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Trishul (missile)

Trishul (IAST: triśūla "Trident") is a low-level quick-reaction short range surface-to-air missile developed in India by Defence Research and Development Organisation (DRDO) as part of the Integrated Guided Missile Development Programme (IGMDP). It can also be used as an anti-sea skimmer from naval ship against low flying missile, attack helicopter and aircraft.

In 2008, Minister of Defence A. K. Antony officially announced the closure of the project on a written reply to Rajya Sabha after completion of Technology Demonstration (TD) phase. The development cost of Trishul Project was inr 2826000000.

History and development
The Trishul missile project was commissioned in 1983 as a part of Integrated Guided Missile Development Programme. The primary objective was to produce short range surface to air missile with a reaction time below 6 seconds. In 1985, Trishul made its first unguided flight from Satish Dhawan Space Centre, Sriharikota. The missile made its first full range guided flight in 1989 but without television guidance (TVM) which was originally planned. Indian Army and Indian Air Force (IAF) wanted Trishul to replace the Soviet-era 9K33 Osa. On the other hand, Indian Navy wanted to purchase Barak 1 and Kashtan CIWS for point-defence role since Pakistan began acquiring Harpoon and Exocet from 1980s. By the late 1990's, DRDO pushed Trishul as an alternative to Barak 1 for Indian Navy. One of the biggest challenge faced by DRDO is to make Trishul skim just 5 meters above the sea waves at supersonic speed.

The project was planned to be completed by 1992 and to be fitted in Brahmaputra-class frigates as an anti-sea skimmer. In 1992, the missile was successfully fired reaching Mach 2 speed following a predetermined trajectory against a target mounted 7 meter above sea but variation in altimeter led to test failure. In 1997, the associated radar systems for detecting the incoming sea-skimmer were operational at INS Dronacharya, but Indian Navy expressed its displeasure in the developmental delay of Trishul for the Brahmaputra-class frigates and finally opted for Barak 1. Trishul was unable to complete all the static trials from a fixed launcher until 1998. By May 1998, Bharat Dynamics Limited (BDL) was able to produce Trishul while the 27 tonne launch system was developed by Bharat Heavy Electricals Limited (BHEL). The first missile produced by BDL was test fired against Northrop BQM-74 Chukar in June.

Upon reviewed by DRDO and the Indian Armed Forces in October 2001, the missile system was found deficient as the tracking radar beam was getting intermittent breaks resulting in the missile missing the target and the heavy BMP-2 chassis did not meet the General Staff Qualitative Requirements (GSQRs) for swift mobility due to heavy weight. On 25 January 2002, the naval variant of Trishul was test fired from INS Dronacharya but failed at sea-skimming capability.

In 2003, Government of India announced that the missile will be a technology demonstrator and de-linked it from Integrated Guided Missile Development Programme. But Ministry of Defence (MoD) was not interested in downgrading the Trishul Missile project. After modification in guidance, sub-systems and propellant composition, four missiles in full combat configuration was launched from BMP-2 from June 22 to June 25, 2003. The test achieved miss distance against moving targets above the specified requirement of the Indian Armed Forces. All the sub-systems, air frames, controls, integrated with ground control system of the combat vehicle worked well. By this time Trishul became more of a research and development oriented project instead of a user driven one backed by the armed forces. Trishul was successfully test fired from Integrated Test Range (ITR) on 10 February, 26 March and 27 March of 2004. On 5 October 2005, Trishul fired towards the sea from ITR was able to hit a pilot-less target aircraft.

Until October 2006, 80 flight tests were already completed and DRDO was in dialogue with the IAF for user trials and induction. In 2006, Minister of Defence Pranab Mukherjee granted one year extension to Trishul project. Due to project delays, and modification of GSQRs and operational requirements over time, Trishul no longer able to meet the need of the end users. For continuation of the project and funding, it was proposed that the missile will be deployed in certain locations to conduct training, fire control, and air defence practice. As per Ministry of Defence (MoD), Trishul Project met the performance parameters set by the original GSQRs but failed to achieve the perfect three-beam guidance and development of millimeter-wave active radar homing seeker. The team of 200 scientists working on Trishul were reassigned for Barak 8, a joint project between DRDO and Israel Aerospace Industries (IAI). IAF finally selected SPYDER as an alternative to Trishul. To fulfill IAF requirement, DRDO made another attempt with MBDA on a joint project called Maitri. But it got cancelled due to lack of interest. All the proven technologies and learning from Trishul later helped DRDO in QRSAM and VL-SRSAM. People who worked on Trishul and Barak 8 termed the basic design flaw as one of the many reasons behind the project failure.

