The Organization of the Petroleum Exporting Countries (OPEC, /ˈoʊpɛk/ OH-pek) is an intergovernmental organisation of 14 nations, founded in 1960 in Baghdad by the first five members (Iran, Iraq, Kuwait, Saudi Arabia, and Venezuela), and headquartered since 1965 in Vienna, Austria. As of September 2018, the then 15 member countries accounted for an estimated 44 percent of global oil production and 81.5 percent of the world's "proven" oil reserves, giving OPEC a major influence on global oil prices that were previously determined by the so called "Seven Sisters” grouping of multinational oil companies.
The stated mission of the organisation is to "coordinate and unify the petroleum policies of its member countries and ensure the stabilization of oil markets, in order to secure an efficient, economic and regular supply of petroleum to consumers, a steady income to producers, and a fair return on capital for those investing in the petroleum industry."[4] The organization is also a significant provider of information about the international oil market. The current OPEC members are the following: Algeria, Angola, Ecuador, Equatorial Guinea, Gabon, Iran, Iraq, Kuwait, Libya, Nigeria, the Republic of the Congo, Saudi Arabia (the de facto leader), United Arab Emirates, and Venezuela. Indonesia and Qatar are former members.
The formation of OPEC marked a turning point toward national sovereignty over natural resources, and OPEC decisions have come to play a prominent role in the global oil market and international relations. The effect can be particularly strong when wars or civil disorders lead to extended interruptions in supply. In the 1970s, restrictions in oil production led to a dramatic rise in oil prices and in the revenue and wealth of OPEC, with long-lasting and far-reaching consequences for the global economy. In the 1980s, OPEC began setting production targets for its member nations; generally, when the targets are reduced, oil prices increase. This has occurred most recently from the organization's 2008 and 2016 decisions to trim oversupply.
Economists often cite OPEC as a textbook example of a cartel that cooperates to reduce market competition, but one whose consultations are protected by the doctrine of state immunity under international law. In December 2014, "OPEC and the oil men" ranked as #3 on Lloyd's list of "the top 100 most influential people in the shipping industry".[5] However, the influence of OPEC on international trade is periodically challenged by the expansion of non-OPEC energy sources, and by the recurring temptation for individual OPEC countries to exceed production targets and pursue conflicting self-interests.
Membership

Current member countries
As of January 2019, OPEC has 14 member countries: five in the Middle East (Western Asia), seven in Africa, and two in South America. According to the U.S. Energy Information Administration (EIA), OPEC's combined rate of oil production (including gas condensate) represented 44 percent of the world's total in 2016,[6] and OPEC accounted for 81.5 percent of the world's "proven" oil reserves.
Approval of a new member country requires agreement by three-quarters of OPEC's existing members, including all five of the founders.[7] In October 2015, Sudan formally submitted an application to join,[8] but it is not yet a member.
Qatar left OPEC on 1 January 2019, after joining the organization in 1961, to focus on natural gas production, of which it is the world's largest exporter in the form of liquified natural gas (LNG).[9][10]

Lapsed members

For countries that export petroleum at relatively low volume, their limited negotiating power as OPEC members would not necessarily justify the burdens imposed by OPEC production quotas and membership costs. Ecuador withdrew from OPEC in December 1992, because it was unwilling to pay the annual US$2million membership fee and felt that it needed to produce more oil than it was allowed under its OPEC quota at the time,[16] although it rejoined in October 2007. Similar concerns prompted Gabon to suspend membership in January 1995;[17] it rejoined in July 2016. In May 2008, Indonesia announced that it would leave OPEC when its membership expired at the end of that year, having become a net importer of oil and being unable to meet its production quota.[18] It rejoined the organization in January 2016,[2] but announced another "temporary suspension" of its membership at year-end when OPEC requested a 5 percent production cut.[19]
Some commentators consider that the United States was a de facto member of OPEC during its formal occupation of Iraq, due to its leadership of the Coalition Provisional Authority in 2003–2004.[20][21] But this is not borne out by the minutes of OPEC meetings, as no US representative attended in an official capacity.[22][23]
Observers
Since the 1980s, representatives from Egypt, Mexico, Norway, Oman, Russia, and other oil-exporting nations have attended many OPEC meetings as observers. This arrangement serves as an informal mechanism for coordinating policies.[24]
Leadership and decision-making

The OPEC Conference is the supreme authority of the organization, and consists of delegations normally headed by the oil ministers of member countries. The chief executive of the organization is the OPEC Secretary General. The Conference ordinarily meets at the Vienna headquarters, at least twice a year and in additional extraordinary sessions when necessary. It generally operates on the principles of unanimity and "one member, one vote", with each country paying an equal membership fee into the annual budget.[7] However, since Saudi Arabia is by far the largest and most-profitable oil exporter in the world, with enough capacity to function as the traditional swing producer to balance the global market, it serves as "OPEC's de facto leader".[25]
International cartel
At various times, OPEC members have displayed apparent anti-competitive cartel behavior through the organization's agreements about oil production and price levels.[26] In fact, economists often cite OPEC as a textbook example of a cartel that cooperates to reduce market competition, as in this definition from OECD's Glossary of Industrial Organisation Economics and Competition Law:[1]
International commodity agreements covering products such as coffee, sugar, tin and more recently oil (OPEC: Organization of Petroleum Exporting Countries) are examples of international cartels which have publicly entailed agreements between different national governments.
OPEC members strongly prefer to describe their organization as a modest force for market stabilization, rather than a powerful anti-competitive cartel. In its defense, the organization was founded as a counterweight against the previous "Seven Sisters" cartel of multinational oil companies, and non-OPEC energy suppliers have maintained enough market share for a substantial degree of worldwide competition.[27] Moreover, because of an economic "prisoner's dilemma" that encourages each member nation individually to discount its price and exceed its production quota,[28] widespread cheating within OPEC often erodes its ability to influence global oil prices through collective action.[29][30]
OPEC has not been involved in any disputes related to the competition rules of the World Trade Organization, even though the objectives, actions, and principles of the two organizations diverge considerably.[31] A key US District Court decision held that OPEC consultations are protected as "governmental" acts of state by the Foreign Sovereign Immunities Act, and are therefore beyond the legal reach of US competition law governing "commercial" acts.[32][33] Despite popular sentiment against OPEC, legislative proposals to limit the organization's sovereign immunity, such as the NOPEC Act, have so far been unsuccessful.[34]
Conflicts
OPEC often has difficulty agreeing on policy decisions because its member countries differ widely in their oil export capacities, production costs, reserves, geological features, population, economic development, budgetary situations, and political circumstances.[35][36] Indeed, over the course of market cycles, oil reserves can themselves become a source of serious conflict, instability and imbalances, in what economists call the "natural resource curse".[37][38] A further complication is that religion-linked conflicts in the Middle East are recurring features of the geopolitical landscape for this oil-rich region.[39][40] Internationally important conflicts in OPEC's history have included the Six-Day War (1967), Yom Kippur War (1973), a hostage siege directed by Palestinian militants (1975), the Iranian Revolution (1979), Iran–Iraq War (1980–1988), Iraqi occupation of Kuwait (1990–1991), September 11 attacks by mostly Saudi hijackers (2001), American occupation of Iraq (2003–2011), Conflict in the Niger Delta (2004–present), Arab Spring (2010–2012), Libyan Crisis (2011–present), and international Embargo against Iran (2012–2016). Although events such as these can temporarily disrupt oil supplies and elevate prices, the frequent disputes and instabilities tend to limit OPEC's long-term cohesion and effectiveness.[41]
Market information
As one area in which OPEC members have been able to cooperate productively over the decades, the organization has significantly improved the quality and quantity of information available about the international oil market. This is especially helpful for a natural-resource industry whose smooth functioning requires months and years of careful planning.
Publications and research

In April 2001, OPEC collaborated with five other international organizations (APEC, Eurostat, IEA, OLADE, UNSD) to improve the availability and reliability of oil data. They launched the Joint Oil Data Exercise, which in 2005 was joined by IEF and renamed the Joint Organisations Data Initiative (JODI), covering more than 90 percent of the global oil market. GECF joined as an eighth partner in 2014, enabling JODI also to cover nearly 90 percent of the global market for natural gas.[42]
Since 2007, OPEC has published the "World Oil Outlook" (WOO) annually, in which it presents a comprehensive analysis of the global oil industry including medium- and long-term projections for supply and demand.[43] OPEC also produces an "Annual Statistical Bulletin" (ASB),[44] and publishes more-frequent updates in its "Monthly Oil Market Report" (MOMR)[45] and "OPEC Bulletin".[46]
Crude oil benchmarks

