Jump up ^ Prediction of coronary heart disease using risk factor categories. Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Circulation. 1998 May 12;97(18):1837-47.
Jump up ^ The distribution of 10-Year risk for coronary heart disease among US adults: findings from the National Health and Nutrition Examination Survey III. Ford ES, Giles WH, Mokdad AH. J Am Coll Cardiol. 2004 May 19;43(10):1791-6.
Jump up ^ "NHLBI, Estimate of 10-Year Risk for CHD". Nhlbi.nih.gov. Retrieved 2013-09-14.
Jump up ^ Development of a risk score for atrial fibrillation (Framingham Heart Study): a community-based cohort study. Schnabel RB, Sullivan LM, Levy D, Pencina MJ, Massaro JM, D'Agostino RB Sr, Newton-Cheh C, Yamamoto JF, Magnani JW, Tadros TM, Kannel WB, Wang TJ, Ellinor PT, Wolf PA, Vasan RS, Benjamin EJ. Lancet. 2009 Feb 28;373(9665):739-45.
Jump up ^ Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Lloyd-Jones DM, Wang TJ, Leip EP, Larson MG, Levy D, Vasan RS, D'Agostino RB, Massaro JM, Beiser A, Wolf PA, Benjamin EJ. Circulation. 2004 Aug 31;110(9):1042-6.
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