Characteristics
Trishul has a range between 300 m to 9 km. DRDO also made an enhanced 11 km range variant for the Indian Air Force. It is powered by a Dual-thrust propulsion stage using high-energy solid propellant. Trishul weighs 130 kg and is capable of carrying a 15 kg warhead. Trishul is 3 m in length and 20 cm in diameter. The modified naval variant use command to line-of-sight guidance mechanism. The missile can be employed against sea skimmers with a fire control radar. Trishul flies at supersonic speed. It has a low altitude radio altimeter and height lock loop control.

title: Trishul (missile)


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Rhonda Ross Kendrick

Rhonda Ross Kendrick (born Rhonda Suzanne Silberstein; August 14, 1971) is an American singer and former actress. Kendrick is the daughter of singer and actress Diana Ross and the biological child of Motown Records founder Berry Gordy; however, her legal father is Robert Ellis Silberstein, as her mother was married to him before she was born and he is the father who raised her.

Early life
At the time of Rhonda's birth, Diana Ross was married to her first husband, Robert Ellis Silberstein. Ross, Gordy, and Silberstein all knew of Rhonda's parentage. She was publicly presented as the daughter of Ross and Silberstein, and he raised her. When she was 13, she was told Gordy was her biological father. Ross Kendrick has said that the revelation came as a relief. She was beginning to notice physical differences between herself and her younger sisters. The revelation gave her an answer to the situation. Rhonda Ross Kendrick is the eldest of Diana Ross' five children and the seventh of Berry Gordy's eight biological children. She is a graduate of Brown University.

Career
Ross Kendrick's most famous acting credit is Toni Burrell on Another World. She played the role from 1997 to 1999 and was nominated for a Daytime Emmy Award in 1998. She also appeared in the movie The Personals (1999) with Malik Yoba as well as The Temptations miniseries with her relative Bianca Lawson. In 2004, she released her debut live album Rhonda Ross Live Featuring Rodney Kendrick.

After working for two years as an agent with the firm Citi Habitats, she founded Ross Realty International, a real-estate brokerage firm in New York City in 2008.

In 2013, she joined her mother on the In the Name of Love Tour as the opening act for her concerts. In July 2016, she released her first studio album In Case You Didn't Know. The album spawned the singles "Summer Day" and "In Case You Didn't Know".

During the COVID-19 lockdown, Rhonda contributed her songwriting talents to her mother's Grammy nominated album Thank You released on Decca Records in late 2021. The album included the single "All is Well" co-written by Rhonda, her mother, and celebrated songwriter and background singer Fred White.

Personal life
On September 14, 1997, she married jazz musician Rodney Kendrick. On August 7, 2009, she gave birth to their son.

Discography

 * Rhonda Ross Live Featuring Rodney Kendrick (2004)
 * In Case You Didn't Know (2016)

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Rhonda Ross Kendrick


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XCBL

xCBL is a collection of XML specifications (both DTD and XML Schema) for use in e-business. It was created by Commerce One Inc. and is maintained by Perfect Commerce.

History
xCBL was originally called Common Business Library (CBL). The xCBL standardization began in 1997.

This led to the creation of xCBL 2.0 which covered 12 different business document specifications, mainly meant for electronic document communication in business-to-business (B2B) procurement over the Internet. xCBL 2.0 was mainly based on existing Electronic Data Interchange (EDI) standards and introduced the Schema for Object-Oriented XML (SOX) schema library for XML validation.

 * xCBL 3.0 contained several new business specifications and categories. It also introduced the use of several XML Schema standards.

 * xCBL 3.5 (October 2001) contained nine new business documents. OASIS used this version as the starting point for defining business documents in Universal Business Language (UBL).

 * xCBL 4.0 (March 2003) is the latest version of xCBL. It consists of 44 business documents in eight categories.