A "crude oil benchmark" is a standardized petroleum product that serves as a convenient reference price for buyers and sellers of crude oil, including standardized contracts in major futures markets since 1983. Benchmarks are used because oil prices differ (usually by a few dollars per barrel) based on variety, grade, delivery date and location, and other legal requirements.[47][48]
The OPEC Reference Basket of Crudes has been an important benchmark for oil prices since 2000. It is calculated as a weighted average of prices for petroleum blends from the OPEC member countries: Saharan Blend (Algeria), Girassol (Angola), Oriente (Ecuador), Rabi Light (Gabon), Iran Heavy (Islamic Republic of Iran), Basra Light (Iraq), Kuwait Export (Kuwait), Es Sider (Libya), Bonny Light (Nigeria), Qatar Marine (Qatar), Arab Light (Saudi Arabia), Murban (UAE), and Merey (Venezuela).[49]
North Sea Brent Crude Oil is the leading benchmark for Atlantic basin crude oils, and is used to price approximately two-thirds of the world's traded crude oil. Other well-known benchmarks are West Texas Intermediate (WTI), Dubai Crude, Oman Crude, and Urals oil.[50]
Spare capacity
The US Energy Information Administration, the statistical arm of the US Department of Energy, defines spare capacity for crude oil market management "as the volume of production that can be brought on within 30 days and sustained for at least 90 days... OPEC spare capacity provides an indicator of the world oil market's ability to respond to potential crises that reduce oil supplies."[51]
In November 2014, the International Energy Agency (IEA) estimated that OPEC's "effective" spare capacity, adjusted for ongoing disruptions in countries like Libya and Nigeria, was 3.5 million barrels per day (560,000m3/d) and that this number would increase to a peak in 2017 of 4.6 million barrels per day (730,000m3/d).[52] By November 2015, the IEA changed its assessment "with OPEC's spare production buffer stretched thin, as Saudi Arabia – which holds the lion's share of excess capacity – and its [Persian] Gulf neighbours pump at near-record rates."[53]
History and impact
Post-WWII situation
In 1949, Venezuela and Iran took the earliest steps in the direction of OPEC, by inviting Iraq, Kuwait and Saudi Arabia to improve communication among petroleum-exporting nations as the world recovered from World War II.[54] At the time, some of the world's largest oil fields were just entering production in the Middle East. The United States had established the Interstate Oil Compact Commission to join the Texas Railroad Commission in limiting overproduction. The US was simultaneously the world's largest producer and consumer of oil; and the world market was dominated by a group of multinational companies known as the "Seven Sisters", five of which were headquartered in the US following the breakup of John D. Rockefeller's original Standard Oil monopoly. Oil-exporting countries were eventually motivated to form OPEC as a counterweight to this concentration of political and economic power.[55]
1959–1960 anger from exporting countries
In February 1959, as new supplies were becoming available, the multinational oil companies (MOCs) unilaterally reduced their posted prices for Venezuelan and Middle Eastern crude oil by 10 percent. Weeks later, the Arab League's first Arab Petroleum Congress convened in Cairo, Egypt, where the influential journalist Wanda Jablonski introduced Saudi Arabia's Abdullah Tariki to Venezuela's observer Juan Pablo Pérez Alfonzo, representing the two then-largest oil-producing nations outside the United States and the Soviet Union. Both oil ministers were angered by the price cuts, and the two led their fellow delegates to establish the Maadi Pact or Gentlemen's Agreement, calling for an "Oil Consultation Commission" of exporting countries, to which MOCs should present price-change plans. Jablonski reported a marked hostility toward the West and a growing outcry against "absentee landlordism" of the MOCs, which at the time controlled all oil operations within the exporting countries and wielded enormous political influence. In August 1960, ignoring the warnings, and with the US favoring Canadian and Mexican oil for strategic reasons, the MOCs again unilaterally announced significant cuts in their posted prices for Middle Eastern crude oil.[54][55][56][57]
1960–1975 founding and expansion

The following month, during 10–14 September 1960, the Baghdad Conference was held at the initiative of Tariki, Pérez Alfonzo, and Iraqi prime minister Abd al-Karim Qasim, whose country had skipped the 1959 congress.[58] Government representatives from Iran, Iraq, Kuwait, Saudi Arabia and Venezuela met in Baghdad to discuss ways to increase the price of crude oil produced by their countries, and ways to respond to unilateral actions by the MOCs. Despite strong US opposition: "Together with Arab and non-Arab producers, Saudi Arabia formed the Organization of Petroleum Export Countries (OPEC) to secure the best price available from the major oil corporations."[59] The Middle Eastern members originally called for OPEC headquarters to be in Baghdad or Beirut, but Venezuela argued for a neutral location, and so the organization chose Geneva, Switzerland. On 1 September 1965, OPEC moved to Vienna, Austria, after Switzerland declined to extend diplomatic privileges.[60]
During 1961–1975, the five founding nations were joined by Qatar (1961), Indonesia (1962–2008, rejoined 2014-2016), Libya (1962), United Arab Emirates (originally just the Emirate of Abu Dhabi, 1967), Algeria (1969), Nigeria (1971), Ecuador (1973–1992, rejoined 2007), and Gabon (1975–1994, rejoined 2016).[2] By the early 1970s, OPEC's membership accounted for more than half of worldwide oil production.[61] Indicating that OPEC is not averse to further expansion, Mohammed Barkindo, OPEC's Acting Secretary General in 2006, urged his African neighbors Angola and Sudan to join,[62] and Angola did in 2007, followed by Equatorial Guinea in 2017.[3] Since the 1980s, representatives from Egypt, Mexico, Norway, Oman, Russia, and other oil-exporting nations have attended many OPEC meetings as observers, as an informal mechanism for coordinating policies.[24]
1973–1974 oil embargo

In October 1973, the Organization of Arab Petroleum Exporting Countries (OAPEC, consisting of the Arab majority of OPEC plus Egypt and Syria) declared significant production cuts and an oil embargo against the United States and other industrialized nations that supported Israel in the Yom Kippur War.[63][64] A previous embargo attempt was largely ineffective in response to the Six-Day War in 1967.[65] However, in 1973, the result was a sharp rise in oil prices and OPEC revenues, from US$3/bbl to US$12/bbl, and an emergency period of energy rationing, intensified by panic reactions, a declining trend in US oil production, currency devaluations,[64] and a lengthy UK coal-miners dispute. For a time, the UK imposed an emergency three-day workweek.[66] Seven European nations banned non-essential Sunday driving.[67] US gas stations limited the amount of gasoline that could be dispensed, closed on Sundays, and restricted the days when gasoline could be purchased, based on license plate numbers.[68][69] Even after the embargo ended in March 1974 following intense diplomatic activity, prices continued to rise. The world experienced a global economic recession, with unemployment and inflation surging simultaneously, steep declines in stock and bond prices, major shifts in trade balances and petrodollar flows, and a dramatic end to the post-WWII economic boom.[70][71]
The 1973–1974 oil embargo had lasting effects on the United States and other industrialized nations, which established the International Energy Agency in response, as well as national emergency stockpiles designed to withstand months of future supply disruptions. Oil conservation efforts included lower speed limits on highways, smaller and more energy-efficient cars and appliances, year-round daylight saving time, reduced usage of heating and air-conditioning, better insulation, increased support of mass transit, and greater emphasis on coal, natural gas, ethanol, nuclear and other alternative energy sources. These long-term efforts became effective enough that US oil consumption would rise only 11 percent during 1980–2014, while real GDP rose 150 percent. But in the 1970s, OPEC nations demonstrated convincingly that their oil could be used as both a political and economic weapon against other nations, at least in the short term.[64][72][73][74][75]
1975–1980 Special Fund, now OFID

OPEC's international aid activities date from well before the 1973–1974 oil price surge. For example, the Kuwait Fund for Arab Economic Development has operated since 1961.[76]
In the years after 1973, as an example of so-called "checkbook diplomacy", certain Arab nations have been among the world's largest providers of foreign aid,[77][78] and OPEC added to its goals the selling of oil for the socio-economic growth of poorer nations. The OPEC Special Fund was conceived in Algiers, Algeria, in March 1975, and was formally established the following January. "A Solemn Declaration 'reaffirmed the natural solidarity which unites OPEC countries with other developing countries in their struggle to overcome underdevelopment,' and called for measures to strengthen cooperation between these countries... [The OPEC Special Fund's] resources are additional to those already made available by OPEC states through a number of bilateral and multilateral channels."[79] The Fund became an official international development agency in May 1980 and was renamed the OPEC Fund for International Development (OFID),[80] with Permanent Observer status at the United Nations.[81]
1975 hostage siege

On 21 December 1975, Saudi Arabia's Ahmed Zaki Yamani, Iran's Jamshid Amuzegar, and the other OPEC oil ministers were taken hostage at their semi-annual conference in Vienna, Austria. The attack, which killed three non-ministers, was orchestrated by a six-person team led by Venezuelan militant "Carlos the Jackal", and which included Gabriele Kröcher-Tiedemann and Hans-Joachim Klein. The self-named "Arm of the Arab Revolution" group declared its goal to be the liberation of Palestine. Carlos planned to take over the conference by force and hold for ransom all eleven attending oil ministers, except for Yamani and Amuzegar who were to be executed.[82]
Carlos arranged bus and plane travel for his team and 42 of the original 63 hostages, with stops in Algiers and Tripoli, planning to fly eventually to Baghdad, where Yamani and Amuzegar were to be killed. All 30 non-Arab hostages were released in Algiers, excluding Amuzegar. Additional hostages were released at another stop in Tripoli before returning to Algiers. With only 10 hostages remaining, Carlos held a phone conversation with Algerian President Houari Boumédienne, who informed Carlos that the oil ministers' deaths would result in an attack on the plane. Boumédienne must also have offered Carlos asylum at this time and possibly financial compensation for failing to complete his assignment. Carlos expressed his regret at not being able to murder Yamani and Amuzegar, then he and his comrades left the plane. All the hostages and terrorists walked away from the situation, two days after it began.[82]
Some time after the attack, Carlos's accomplices revealed that the operation was commanded by Wadie Haddad, a founder of the Popular Front for the Liberation of Palestine. They also claimed that the idea and funding came from an Arab president, widely thought to be Muammar al-Gaddafi of Libya, itself an OPEC member. Fellow militants Bassam Abu Sharif and Klein claimed that Carlos received and kept a ransom between US$20million and US$50million from "an Arab president". Carlos claimed that Saudi Arabia paid ransom on behalf of Iran, but that the money was "diverted en route and lost by the Revolution".[82][83] He was finally captured in 1994 and is serving life sentences for at least 16 other murders.[84]
1979–1980 oil crisis and 1980s oil glut