Use
As an XML document standard, xCBL is used primarily in B2B procurement tools for buyers, order and invoice management tools for suppliers and document routing tools for public and private marketplaces.

For xCBL message transport, Commerce One created an envelope messaging standard called MML (Marketsite Messaging Layer) based on the SMTP MIME format to provide both payload (xCBL) and attachment support.

title: XCBL


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Kazimierz Kutz

Kazimierz Julian Kutz (16 February 1929 – 18 December 2018) was a Polish film director, author, journalist and politician, one of the representatives of the Polish Film School and a deputy speaker of the Senate of Poland.

Biography
Kazimierz Kutz was born on 16 February 1929 in Szopienice, since 1960 district of Katowice, to a railway worker and a former partisan of the Silesian Uprisings. After the World War II Kutz graduated from gymnasium in Mysłowice and in 1949 was admitted to the Łódź Film School. After finishing his studies in 1954 he started working as an assistant to Andrzej Wajda.

His film debut was Krzyż Walecznych (1959). Since then he finished more than 20 pictures, including six about his home region - Silesia. He is also famous for directing theatre plays on some of the most prominent scenes of Poland, including National Stary Theatre in Kraków and National Theatre in Warsaw, as well as several plays for the Polish television. In 1972, he founded the Silesia Film Company in Katowice and, until 1978, was its Artistic Director.

In the 1970s he became the main director of the Polish Television branch in Katowice. He was also working for several branch and cultural organisations. After the Martial Law had been imposed in Poland in 1981 Kutz was interned by the communist authorities, but was released soon afterwards. Between 1981 and 1983, lectured in the Radio and Television Faculty at Silesian University in Katowice, and, between 1985 and 1991, taught directing at the Higher Theatre School in Kraków. Since 1987, was Principal Director in the Polish Television Centre in Katowice and, between 1990 and 1991, headed the Centre. After the peaceful transition to democracy in 1989 Kutz became the head of the Polish TV branch in Kraków (until 1991).

For his involvement in the matters of Silesia, and for his films depicting the traditions and problems of that part of Poland, he was considered by some the spokesman of all Silesians. In a plebiscite organised by Gazeta Wyborcza newspaper he was chosen the third most famous Silesian ever and the first among the people living at the time. In 1997 he was awarded with the title of doctor honoris causa by the University of Opole. He was a promoter and patron of several Silesia-based cultural feasts and societies, including the Festiwal Filmów Kultowych, Festiwal Sztuki Reżyserskiej, Cultural Congress of the Upper Silesia, Council of Culture of the Silesian Voivodship, Academy of Fine Arts in Katowice and Committee for the Construction of Silesian Museum. He was also one of the supporters of development of the Silesian language.

His 1995 film Reverted was entered into the 19th Moscow International Film Festival.

In 1997 Kutz took part in the elections to the Senate of Poland (from the list of Freedom Union party, Katowice constituency) and was supported by approximately 500,000 Silesians. In 2001 he was elected for his second term as a non-partisan candidate, and in 2005 re-elected for the third term. Recently, he was the deputy speaker of the Senate of Poland. For his social involvements he was awarded with many of the highest Polish awards.

Kazimierz Kutz was married to Iwona and had two sons (Gabriel and Tymoteusz) and two daughters (Wiktoria and Kamila).

Filmography

 * 1958 - Krzyż walecznych
 * 1960 - Nikt nie woła
 * 1961 - Tarpany
 * 1961 - Ludzie z pociągu
 * 1963 - Milczenie
 * 1964 - Upał
 * 1966 - Ktokolwiek wie...
 * 1967 - Skok
 * 1969 - Salt of the Black Earth (Sól ziemi czarnej)
 * 1971 - Pearl in the Crown (Perła w koronie)
 * 1974 - Linia
 * 1975 - Znikąd donikąd
 * 1979 - The Beads of One Rosary (Paciorki jednego różańca)
 * 1983 - Na straży swej stać będę
 * 1986 - Wkrótce nadejdą bracia
 * 1993 - Straszny sen Dzidziusia Górkiewicza
 * 1994 - Reverted (Zawrócony)
 * 1994 - Śmierć jak kromka chleba
 * 1995 - Colonel Kwiatkowski (Pułkownik Kwiatkowski)
 * 1997 - Sława i chwała
 * 2004 - Stare srebra

title: Kazimierz Kutz


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Giuseppe Di Stefano

Giuseppe Di Stefano (24 July 1921 – 3 March 2008) was an Italian operatic tenor who sang professionally from the mid-1940s until the early 1990s. Called Pippo by both fans and friends, he was known as the "Golden voice" or "The most beautiful voice", as the true successor of Beniamino Gigli. Luciano Pavarotti said he modeled himself after Di Stefano. In an interview Pavarotti said "Di Stefano is my idol. There is a solar voice...It was the most incredible, open voice you could hear. The musicality of Di Stefano is as natural and beautiful as the voice is phenomenal". Di Stefano was also the tenor who most inspired José Carreras. He died on 3 March 2008 as a result of injuries from an attack by unknown assailants.

Early life and musical training
Giuseppe Di Stefano was born in Motta Sant'Anastasia, a village near Catania, Sicily, in 1921. He moved to Milan with his parents when he was six. He was the only son of a carabiniere turned cobbler and his dressmaker wife. Di Stefano was educated at a Jesuit seminary and briefly contemplated entering the priesthood.

When he was 16, he burst into song after losing a game of cards, and the friend with whom he was playing said he must get his voice trained. Two years later he began studying in earnest with the baritones Luigi Montesanto and Mariano Stabile, the latter impressing on the young tenor the importance of clear diction, advice he readily followed.

World War Two interrupted Di Stefano's early career as he had to join the Italian army, where he often entertained the troops with his singing. He was considered such a bad soldier that his commanding officer decided that he would better serve his country by leaving the forces in order to sing. He performed under the pseudonym Nino Florio until Italy was defeated, when he fled to Switzerland. After a period of internment he was allowed to sing on Lausanne Radio, where he made the first of his recordings, disclosing a tenor voice of decided beauty and a singer with personality. He recorded many of his native Sicilian songs, records of which first brought him to the attention of discerning ears outside Italy in the late 1940s.

Career
He began his career as a lyric tenor, notable in roles such as Nemorino in Donizetti's L'Elisir d'Amore and Alfredo in Verdi's La Traviata. He made his New York debut at the Metropolitan Opera in February 1948 as the Duke of Mantua in Verdi's Rigoletto after singing the role in Riccione with Hjördis Schymberg in August of the previous year. After his performance in Manon a month later, Musical America wrote that Di Stefano "had the rich velvety sound we have seldom heard since the days of Gigli". He went on to perform regularly in New York for many years. In 1957, Di Stefano made his British debut at the Edinburgh Festival as Nemorino in L'elisir d'amore and his Royal Opera House, Covent Garden, debut in 1961, as Cavaradossi in Tosca.

As a singer, Di Stefano was admired for his excellent diction, unique timbre, passionate delivery and, in particular, for the sweetness of his soft singing. In his Metropolitan Opera radio broadcast debut in Faust, he attacked the high C forte and then softened to a pianissimo. Sir Rudolf Bing said in his memoirs, "The most spectacular single moment in my observation year had come when I heard his diminuendo on the high C in "Salut! demeure" in Faust: I shall never as long as I live forget the beauty of that sound".

During his years of international celebrity, Di Stefano won a gold Orfeo, an Italian musical award.

In 1953 Walter Legge, leader of EMI's classical wing, wanted a tenor to record all the popular Italian operas with Maria Callas, and chose Di Stefano. Among their recording achievements was the famous 1953 studio recording of Tosca under Victor de Sabata, which is considered "as being one of the great performances in the history of the gramophone". The two also performed together on stage frequently, from 1951 in South America to the end of 1957 in Un ballo in maschera at La Scala, the last time the two collaborated in an opera. He sang Alfredo in the famous Visconti production of La traviata in 1955 at La Scala, as well as Edgardo to her Lucia under Herbert von Karajan at La Scala, Berlin and Vienna. Rudolf Bing of the Metropolitan Opera House lamented Di Stefano's playboy lifestyle, which he felt was the cause of his vocal decline, although Di Stefano himself blamed allergies to synthetic fibres for permanently damaging his vocal cords.