In response to a wave of oil nationalizations and the high prices of the 1970s, industrial nations took steps to reduce their dependence on OPEC oil, especially after prices reached new peaks approaching US$40/bbl in 1979–1980[87][88] when the Iranian Revolution and Iran–Iraq War disrupted regional stability and oil supplies. Electric utilities worldwide switched from oil to coal, natural gas, or nuclear power;[89] national governments initiated multibillion-dollar research programs to develop alternatives to oil;[90][91] and commercial exploration developed major non-OPEC oilfields in Siberia, Alaska, the North Sea, and the Gulf of Mexico.[92] By 1986, daily worldwide demand for oil dropped by 5million barrels, non-OPEC production rose by an even-larger amount,[93] and OPEC's market share sank from approximately 50 percent in 1979 to less than 30 percent in 1985.[61] Illustrating the volatile multi-year timeframes of typical market cycles for natural resources, the result was a six-year decline in the price of oil, which culminated by plunging more than half in 1986 alone.[94] As one oil analyst summarized succinctly: "When the price of something as essential as oil spikes, humanity does two things: finds more of it and finds ways to use less of it."[61]
To combat falling revenue from oil sales, in 1982 Saudi Arabia pressed OPEC for audited national production quotas in an attempt to limit output and boost prices. When other OPEC nations failed to comply, Saudi Arabia first slashed its own production from 10million barrels daily in 1979–1981 to just one-third of that level in 1985. When even this proved ineffective, Saudi Arabia reversed course and flooded the market with cheap oil, causing prices to fall below US$10/bbl and higher-cost producers to become unprofitable.[93][95]:127-128,136-137 Faced with increasing economic hardship (which ultimately contributed to the collapse of the Soviet bloc in 1989),[96][97] the "free-riding" oil exporters that had previously failed to comply with OPEC agreements finally began to limit production to shore up prices, based on painstakingly negotiated national quotas that sought to balance oil-related and economic criteria since 1986.[93][98] (Within their sovereign-controlled territories, the national governments of OPEC members are able to impose production limits on both government-owned and private oil companies.)[99] Generally when OPEC production targets are reduced, oil prices increase.[51]
1990–2003 ample supply and modest disruptions

Leading up to his August 1990 Invasion of Kuwait, Iraqi President Saddam Hussein was pushing OPEC to end overproduction and to send oil prices higher, in order to help OPEC members financially and to accelerate rebuilding from the 1980–1988 Iran–Iraq War.[102] But these two Iraqi wars against fellow OPEC founders marked a low point in the cohesion of the organization, and oil prices subsided quickly after the short-term supply disruptions. The September 2001 Al Qaeda attacks on the US and the March 2003 US invasion of Iraq had even milder short-term impacts on oil prices, as Saudi Arabia and other exporters again cooperated to keep the world adequately supplied.[101]
In the 1990s, OPEC lost its two newest members, who had joined in the mid-1970s. Ecuador withdrew in December 1992, because it was unwilling to pay the annual US$2million membership fee and felt that it needed to produce more oil than it was allowed under the OPEC quota,[16] although it rejoined in October 2007. Similar concerns prompted Gabon to suspend membership in January 1995;[17] it rejoined in July 2016.[2] Iraq has remained a member of OPEC since the organization's founding, but Iraqi production was not a part of OPEC quota agreements from 1998 to 2016, due to the country's daunting political difficulties.[44][103]
Lower demand triggered by the 1997–1998 Asian financial crisis saw the price of oil fall back to 1986 levels. After oil slumped to around US$10/bbl, joint diplomacy achieved a gradual slowing of oil production by OPEC, Mexico and Norway.[104]  After prices slumped again in Nov. 2001, OPEC, Norway, Mexico, Russia, Oman and Angola agreed to cut production on 1 Jan. 2002 for 6 months. OPEC contributed 1.5 million barrels a day (mbpd) to the approximately 2 mbpd of cuts announced.[95]
In June 2003, the International Energy Agency (IEA) and OPEC held their first joint workshop on energy issues. They have continued to meet regularly since then, "to collectively better understand trends, analysis and viewpoints and advance market transparency and predictability."[105]
2003–2011 volatility

Widespread insurgency and sabotage occurred during the 2003–2008 height of the American occupation of Iraq, coinciding with rapidly increasing oil demand from China and commodity-hungry investors, recurring violence against the Nigerian oil industry, and dwindling spare capacity as a cushion against potential shortages. This combination of forces prompted a sharp rise in oil prices to levels far higher than those previously targeted by OPEC.[106][107][108] Price volatility reached an extreme in 2008, as WTI crude oil surged to a record US$147/bbl in July and then plunged back to US$32/bbl in December, during the worst global recession since World War II.[109] OPEC's annual oil export revenue also set a new record in 2008, estimated around US$1trillion, and reached similar annual rates in 2011–2014 (along with extensive petrodollar recycling activity) before plunging again.[86] By the time of the 2011 Libyan Civil War and Arab Spring, OPEC started issuing explicit statements to counter "excessive speculation" in oil futures markets, blaming financial speculators for increasing volatility beyond market fundamentals.[110]
In May 2008, Indonesia announced that it would leave OPEC when its membership expired at the end of that year, having become a net importer of oil and being unable to meet its production quota.[18] A statement released by OPEC on 10 September 2008 confirmed Indonesia's withdrawal, noting that OPEC "regretfully accepted the wish of Indonesia to suspend its full membership in the organization, and recorded its hope that the country would be in a position to rejoin the organization in the not-too-distant future."[111]
2008 production dispute

The differing economic needs of OPEC member states often affect the internal debates behind OPEC production quotas. Poorer members have pushed for production cuts from fellow members, to increase the price of oil and thus their own revenues.[112] These proposals conflict with Saudi Arabia's stated long-term strategy of being a partner with the world's economic powers to ensure a steady flow of oil that would support economic expansion.[113]  Part of the basis for this policy is the Saudi concern that overly expensive oil or unreliable supply will drive industrial nations to conserve energy and develop alternative fuels, curtailing the worldwide demand for oil and eventually leaving unneeded barrels in the ground.[114]  To this point, Saudi Oil Minister Yamani famously remarked in 1973: "The Stone Age didn't end because we ran out of stones."[115]
On 10 September 2008, with oil prices still near US$100/bbl, a production dispute occurred when the Saudis reportedly walked out of a negotiating session where rival members voted to reduce OPEC output. Although Saudi delegates officially endorsed the new quotas, they stated anonymously that they would not observe them. The New York Times quoted one such delegate as saying: "Saudi Arabia will meet the market's demand. We will see what the market requires and we will not leave a customer without oil. The policy has not changed."[36] Over the next few months, oil prices plummeted into the $30s, and did not return to $100 until the Libyan Civil War in 2011.[116]
2014–2017 oil glut

During 2014–2015, OPEC members consistently exceeded their production ceiling, and China experienced a slowdown in economic growth. At the same time, US oil production nearly doubled from 2008 levels and approached the world-leading "swing producer" volumes of Saudi Arabia and Russia, due to the substantial long-term improvement and spread of shale "fracking" technology in response to the years of record oil prices. These developments led in turn to a plunge in US oil import requirements (moving closer to energy independence), a record volume of worldwide oil inventories, and a collapse in oil prices that continued into early 2016.[116][118][119]
In spite of global oversupply, on 27 November 2014 in Vienna, Saudi Oil Minister Ali Al-Naimi blocked appeals from poorer OPEC members for production cuts to support prices. Naimi argued that the oil market should be left to rebalance itself competitively at lower price levels, strategically rebuilding OPEC's long-term market share by ending the profitability of high-cost US shale oil production.[120] As he explained in an interview:[35]
Is it reasonable for a highly efficient producer to reduce output, while the producer of poor efficiency continues to produce? That is crooked logic. If I reduce, what happens to my market share? The price will go up and the Russians, the Brazilians, US shale oil producers will take my share... We want to tell the world that high-efficiency producing countries are the ones that deserve market share. That is the operative principle in all capitalist countries... One thing is for sure: Current prices [roughly US$60/bbl] do not support all producers.
A year later, when OPEC met in Vienna on 4 December 2015, the organization had exceeded its production ceiling for 18 consecutive months, US oil production had declined only slightly from its peak, world markets appeared to be oversupplied by at least 2 million barrels per day despite war-torn Libya pumping 1 million barrels below capacity, oil producers were making major adjustments to withstand prices as low as the $40s, Indonesia was rejoining the export organization, Iraqi production had surged after years of disorder, Iranian output was poised to rebound with the lifting of international sanctions, hundreds of world leaders at the Paris Climate Agreement were committing to limit carbon emissions from fossil fuels, and solar technologies were becoming steadily more competitive and prevalent. In light of all these market pressures, OPEC decided to set aside its ineffective production ceiling until the next ministerial conference in June 2016.[25][119][121][122][123][124] By 20 January 2016, the OPEC Reference Basket was down to US$22.48/bbl – less than one-fourth of its high from June 2014 ($110.48), less than one-sixth of its record from July 2008 ($140.73), and back below the April 2003 starting point ($23.27) of its historic run-up.[116]
As 2016 continued, the oil glut was partially trimmed with significant production offline in the US, Canada, Libya, Nigeria and China, and the basket price gradually rose back into the $40s. OPEC regained a modest percentage of market share, saw the cancellation of many competing drilling projects, maintained the status quo at its June conference, and endorsed "prices at levels that are suitable for both producers and consumers", although many producers were still experiencing serious economic difficulties.[125][126][127][128]
2017–2018 production cut
As OPEC members grew weary of a multi-year supply contest with diminishing returns and shrinking financial reserves, the organization finally attempted its first production cut since 2008. Despite many political obstacles, a September 2016 decision to trim approximately 1 million barrels per day was codified by a new quota agreement at the November 2016 OPEC conference. The agreement (which exempted disruption-ridden members Libya and Nigeria) covered the first half of 2017 – alongside promised reductions from Russia and ten other non-members, offset by expected increases in the US shale sector, Libya, Nigeria, spare capacity, and surging late-2016 OPEC production before the cuts took effect. Indonesia announced another "temporary suspension" of its OPEC membership, rather than accepting the organization's requested 5 percent production cut. Prices fluctuated around US$50/bbl, and OPEC in May 2017 decided to extend the new quotas through March 2018, with the world waiting to see if and how the oil inventory glut might be fully siphoned-off by then.[19][129][130][131][132][133][3] Longtime oil analyst Daniel Yergin "described the relationship between OPEC and shale as 'mutual coexistence', with both sides learning to live with prices that are lower than they would like."[134]
In December 2017, Russia and OPEC agreed to extend the production cut of 1.8million barrels/day until the end of 2018.[135][136]
Qatar announced it will withdraw from OPEC effective 1st of January 2019.[137] According to the New York Times, this constitutes a strategic response to the ongoing Qatar boycott by Saudi Arabia, United Arab Emirates, Bahrain, and Egypt.[138]

See also
List of country groupings
List of intergovernmental organizations

Further reading
Evans, John. OPEC, Its Member States and the World Energy Market (1986), 679 pages
Fesharaki, Fereidun. OPEC, the Gulf, and the World Petroleum Market: A Study in Government Policy and Downstream Operations (1983).