In 1973, Di Stefano and Maria Callas went together for a recital tour that ended in 1974: critics remarked that Maria Callas had lost her voice, but the public reaction was nevertheless enthusiastic everywhere. It was during this period that there were rumors of a brief romantic relationship between the two singers. Di Stefano continued to sing successfully and his final operatic role was as the Emperor in Turandot, in July 1992.

Private life and death
In 1949 he married the conservatory student Maria Girolami in New York, with whom he had three children. The pair separated in 1976. In 1977 he began a new romantic relationship with Monika Curth, an operetta soprano originally from Hamburg, whom he married in 1993.

His last public appearance was on 24 October 2004 in Oderzo to receive an award.

On 3 December 2004, he was seriously injured during a robbery at his home in Diani Beach in Kenya by unknown assailants who left him on the ground bloodied and unconscious. After being admitted to a hospital in Mombasa, his condition proved to be more serious than it had appeared at first. After undergoing at least three operations, he went into a coma on 7 December. On 23 December, he was transferred to Italy, where he was hospitalised in Milan. Eventually he awoke from the coma, but his health never fully improved. He died in his home in Santa Maria Hoè, north of Milan, on 3 March 2008 at the age of 86.

Vocal and singing style
Di Stefano was a lyric tenor with a soft voice, an unmistakable warm and rich timbre and, at least in the early years, was very expansive. He was admired for his vocal skills, clear diction, passionate phrasing, captivating interpretation and the exquisite lightness of pianissimo and shades. Far from the studious precision and "aplomb" of a Bjorling or a Kraus, or the vocal overpowering of a Del Monaco or stylistic rigour of a Bergonzi, Di Stefano had a natural musicality, with a generous, instinctive and communicative style of singing.

Di Stefano can be placed in the tradition of tenori lirici post-romantic of the Italian and French repertoire, where he gave memorable performances especially in the first part of his career (Rigoletto, La traviata, La bohème, The pearl fishermen, Manon, Faust). In the following years he developed into roles of the lyrical repertoire, with more drive and drama (Tosca, La forza del destino, Turandot, Carmen, up to Pagliacci and Andrea Chénier).

Recordings with Maria Callas

Di Stefano and Maria Callas recorded many operas together, all of which for EMI. Together they recorded the following complete operas:

 * Lucia di Lammermoor – 1953
 * I puritani – 1953
 * Cavalleria rusticana – 1953
 * Tosca – 1953
 * Pagliacci – 1954
 * Rigoletto – 1955
 * Il trovatore – 1956
 * La bohème – 1956
 * Un ballo in maschera – 1956
 * Manon Lescaut – 1957

A series of duets with Di Stefano and Callas was recorded by the Philips label in the period November–December 1972, with Antonio de Almeida conducting the London Symphony Orchestra. These recordings were not published officially, but a 'pirate' version did appear.

Other recordings
Di Stefano also made many other recordings with other wonderful singers, complete EMI sets of Madama Butterfly (opposite Victoria de los Ángeles, 1954) and La traviata (with Antonietta Stella and Tito Gobbi, 1955).

For English Decca he recorded L'elisir d'amore with Hilde Gueden and Fernando Corena (1955), La Gioconda (with Zinka Milanov and Leonard Warren, 1957), La forza del destino (1958) and Tosca (with Leontyne Price and Giuseppe Taddei, Herbert von Karajan conducting, 1962).

For Ricordi (Ricordi MRO 104/105), he made a complete stereo Lucia di Lammermoor with Renata Scotto, Ettore Bastianini and Ivo Vinco in 1958, with Nino Sanzogno conducting the Orchestra and Chorus of La Scala, Milan.

In 1995, VAI issued an approved version of La bohème, from a 1959 performance in New Orleans, with the tenor starring opposite Licia Albanese, Audrey Schuh, Giuseppe Valdengo and Norman Treigle. Additionally, in 1962 the tenor recorded excerpts from Massenet's Manon, with Anna Moffo, conducted by René Leibowitz.

In 1951, Di Stefano sang in a performance of Verdi's Requiem, at Carnegie Hall, conducted by Arturo Toscanini, the other soloists being Herva Nelli, Fedora Barbieri and Cesare Siepi. It was released as a recording by RCA.