Painter, David S. "Oil and geopolitics: The oil crises of the 1970s and the cold war." Historical Social Research/Historische Sozialforschung (2014): 186-208.
Skeet, Ian. OPEC: Twenty-five Years of Prices and Politics (Cambridge UP, 1988).
Yergin, Daniel.  The Prize: The Epic Quest for Oil, Money, and Power (1991)

What were the founding members of the Organization of Petroleum Exporting Countries?


Alzheimer's disease (AD), also referred to simply as Alzheimer's, is a chronic neurodegenerative disease that usually starts slowly and worsens over time.[1][2] It is the cause of 60–70% of cases of dementia.[1][2] The most common early symptom is difficulty in remembering recent events (short-term memory loss).[1] As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, not managing self care, and behavioural issues.[1][2] As a person's condition declines, they often withdraw from family and society.[1] Gradually, bodily functions are lost, ultimately leading to death.[10] Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.[7][11]

The cause of Alzheimer's disease is poorly understood.[1] About 70% of the risk is believed to be genetic with many genes usually involved.[4] Other risk factors include a history of head injuries, depression, or hypertension.[1] The disease process is associated with plaques and tangles in the brain.[4] A probable diagnosis is based on the history of the illness and cognitive testing with medical imaging and blood tests to rule out other possible causes.[5] Initial symptoms are often mistaken for normal ageing.[1] Examination of brain tissue is needed for a definite diagnosis.[4] Mental and physical exercise, and avoiding obesity may decrease the risk of AD; however, evidence to support these recommendations is not strong.[4][12] There are no medications or supplements that have been shown to decrease risk.[13]

No treatments stop or reverse its progression, though some may temporarily improve symptoms.[2] Affected people increasingly rely on others for assistance, often placing a burden on the caregiver; the pressures can include social, psychological, physical, and economic elements.[14] Exercise programmes may be beneficial with respect to activities of daily living and can potentially improve outcomes.[15] Behavioural problems or psychosis due to dementia are often treated with antipsychotics, but this is not usually recommended, as there is little benefit with an increased risk of early death.[16][17]

In 2015, there were approximately 29.8 million people worldwide with AD.[2][8] It most often begins in people over 65years of age, although 4% to 5% of cases are early-onset Alzheimer's which begin before this.[3] It affects about 6% of people 65 years and older.[1] In 2015, dementia resulted in about 1.9 million deaths.[9] It was first described by, and later named after, German psychiatrist and pathologist Alois Alzheimer in 1906.[18]  In developed countries, AD is one of the most financially costly diseases.[19][20]

Signs and symptoms

Stages of Alzheimer's disease[21]

Effects of ageing on memory but not AD
Forgetting things occasionally
Misplacing items sometimes
Minor short-term memory loss
Not remembering exact details
Early stage Alzheimer's
Not remembering episodes of forgetfulness
Forgets names of family or friends
Changes may only be noticed by close friends or relatives
Some confusion in situations outside the familiar
Middle stage Alzheimer's
Greater difficulty remembering recently learned information
Deepening confusion in many circumstances
Problems with sleep
Trouble determining their location
Late stage Alzheimer's
Poor ability to think
Problems speaking
Repeats same conversations
More abusive, anxious, or paranoid

The disease course is divided into four stages, with a progressive pattern of cognitive and functional impairment.
Pre-dementia
The first symptoms are often mistakenly attributed to ageing or stress.[22] Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfils the clinical criteria for diagnosis of AD.[23] These early symptoms can affect the most complex activities of daily living.[24] The most noticeable deficit is short term memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information.[23][25]
Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory (memory of meanings, and concept relationships) can also be symptomatic of the early stages of AD.[23] Apathy can be observed at this stage, and remains the most persistent neuropsychiatric symptom throughout the course of the disease.[26] Depressive symptoms, irritability and reduced awareness of subtle memory difficulties are also common.[27]
The preclinical stage of the disease has also been termed mild cognitive impairment (MCI).[25] This is often found to be a transitional stage between normal ageing and dementia. MCI can present with a variety of symptoms, and when memory loss is the predominant symptom, it is termed "amnestic MCI" and is frequently seen as a prodromal stage of Alzheimer's disease.[28]
Early
In people with AD, the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small percentage, difficulties with language, executive functions, perception (agnosia), or execution of movements (apraxia) are more prominent than memory problems.[29] AD does not affect all memory capacities equally. Older memories of the person's life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat or how to drink from a glass) are affected to a lesser degree than new facts or memories.[30][31]
Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency, leading to a general impoverishment of oral and written language.[29][32] In this stage, the person with Alzheimer's is usually capable of communicating basic ideas adequately.[29][32][33]  While performing fine motor tasks such as writing, drawing or dressing, certain movement coordination and planning difficulties (apraxia) may be present, but they are commonly unnoticed.[29] As the disease progresses, people with AD can often continue to perform many tasks independently, but may need assistance or supervision with the most cognitively demanding activities.[29]
Moderate
Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living.[29] Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost.[29][33] Complex motor sequences become less coordinated as time passes and AD progresses, so the risk of falling increases.[29] During this phase, memory problems worsen, and the person may fail to recognise close relatives.[29] Long-term memory, which was previously intact, becomes impaired.[29]
Behavioural and neuropsychiatric changes become more prevalent. Common manifestations are wandering, irritability and labile affect, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving.[29] Sundowning can also appear.[34] Approximately 30% of people with AD develop illusionary misidentifications and other delusional symptoms.[29] Subjects also lose insight of their disease process and limitations (anosognosia).[29] Urinary incontinence can develop.[29] These symptoms create stress for relatives and carers, which can be reduced by moving the person from home care to other long-term care facilities.[29][35]
Advanced
During the final stages, the patient is completely dependent upon caregivers.[29] Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech.[29][33] Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common symptoms. People with Alzheimer's disease will ultimately not be able to perform even the simplest tasks independently; muscle mass and mobility deteriorates to the point where they are bedridden and unable to feed themselves. The cause of death is usually an external factor, such as infection of pressure ulcers or pneumonia, not the disease itself.[29]
Cause
The cause for most Alzheimer's cases is still mostly unknown except for 1% to 5% of cases where genetic differences have been identified.[36][37] Several competing hypotheses exist trying to explain the cause of the disease.
Genetic
The genetic heritability of Alzheimer's disease (and memory components thereof), based on reviews of twin and family studies, ranges from 49% to 79%.[38][39] Around 0.1% of the cases are familial forms of autosomal (not sex-linked) dominant inheritance, which have an onset before age 65.[40] This form of the disease is known as early onset familial Alzheimer's disease. Most of autosomal dominant familial AD can be attributed to mutations in one of three genes: those encoding amyloid precursor protein (APP) and presenilins 1 and 2.[41] Most mutations in the APP and presenilin genes increase the production of a small protein called Aβ42, which is the main component of senile plaques.[42] Some of the mutations merely alter the ratio between Aβ42 and the other major forms—particularly Aβ40—without increasing Aβ42 levels.[43][44]
Most cases of Alzheimer's disease do not exhibit autosomal-dominant inheritance and are termed sporadic AD, in which environmental and genetic differences may act as risk factors. The best known genetic risk factor is the inheritance of the ε4 allele of the apolipoprotein E (APOE).[45][46] Between 40 and 80% of people with AD possess at least one APOEε4 allele.[46] The APOEε4 allele increases the risk of the disease by three times in heterozygotes and by 15 times in homozygotes.[40] Like many human diseases, environmental effects and genetic modifiers result in incomplete penetrance. For example, certain Nigerian populations do not show the relationship between dose of APOEε4 and incidence or age-of-onset for Alzheimer's disease seen in other human populations.[47][48] Early attempts to screen up to 400 candidate genes for association with late-onset sporadic AD (LOAD) resulted in a low yield.[40][41] More recent genome-wide association studies (GWAS) have found 19 areas in genes that appear to affect the risk.[49] These genes include: CASS4, CELF1, FERMT2, HLA-DRB5, INPP5D, MEF2C, NME8, PTK2B, SORL1, ZCWPW1, SlC24A4, CLU, PICALM, CR1, BIN1, MS4A, ABCA7, EPHA1, and CD2AP.[49]
Alleles in the TREM2 gene have been associated with a 3 to 5 times higher risk of developing Alzheimer's disease.[50][51] A suggested mechanism of action is that in some variants in TREM2 white blood cells in the brain are no longer able to control the amount of beta amyloid present. Many SNPs are associated with Alzheimer's with a 2018 study adding 30 SNPs by differentiating AD into 6 categories, including memory, language, visuospatial, and executive functioning.[52]
Cholinergic hypothesis
The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis,[53] which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective.[54]
Amyloid hypothesis
In 1991, the amyloid hypothesis postulated that extracellular amyloid beta (Aβ) deposits are the fundamental cause of the disease.[55][56] Support for this postulate comes from the location of the gene for the amyloid precursor protein (APP) on chromosome 21, together with the fact that people with trisomy 21 (Down Syndrome) who have an extra gene copy almost universally exhibit at least the earliest symptoms of AD by 40years of age.[57][58] Also, a specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for AD. While apolipoproteins enhance the breakdown of beta amyloid, some isoforms are not very effective at this task (such as APOE4), leading to excess amyloid buildup in the brain.[59] Further evidence comes from the finding that transgenic mice that express a mutant form of the human APP gene develop fibrillar amyloid plaques and Alzheimer's-like brain pathology with spatial learning deficits.[60]
An experimental vaccine was found to clear the amyloid plaques in early human trials, but it did not have any significant effect on dementia.[61] Researchers have been led to suspect non-plaque Aβ oligomers (aggregates of many monomers) as the primary pathogenic form of Aβ. These toxic oligomers, also referred to as amyloid-derived diffusible ligands (ADDLs), bind to a surface receptor on neurons and change the structure of the synapse, thereby disrupting neuronal communication.[62] One receptor for Aβ oligomers may be the prion protein, the same protein that has been linked to mad cow disease and the related human condition, Creutzfeldt–Jakob disease, thus potentially linking the underlying mechanism of these neurodegenerative disorders with that of Alzheimer's disease.[63]
In 2009, this theory was updated, suggesting that a close relative of the beta-amyloid protein, and not necessarily the beta-amyloid itself, may be a major culprit in the disease. The theory holds that an amyloid-related mechanism that prunes neuronal connections in the brain in the fast-growth phase of early life may be triggered by ageing-related processes in later life to cause the neuronal withering of Alzheimer's disease.[64] N-APP, a fragment of APP from the peptide's N-terminus, is adjacent to beta-amyloid and is cleaved from APP by one of the same enzymes. N-APP triggers the self-destruct pathway by binding to a neuronal receptor called death receptor 6 (DR6, also known as TNFRSF21).[64] DR6 is highly expressed in the human brain regions most affected by Alzheimer's, so it is possible that the N-APP/DR6 pathway might be hijacked in the ageing brain to cause damage. In this model, beta-amyloid plays a complementary role, by depressing synaptic function.
In early 2017, a trial of verubecestat, which inhibits the beta-secretase protein responsible for creating beta-amyloid protein was discontinued as an independent panel found "virtually no chance of finding a positive clinical effect".[65]
Tau hypothesis

The tau hypothesis proposes that tau protein abnormalities initiate the disease cascade.[56] In this model, hyperphosphorylated tau begins to pair with other threads of tau. Eventually, they form neurofibrillary tangles inside nerve cell bodies.[66] When this occurs, the microtubules disintegrate, destroying the structure of the cell's cytoskeleton which collapses the neuron's transport system.[67] This may result first in malfunctions in biochemical communication between neurons and later in the death of the cells.[68]
Other hypotheses
A neurovascular hypothesis has been proposed which states that poor functioning of the blood–brain barrier may be involved.[69]
The cellular homeostasis of biometals such as ionic copper, iron, and zinc is disrupted in AD, though it remains unclear whether this is produced by or causes the changes in proteins. These ions affect and are affected by tau, APP, and APOE,[70] and their dysregulation may cause  oxidative stress that may contribute to the pathology.[71][72][73][74][75] The quality of some of these studies has been criticised,[76][77] and the link remains controversial.[78] The majority of researchers do not support a causal connection with aluminium.[77]
Smoking is a significant AD risk factor.[79] Systemic markers of the innate immune system are risk factors for late-onset AD.[80]
There is tentative evidence that exposure to air pollution may be a contributing factor to the development of Alzheimer's disease.[81]
Gum disease: An infection with Spirochetes (a bacterium) in gum disease may cause dementia and may be involved in the pathogenesis of Alzheimer's disease.[82] A fungal infection may also be a factor.[83]
One hypothesis posits that dysfunction of oligodendrocytes and their associated myelin during aging contributes to axon damage, which then causes amyloid production and tau hyper-phosphorylation as a side effect.[84][85]
Retrogenesis is a medical hypothesis about the development and progress of Alzheimer's disease proposed by Barry Reisberg in the 1980s.[86] The hypothesis is that just as the fetus goes through a process of neurodevelopment beginning with neurulation and ending with myelination, the brains of people with AD go through a reverse neurodegeneration process starting with demyelination and death of axons (white matter) and ending with the death of grey matter.[87] Likewise the hypothesis is, that as infants go through states of cognitive development, people with AD go through the reverse process of progressive cognitive impairment.[86] Reisberg developed the caregiving assessment tool known as "FAST" (Functional Assessment Staging Tool) which he says allows those caring for AD patients to identify the stages of disease progression and that provides advice about the kind of care needed at each stage.[86][88]
Pathophysiology

Neuropathology
Alzheimer's disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus.[89] Degeneration is also present in brainstem nuclei like the locus coeruleus.[90] Studies using MRI and PET have documented reductions in the size of specific brain regions in people with AD as they progressed from mild cognitive impairment to Alzheimer's disease, and in comparison with similar images from healthy older adults.[91][92]
Both amyloid plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those afflicted by AD.[93] Plaques are dense, mostly insoluble deposits of beta-amyloid peptide and cellular material outside and around neurons. Tangles (neurofibrillary tangles) are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves. Although many older individuals develop some plaques and tangles as a consequence of ageing, the brains of people with AD have a greater number of them in specific brain regions such as the temporal lobe.[94] Lewy bodies are not rare in the brains of people with AD.[95]
Biochemistry

Alzheimer's disease has been identified as a protein misfolding disease (proteopathy), caused by plaque accumulation of abnormally folded amyloid beta protein and tau protein in the brain.[96] Plaques are made up of small peptides, 39–43amino acids in length, called amyloid beta (Aβ). Aβ is a fragment from the larger amyloid precursor protein (APP). APP is a transmembrane protein that penetrates through the neuron's membrane. APP is critical to neuron growth, survival, and post-injury repair.[97][98] In Alzheimer's disease, gamma secretase and beta secretase act together in a proteolytic process which causes APP to be divided into smaller fragments.[99] One of these fragments gives rise to fibrils of amyloid beta, which then form clumps that deposit outside neurons in dense formations known as senile plaques.[93][100]
AD is also considered a tauopathy due to abnormal aggregation of the tau protein. Every neuron has a cytoskeleton, an internal support structure partly made up of structures called microtubules. These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the axon and back. A protein called tau stabilises the microtubules when phosphorylated, and is therefore called a microtubule-associated protein. In AD, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neuron's transport system.[101] Pathogenic tau can also cause neuronal death through transposable element dysregulation.[102]
Disease mechanism
Exactly how disturbances of production and aggregation of the beta-amyloid peptide give rise to the pathology of AD is not known.[103][104]
The amyloid hypothesis traditionally points to the accumulation of beta-amyloid peptides as the central event triggering neuron degeneration. Accumulation of aggregated amyloid fibrils, which are believed to be the toxic form of the protein responsible for disrupting the cell's calcium ion homeostasis, induces programmed cell death (apoptosis).[105] It is also known that Aβ selectively builds up in the mitochondria in the cells of Alzheimer's-affected brains, and it also inhibits certain enzyme functions and the utilisation of glucose by neurons.[106]
Various inflammatory processes and cytokines may also have a role in the pathology of Alzheimer's disease. Inflammation is a general marker of tissue damage in any disease, and may be either secondary to tissue damage in AD or a marker of an immunological response.[107] There is increasing evidence of a strong interaction between the neurons and the immunological mechanisms in the brain. Obesity and systemic inflammation may interfere with immunological processes which promote disease progression.[108]
Alterations in the distribution of different neurotrophic factors and in the expression of their receptors such as the brain-derived neurotrophic factor (BDNF) have been described in AD.[109][110]
Diagnosis

Alzheimer's disease is usually diagnosed based on the person's medical history, history from relatives, and behavioural observations. The presence of characteristic neurological and neuropsychological features and the absence of alternative conditions is supportive.[111][112] Advanced medical imaging with computed tomography (CT) or magnetic resonance imaging (MRI), and with single-photon emission computed tomography (SPECT) or positron emission tomography (PET) can be used to help exclude other cerebral pathology or subtypes of dementia.[113] Moreover, it may predict conversion from prodromal stages (mild cognitive impairment) to Alzheimer's disease.[114]
Assessment of intellectual functioning including memory testing can further characterise the state of the disease.[22] Medical organisations have created diagnostic criteria to ease and standardise the diagnostic process for practising physicians. The diagnosis can be confirmed with very high accuracy post-mortem when brain material is available and can be examined histologically.[115]
Criteria
The National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and the Alzheimer's Disease and Related Disorders Association (ADRDA, now known as the Alzheimer's Association) established the most commonly used NINCDS-ADRDA Alzheimer's Criteria for diagnosis in 1984,[115] extensively updated in 2007.[116] These criteria require that the presence of cognitive impairment, and a suspected dementia syndrome, be confirmed by neuropsychological testing for a clinical diagnosis of possible or probable AD. A histopathologic confirmation including a microscopic examination of brain tissue is required for a definitive diagnosis. Good statistical reliability and validity have been shown between the diagnostic criteria and definitive histopathological confirmation.[117] Eight intellectual domains are most commonly impaired in AD—memory, language, perceptual skills, attention, motor skills, orientation, problem solving and executive functional abilities. These domains are equivalent to the NINCDS-ADRDA Alzheimer's Criteria as listed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) published by the American Psychiatric Association.[118][119]
Techniques

Neuropsychological tests such as the mini–mental state examination (MMSE) are widely used to evaluate the cognitive impairments needed for diagnosis. More comprehensive test arrays are necessary for high reliability of results, particularly in the earliest stages of the disease.[120][121] Neurological examination in early AD will usually provide normal results, except for obvious cognitive impairment, which may not differ from that resulting from other diseases processes, including other causes of dementia.
Further neurological examinations are crucial in the differential diagnosis of AD and other diseases.[22] Interviews with family members are also utilised in the assessment of the disease. Caregivers can supply important information on the daily living abilities, as well as on the decrease, over time, of the person's mental function.[122] A caregiver's viewpoint is particularly important, since a person with AD is commonly unaware of his own deficits.[123] Many times, families also have difficulties in the detection of initial dementia symptoms and may not communicate accurate information to a physician.[124]
Supplemental testing provides extra information on some features of the disease or is used to rule out other diagnoses. Blood tests can identify other causes for dementia than AD[22]—causes which may, in rare cases, be reversible.[125] It is common to perform thyroid function tests, assess B12, rule out syphilis, rule out metabolic problems (including tests for kidney function, electrolyte levels and for diabetes), assess levels of heavy metals (e.g. lead, mercury) and anaemia. (It is also necessary to rule out delirium).
Psychological tests for depression are employed, since depression can either be concurrent with AD (see Depression of Alzheimer disease), an early sign of cognitive impairment,[126] or even the cause.[127][128]
Due to low accuracy, the C-PIB-PET scan is not recommended to be used as an early diagnostic tool or for predicting the development of Alzheimer's disease when people show signs of mild cognitive impairment (MCI).[129] The use of ¹⁸F-FDG PET scans, as a single test, to identify people who may develop Alzheimer's disease is also not supported by evidence.[130]
Prevention

There is no definitive evidence to support that any particular measure is effective in preventing AD.[13] Global studies of measures to prevent or delay the onset of AD have often produced inconsistent results.
Epidemiological studies have proposed relationships between certain modifiable factors, such as diet, cardiovascular risk, pharmaceutical products, or intellectual activities among others, and a population's likelihood of developing AD. Only further research, including clinical trials, will reveal whether these factors can help to prevent AD.[13]
Medication
Although cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and course of AD,[131][132] statins, which are cholesterol lowering drugs, have not been effective in preventing or improving the course of the disease.[133][134][135]
Long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs) were thought in 2007 to be associated with a reduced likelihood of developing AD.[136] Evidence also suggested the notion that NSAIDs could reduce inflammation related to amyloid plaques, but trials were suspended due to high adverse events.[13] No prevention trial has been completed.[13] They do not appear to be useful as a treatment, but as of 2011 were thought to be candidates as presymptomatic preventatives.[137] Hormone replacement therapy in menopause, although previously used, may increase the risk of dementia.[138]
Lifestyle
People who engage in intellectual activities such as reading, playing board games, completing crossword puzzles, playing musical instruments, or regular social interaction show a reduced risk for Alzheimer's disease.[139] This is compatible with the cognitive reserve theory, which states that some life experiences result in more efficient neural functioning providing the individual a cognitive reserve that delays the onset of dementia manifestations.[139] Education delays the onset of AD syndrome without changing the duration of the disease.[140] Learning a second language even later in life seems to delay getting Alzheimer disease.[141]
Physical activity is also associated with a reduced risk of AD.[140] Physical exercise is associated with decreased rate of dementia.[142] Physical exercise is also effective in reducing symptom severity in those with Alzheimers.[143]
Diet

People who maintain a healthy, Japanese, or Mediterranean diet have a reduced risk of AD.[144] A Mediterranean diet may improve outcomes in those with the disease.[145] Those who eat a diet high in saturated fats and simple carbohydrates (mono- and disaccharide) have a higher risk.[146] The Mediterranean diet's beneficial cardiovascular effect has been proposed as the mechanism of action.[147]

Conclusions on dietary components have at times been difficult to ascertain as results have differed between population-based studies and randomised controlled trials.[144] There is limited evidence that light to moderate use of alcohol, particularly red wine, is associated with lower risk of AD.[144] There is tentative evidence that caffeine may be protective.[148] A number of foods high in flavonoids such as cocoa, red wine, and tea may decrease the risk of AD.[149][150]

Reviews on the use of vitamins and minerals have not found enough consistent evidence to recommend them. This includes vitamin A,[151][152] C,[153][154] the alpha-tocopherol form of vitamin E,[155] selenium,[156] zinc,[157][158] and folic acid with or without vitamin B12.[159] Evidence from one randomized controlled trial indicated that the alpha-tocopherol form of vitamin E may slow cognitive decline, this evidence was judged to be "moderate" in quality.[155] Trials examining folic acid (B9) and other B vitamins failed to show any significant association with cognitive decline.[160] Omega-3 fatty acid supplements from plants and fish, and dietary docosahexaenoic acid (DHA), do not appear to benefit people with mild to moderate Alzheimer's disease.[161][162]

Curcumin as of 2010 had not shown benefit in people even though there is tentative evidence in animals.[163] There was inconsistent and unconvincing evidence that ginkgo has any positive effect on cognitive impairment and dementia.[164] As of 2008 there was no concrete evidence that cannabinoids are effective in improving the symptoms of AD or dementia;[165] however, some research into endocannabinoids looked promising.[166]
Management
There is no cure for Alzheimer's disease; available treatments offer relatively small symptomatic benefit but remain palliative in nature. Current treatments can be divided into pharmaceutical, psychosocial and caregiving.
Medications

Five medications are currently used to treat the cognitive problems of AD: four are acetylcholinesterase inhibitors (tacrine, rivastigmine, galantamine and donepezil) and the other (memantine) is an NMDA receptor antagonist. The benefit from their use is small.[6][167][168] No medication has been clearly shown to delay or halt the progression of the disease.
Reduction in the activity of the cholinergic neurons is a well-known feature of Alzheimer's disease.[169] Acetylcholinesterase inhibitors are employed to reduce the rate at which acetylcholine (ACh) is broken down, thereby increasing the concentration of ACh in the brain and combating the loss of ACh caused by the death of cholinergic neurons.[170] There is evidence for the efficacy of these medications in mild to moderate Alzheimer's disease,[171][168][167] and some evidence for their use in the advanced stage.[167] The use of these drugs in mild cognitive impairment has not shown any effect in a delay of the onset of AD.[172] The most common side effects are nausea and vomiting, both of which are linked to cholinergic excess. These side effects arise in approximately 10–20% of users, are mild to moderate in severity, and can be managed by slowly adjusting medication doses.[173] Less common secondary effects include muscle cramps, decreased heart rate (bradycardia), decreased appetite and weight, and increased gastric acid production.[171]
Glutamate is an excitatory neurotransmitter of the nervous system, although excessive amounts in the brain can lead to cell death through a process called excitotoxicity which consists of the overstimulation of glutamate receptors. Excitotoxicity occurs not only in Alzheimer's disease, but also in other neurological diseases such as Parkinson's disease and multiple sclerosis.[174] Memantine is a noncompetitive NMDA receptor antagonist first used as an anti-influenza agent. It acts on the glutamatergic system by blocking NMDA receptors and inhibiting their overstimulation by glutamate.[174][175] Memantine has been shown to have a small benefit in the treatment of Alzheimer's disease.[176] Reported adverse events with memantine are infrequent and mild, including hallucinations, confusion, dizziness, headache and fatigue.[177] The combination of memantine and donepezil has been shown to be "of statistically significant but clinically marginal effectiveness".[178]
Atypical antipsychotics are modestly useful in reducing aggression and psychosis in people with Alzheimer's disease, but their advantages are offset by serious adverse effects, such as stroke, movement difficulties or cognitive decline.[179] When used in the long-term, they have been shown to associate with increased mortality.[180] Stopping antipsychotic use in this group of people appears to be safe.[181]
Huperzine A while promising, requires further evidence before its use can be recommended.[182]
Psychosocial intervention
Psychosocial interventions are used as an adjunct to pharmaceutical treatment and can be classified within behaviour-, emotion-, cognition- or stimulation-oriented approaches. Research on efficacy is unavailable and rarely specific to AD, focusing instead on dementia in general.[183]
Behavioural interventions attempt to identify and reduce the antecedents and consequences of problem behaviours. This approach has not shown success in improving overall functioning,[184] but can help to reduce some specific problem behaviours, such as incontinence.[185] There is a lack of high quality data on the effectiveness of these techniques in other behaviour problems such as wandering.[186][187] Music therapy is effective in reducing behavioural and psychological symptoms.[188]
Emotion-oriented interventions include reminiscence therapy, validation therapy, supportive psychotherapy, sensory integration, also called snoezelen, and simulated presence therapy. A Cochrane review has found no evidence that this is effective.[189] Supportive psychotherapy has received little or no formal scientific study, but some clinicians find it useful in helping mildly impaired people adjust to their illness.[183] Reminiscence therapy (RT) involves the discussion of past experiences individually or in group, many times with the aid of photographs, household items, music and sound recordings, or other familiar items from the past. A 2018 review of the effectiveness of RT found that effects were inconsistent, small in size and of doubtful clinical significance, and varied by setting.[190] Simulated presence therapy (SPT) is based on attachment theories and involves playing a recording with voices of the closest relatives of the person with Alzheimer's disease. There is partial evidence indicating that SPT may reduce challenging behaviours.[191]
Finally, validation therapy is based on acceptance of the reality and personal truth of another's experience, while sensory integration is based on exercises aimed to stimulate senses. There is no evidence to support the usefulness of these therapies.[192][193]
The aim of cognition-oriented treatments, which include reality orientation and cognitive retraining, is the reduction of cognitive deficits. Reality orientation consists in the presentation of information about time, place or person to ease the understanding of the person about its surroundings and his or her place in them. On the other hand, cognitive retraining tries to improve impaired capacities by exercitation of mental abilities. Both have shown some efficacy improving cognitive capacities,[194][195] although in some studies these effects were transient and negative effects, such as frustration, have also been reported.[183]
Stimulation-oriented treatments include art, music and pet therapies, exercise, and any other kind of recreational activities. Stimulation has modest support for improving behaviour, mood, and, to a lesser extent, function. Nevertheless, as important as these effects are, the main support for the use of stimulation therapies is the change in the person's routine.[183] The efficacy of non-invasive brain stimulation and invasive brain stimulation in AD remains uncertain.[196]
Caregiving

Since Alzheimer's has no cure and it gradually renders people incapable of tending for their own needs, caregiving is essentially the treatment and must be carefully managed over the course of the disease.
During the early and moderate stages, modifications to the living environment and lifestyle can increase patient safety and reduce caretaker burden.[197][198] Examples of such modifications are the adherence to simplified routines, the placing of safety locks, the labelling of household items to cue the person with the disease or the use of modified daily life objects.[183][199][200] If eating becomes problematic, food will need to be prepared in smaller pieces or even pureed.[201] When swallowing difficulties arise, the use of feeding tubes may be required. In such cases, the medical efficacy and ethics of continuing feeding is an important consideration of the caregivers and family members.[202][203] The use of physical restraints is rarely indicated in any stage of the disease, although there are situations when they are necessary to prevent harm to the person with AD or their caregivers.[183]
As the disease progresses, different medical issues can appear, such as oral and dental disease, pressure ulcers, malnutrition, hygiene problems, or respiratory, skin, or eye infections. Careful management can prevent them, while professional treatment is needed when they do arise.[204][205] During the final stages of the disease, treatment is centred on relieving discomfort until death, often with the help of hospice.[206]
Prognosis

The early stages of Alzheimer's disease are difficult to diagnose. A definitive diagnosis is usually made once cognitive impairment compromises daily living activities, although the person may still be living independently. The symptoms will progress from mild cognitive problems, such as memory loss through increasing stages of cognitive and non-cognitive disturbances, eliminating any possibility of independent living, especially in the late stages of the disease.[29]
Life expectancy of people with AD is reduced.[207] Following diagnosis it typically ranges from three to ten years.[207]
Fewer than 3% of people live more than fourteen years.[208] Disease features significantly associated with reduced survival are an increased severity of cognitive impairment, decreased functional level, history of falls, and disturbances in the neurological examination. Other coincident diseases such as heart problems, diabetes or history of alcohol abuse are also related with shortened survival.[209][210][211] While the earlier the age at onset the higher the total survival years, life expectancy is particularly reduced when compared to the healthy population among those who are younger.[212] Men have a less favourable survival prognosis than women.[208][213]
Pneumonia and dehydration are the most frequent immediate causes of death brought by AD, while cancer is a less frequent cause of death than in the general population.[213]

Epidemiology

Two main measures are used in epidemiological studies: incidence and prevalence. Incidence is the number of new cases per unit of person–time at risk (usually number of new cases per thousand person–years); while prevalence is the total number of cases of the disease in the population at any given time.
Regarding incidence, cohort longitudinal studies (studies where a disease-free population is followed over the years) provide rates between 10 and 15 per thousand person–years for all dementias and 5–8 for AD,[214][215] which means that half of new dementia cases each year are AD. Advancing age is a primary risk factor for the disease and incidence rates are not equal for all ages: every five years after the age of 65, the risk of acquiring the disease approximately doubles, increasing from 3 to as much as 69 per thousand person years.[214][215] There are also sex differences in the incidence rates, women having a higher risk of developing AD particularly in the population older than 85.[215][216] In the United States, the risk of dying from Alzheimer's disease is 26% higher among the non-Hispanic white population than among the non-Hispanic black population, whereas the Hispanic population has a 30% lower risk than the non-Hispanic white population.[217]

Prevalence of AD in populations is dependent upon different factors including incidence and survival. Since the incidence of AD increases with age, it is particularly important to include the mean age of the population of interest. In the United States, Alzheimer prevalence was estimated to be 1.6% in 2000 both overall and in the 65–74 age group, with the rate increasing to 19% in the 75–84 group and to 42% in the greater than 84 group.[218] Prevalence rates in less developed regions are lower.[219] The World Health Organization estimated that in 2005, 0.379% of people worldwide had dementia, and that the prevalence would increase to 0.441% in 2015 and to 0.556% in 2030.[220] Other studies have reached similar conclusions.[219] Another study estimated that in 2006, 0.40% of the world population (range 0.17–0.89%; absolute number 26.6 million, range 11.4–59.4 million) were afflicted by AD, and that the prevalence rate would triple and the absolute number would quadruple by 2050.[221]
History

The ancient Greek and Roman philosophers and physicians associated old age with increasing dementia.[18] It was not until 1901 that German psychiatrist Alois Alzheimer identified the first case of what became known as Alzheimer's disease, named after him, in a fifty-year-old woman he called Auguste D. He followed her case until she died in 1906, when he first reported publicly on it.[222] During the next five years, eleven similar cases were reported in the medical literature, some of them already using the term Alzheimer's disease.[18] The disease was first described as a distinctive disease by Emil Kraepelin after suppressing some of the clinical (delusions and hallucinations) and pathological features (arteriosclerotic changes) contained in the original report of Auguste D.[223] He included Alzheimer's disease, also named presenile dementia by Kraepelin, as a subtype of senile dementia in the eighth edition of his Textbook of Psychiatry, published on 15 July, 1910.[224]
For most of the 20th century, the diagnosis of Alzheimer's disease was reserved for individuals between the ages of 45 and 65 who developed symptoms of dementia. The terminology changed after 1977 when a conference on AD concluded that the clinical and pathological manifestations of presenile and senile dementia were almost identical, although the authors also added that this did not rule out the possibility that they had different causes.[225] This eventually led to the diagnosis of Alzheimer's disease independent of age.[226] The term senile dementia of the Alzheimer type (SDAT) was used for a time to describe the condition in those over 65, with classical Alzheimer's disease being used to describe those who were younger. Eventually, the term Alzheimer's disease was formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease course, and neuropathology.[227]
Society and culture

Social costs
Dementia, and specifically Alzheimer's disease, may be among the most costly diseases for society in Europe and the United States,[19][20] while their costs in other countries such as Argentina,[228] and South Korea,[229] are also high and rising. These costs will probably increase with the ageing of society, becoming an important social problem. AD-associated costs include direct medical costs such as nursing home care, direct nonmedical costs such as in-home day care, and indirect costs such as lost productivity of both patient and caregiver.[20] Numbers vary between studies but dementia costs worldwide have been calculated around $160billion,[230] while costs of Alzheimer's disease in the United States may be $100billion each year.[20]
The greatest origin of costs for society is the long-term care by health care professionals and particularly institutionalisation, which corresponds to 2/3 of the total costs for society.[19] The cost of living at home is also very high,[19] especially when informal costs for the family, such as caregiving time and caregiver's lost earnings, are taken into account.[231]
Costs increase with dementia severity and the presence of behavioural disturbances,[232] and are related to the increased caregiving time required for the provision of physical care.[231] Therefore, any treatment that slows cognitive decline, delays institutionalisation or reduces caregivers' hours will have economic benefits. Economic evaluations of current treatments have shown positive results.[20]
Caregiving burden

The role of the main caregiver is often taken by the spouse or a close relative.[233] Alzheimer's disease is known for placing a great burden on caregivers which includes social, psychological, physical or economic aspects.[14][234][235] Home care is usually preferred by people with AD and their families.[236] This option also delays or eliminates the need for more professional and costly levels of care.[236][237] Nevertheless, two-thirds of nursing home residents have dementias.[183]
Dementia caregivers are subject to high rates of physical and mental disorders.[238] Factors associated with greater psychosocial problems of the primary caregivers include having an affected person at home, the carer being a spouse, demanding behaviours of the cared person such as depression, behavioural disturbances, hallucinations, sleep problems or walking disruptions and social isolation.[239][240] Regarding economic problems, family caregivers often give up time from work to spend 47hours per week on average with the person with AD, while the costs of caring for them are high. Direct and indirect costs of caring for an Alzheimer's patient average between $18,000 and $77,500 per year in the United States, depending on the study.[231][233]
Cognitive behavioural therapy and the teaching of coping strategies either individually or in group have demonstrated their efficacy in improving caregivers' psychological health.[14][241]
Media

AD has been portrayed in films such as: Iris (2001), based on John Bayley's memoir of his wife Iris Murdoch;[242] The Notebook (2004), based on Nicholas Sparks' 1996 novel of the same name;[243] A Moment to Remember (2004);Thanmathra (2005);[244] Memories of Tomorrow (Ashita no Kioku) (2006), based on Hiroshi Ogiwara's novel of the same name;[245] Away from Her (2006), based on Alice Munro's short story "The Bear Came over the Mountain";[246] Still Alice (2014), about a Columbia University professor who has early onset Alzheimer's disease, based on Lisa Genova's 2007 novel of the same name and featuring Julianne Moore in the title role. Documentaries on Alzheimer's disease include Malcolm and Barbara: A Love Story (1999) and Malcolm and Barbara: Love's Farewell (2007), both featuring Malcolm Pointon.[247][248][249]
Research directions

Drugs
In the decade 2002–2012, 244 compounds were assessed in Phase I, Phase II, or Phase III trials, and only one of these (memantine) received FDA approval (though others were still in the pipeline).[250] Solanezumab failed to show effectiveness in patients who already had Alzheimer's symptoms.
One area of clinical research is focused on treating the underlying disease pathology. Reduction of beta-amyloid levels is a common target of compounds[251] (such as apomorphine) under investigation. Immunotherapy or vaccination for the amyloid protein is one treatment modality under study.[252] Unlike preventative vaccination, the putative therapy would be used to treat people already diagnosed. It is based upon the concept of training the immune system to recognise, attack, and reverse deposition of amyloid, thereby altering the course of the disease.[253] An example of such a vaccine under investigation was ACC-001,[254][255] although the trials were suspended in 2008.[256] Another similar agent is bapineuzumab, an antibody designed as identical to the naturally induced anti-amyloid antibody.[257] However, immunotherapeutic agents have been found to cause some concerning adverse drug reactions, such as amyloid-related imaging abnormalities.[258] Other approaches are neuroprotective agents, such as AL-108,[259] and metal-protein interaction attenuation agents, such as PBT2.[260] A TNFα receptor-blocking fusion protein, etanercept has showed encouraging results.[261]
In 2008, two separate clinical trials showed positive results in modifying the course of disease in mild to moderate AD with methylthioninium chloride, a drug that inhibits tau aggregation,[262][263] and dimebon, an antihistamine.[264]
The consecutive phase-III trial of dimebon failed to show positive effects in the primary and secondary endpoints.[265][266][267] Work with methylthioninium chloride showed that bioavailability of methylthioninium from the gut was affected by feeding and by stomach acidity, leading to unexpectedly variable dosing.[268] A new stabilised formulation, as the prodrug LMTX, is in phase-III trials (in 2014).[269]
Behavioral prevention
Preliminary research on the effects of meditation on retrieving memory and cognitive functions have been encouraging.[270]  A 2015 review suggests that mindfulness-based interventions may prevent or delay the onset of mild cognitive impairment and Alzheimer's disease.[271]
Possible transmission
Rare cases of possible transmission between people are being studied,[272] e.g. to growth hormone patients.[273]
Infections
The herpes simplex virus HSV-1 has been found in the same areas as amyloid plaques.[274] This suggested the possibility that AD could be treated or prevented with antiviral medication.[274][275] Studies of antivirals in cell cultures have shown promising results.[276]
Fungal infection of AD brain has also been described.[277]
This hypothesis was proposed by the microbiologist L. Carrasco when his group found statistical correlation between disseminated mycoses and AD.[278]
Further work revealed that fungal infection is present in different brain regions of AD patients, but not in the control individuals.[279]
[280]
A fungal infection explains the symptoms observed in AD patients. The slow progression of AD fits with the chronic nature of some systemic fungal infections, which can be asymptomatic and thus, unnoticed and untreated.[279]
The fungal hypotheses are also compatible with some other established AD hypotheses, like the amyloid hypothesis, that can be explained as an immune system response to an infection in the CNS,[281][282][283] as found by R. Moir and R. Tanzi in mouse and worm models of AD.
Imaging

Of the many medical imaging techniques available, single photon emission computed tomography (SPECT) appears to be superior in differentiating Alzheimer's disease from other types of dementia, and this has been shown to give a greater level of accuracy compared with mental testing and medical history analysis.[284] Advances have led to the proposal of new diagnostic criteria.[22][116]
PiB PET remains investigational, but a similar PET scanning radiopharmaceutical called florbetapir, containing the longer-lasting radionuclide fluorine-18, is a diagnostic tool in Alzheimer's disease.[285][286]
Amyloid imaging is likely to be used in conjunction with other markers rather than as an alternative.[287] Volumetric MRI can detect changes in the size of brain regions. Measuring those regions that atrophy during the progress of Alzheimer's disease is showing promise as a diagnostic indicator. It may prove less expensive than other imaging methods currently under study.[288]
In 2011 An FDA panel voted unanimously to recommend approval of florbetapir. The imaging agent can help to detect Alzheimer's brain plaques.[289] A negative scan indicates sparse or no plaques, which is not consistent with a diagnosis of AD.[290]
Early diagnosis
Emphasis in Alzheimer's research has been placed on diagnosing the condition before symptoms begin.[291] A number of biochemical tests have been developed to enable earlier detection. Some such tests involve the analysis of cerebrospinal fluid for beta-amyloid, total tau protein and phosphorylated tau181P protein concentrations.[292] Because drawing CSF can be painful, repeated draws are avoided. A blood test for circulatory miRNA and inflammatory biomarkers is a potential alternative indicator.[292]

Further reading

Library resources about
 Alzheimer's Disease

 at Curlie


The South Beach Diet is a popular fad diet developed by Arthur Agatston and promoted in a best-selling 2003 book.[1][2][3]  It emphasizes eating high-fiber, low-glycemic carbohydrates, unsaturated fats, and lean protein, and categorizes carbohydrates and fats as "good" or "bad".[4] Like other fad diets,[5] it may have elements which are generally recognized as sensible, but it promises benefits not backed by supporting evidence or sound science.[1][6]
Technique
The diet has three stages, and gradually increases the proportion of carbohydrate consumed as it progresses while simultaneously decreasing the proportions of fat and protein.[7] It includes a number of recommended foods such as lean meats and vegetables, and has a concept of "good" (mostly monounsaturated) fats.[7] It makes no restriction on calorie intake, includes an exercise program, and is based around taking three main meals and two snacks per day.[8]
The first stage of the diet aims for rapid weight loss (13lbs in two weeks).  According to the UK's National Health Service (NHS), the severity of the first stage of the diet may result in the loss of some vitamins, minerals and fiber. The NHS reports that dietary restrictions during stage one may cause side effects including "bad breath, a dry mouth, tiredness, dizziness, insomnia, nausea and constipation."[8] Such symptoms would be rectified once the less extreme phases of the diet then began.[8]
Health effects
Like other fad diets, the South Beach Diet has been marketed with bold claims that are not supported by evidence and with an unrealistic promise of easy weight loss.[6] The book which promotes it also contains some incorrect and misleading information.[1][4] Nevertheless, some aspects of the diet correspond with dietary advice which is recognized as sensible:[6] its last two stages are sufficiently nutritious to be considered healthy.[8] Like other high-fat diets, its short-term safety has been established, but its long-term safety has not.[9]
The diet is promoted as improving risk factors associated with cardiovascular disease, but the effectiveness for improving these risk factors is unclear because no evidence on its effects is available.[10] A trial found no change in weight loss compared to usual care.[10]
South Beach Diet and other low carbohydrate diets lack dietary fiber. Fiber is generally considered to aid weight loss and to help prevent obesity.[11]
Difference from other low-carb diets
Many sources place the South Beach Diet on lists of "low carb" diets such as the Atkins Diet. While the South Beach diet does prohibit foods rich in simple carbohydrates such as white bread, white potatoes and white rice,[12] it does not require dieters to forgo carbohydrates entirely or even measure their intake. Instead, it focuses on the "glycemic impact" (short term change in blood glucose) of foods.  (Nutritionists continue, however, to question the net benefit of the first phase to dieters not affected by impaired glucose metabolism.) Many vegetables are permitted even in phase 1. Complex, fiber-rich carbohydrate sources such as brown rice and 100% whole grain bread are permitted during phase 2. Agatston has tried to distance the South Beach Diet from "low carb" approaches; in the South Beach Diet book he wrote: "It is my purpose to teach neither low-fat nor low-carb. I want you to learn to choose the right fats and the right carbs."[13]:22–23
History
The South Beach Diet was developed in the mid-1990s by celebrity doctor Arthur Agatston with the assistance of Marie Almon, the former chief dietitian at Mount Sinai Medical Center in Miami Beach, Florida.[14][15][16] Originally called the Modified Carbohydrate Diet, the plan was renamed the South Beach Diet after the South Beach neighborhood in Miami Beach near Agatston's practice.[15]
The diet plan was initially developed for Agatston's own patients.  Agatston noticed that the American Heart Association's then-recommended low-fat and high-carbohydrate diet was not lowering his patients' weight, cholesterol or blood sugar levels, but that his patients on the Atkins diet were experiencing weight loss. Unwilling to prescribe the Atkins approach to patients with cardiac issues due to the diet's allowance of saturated fat and limitation of carbohydrates containing fiber and other nutrients, Agatston referenced medical research to build an eating plan that categorized fats and carbohydrates as good or bad and emphasized lean protein and fiber.[17]
The plan grew in popularity as a method of weight loss as Agatston reported the results at conferences and patients distributed photocopies outlining the diet throughout the late 1990s and early 2000s.[17] In 1999 a Miami TV news show put people on the diet and broadcast the results, popularizing the diet locally.[16][18]
The first book describing the diet, The South Beach Diet, was written by Agatston and was released in April 2003.[4][15][19]  By 2004 there about 8 million copies in print, a trade paperback South Beach Diet Good Fats/Good Carbs Guide had 3 million copies in print, and The South Beach Diet Cookbook went on sale with a printing of 1.75 million copies.[15]
In 2004, the former US President Bill Clinton was reported as being on the diet.[20]
In 2008, Agatston published The South Beach Diet Supercharged, written with Joseph Signorile, a professor of exercise physiology; it included an interval training program.[21] A review for the Academy of Nutrition and Dietetics found that "Readers are likely to see success using this diet and fitness book. I recommend skipping the restrictive Phase One meal plans and instead follow the more balanced Phase Two diet. The simple 20-minute-a-day exercise program is a realistic and inexpensive approach to fitness."[21]
SBD Enterprises LLC, of which Agatston is a part owner,[22] owns the "South Beach Diet" trademark.[23]  In December 2015 Nutrisystem acquired SBD for $15 million.[22][24]:20–21[25]  Nutrisystem, a publicly traded company, reported that in 2015 it spent $124 million in marketing[24]:13 and had $463M in revenue.[24]:24  It also said that it planned to launch new lines of South Beach products by 2017 that it would market through retail stores and on the internet.[22][24]:21
See also
List of diets
Low-glycemic index diet
Online weight loss plans

Further reading