Single songs

 * Che gelida manina, Pourquoi me revéiller, Una furtiva lagrima, E lucevan le stelle, Del tempio al limitar (con Giuseppe Marchiò) RADIO LOSANNA-EMI 1945
 * È la solita storia del pastore, Oh dolce incanto, Ed anche Beppe amò, Mi par d'udire ancora RADIO LOSANNA-EMI 1946
 * Ah dispar vision, E lucevan le stelle, De' miei bollenti spiriti, È la solita storia del pastore, Addio Mignon, Ah non-credevi tu HMV 1947
 * Com'è gentil, Pourquoi me revellier EMI 1951
 * Firenze è come un albero fiorito, Non piangere Liù, Nessun dorma, Ch'ella mi creda, Or son sei mesi, Oh tu che in seno agli angeli EMI 1955
 * Ah mi parla di lei, Tardi si fa, Notte d'amor, Già nella notte densa, Oh come al tuo sottile, Leila, Leila mia, Non hai compreso (con Rosanna Carteri) EMI 1957
 * Un dì all'azzurro spazio, Come un bel dì di maggio, Recondita armonia, E lucevan le stelle, Non piangere Liù, Nessun dorma, Pourqoui me revellier, En fermant les yeux, La fleur, Salut demeure, De mon amie, fleur endormie Decca 1958

title: Giuseppe Di Stefano


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User talk:Hangleton79

Welcome!

Hello, and welcome to Wikipedia. Thank you for your contributions. I hope you like the place and decide to stay. Here are a few good links for newcomers: I hope you enjoy editing here and being a Wikipedian! By the way, you can sign your name on Talk and vote pages using three tildes, like this: ~ ~ ~. Four tildes (~ ~ ) produces your name and the current date. If you have any questions, see the help pages, add a question to the village pump or ask me on my Talk page. Again, welcome! -- [[User:MacGyverMagic|Mgm|(talk)]] 12:25, Dec 6, 2004 (UTC)
 * How to edit a page
 * Editing tutorial
 * Picture tutorial
 * How to write a great article
 * Naming conventions
 * Manual of Style

title: User talk:Hangleton79


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Charles Kirk Clarke

Charles Kirk Clarke (1857 – 20 January 1924) was a psychiatrist who was influential in Canadian politics.

Early life
Clarke was born on 16 February 1857 in Elora, Canada West, son of a prominent Ontario parliamentarian.

Career
Clarke graduated from University of Toronto in 1879 and went on to found the Canadian National Committee for Mental Hygiene (now the Canadian Mental Health Association) in 1914 with Clarence Hincks.

As Dean of the Faculty of Medicine at University of Toronto, he oversaw creation of the Department of Psychiatry, and development of the medical school.

Clarke first practised psychiatry at the 999 Queen Street institution in Toronto, Ontario. In 1880, then took a post at the Hamilton, Ontario asylum.

Clarke was a student and brother-in-law of Joseph Workman, Superintendent of the Toronto Asylum. Clarke was an early proponents of eugenics, emphasizing the importance of restrictive laws that would limit the immigration and marriage of the "mentally defective." To them, such laws seemed necessary to stem the explosive growth of state and provincial mental asylums where foreign-born patients made up more than 50 percent of the hospital population. Further, the growth of hereditarian views in science supported eugenic proposals; psychiatry's desire for greater respectability in the medical profession made eugenic "science" attractive. By 1905, Clarke had abandoned the movement, and many of the other leading psychiatrists would follow suit by the end of World War I, when it was clear that eugenic measures were not having the desired effects.

Clarke joined his other brother-in-law, William Metcalfe at the Rockwood Asylum for the Criminally Insane, the psychiatric hospital in Kingston in 1881 and began a series of reforms in the care of the insane. One of these was freeing patients from confinement. On 13 August 1885, a paranoid patient attacked them both and killed Metcalfe. Clarke survived and succeeded his brother-in-law as Medical superintendent of facility. Clarke carried on in Kingston until 1905 when he succeeded Daniel Clark as superintendent of the Toronto Asylum. In 1911 he resigned from government service and was appointed superintendent of the Toronto General Hospital.

Family
Clarke was married to Margaret DeVeber (from 1880 until her death in 1902 ) with whom he had four sons and two daughters. Three of his sons were active as ice hockey players on professional or amateur levels in Canada and the United States. Charles Marshall Clarke (1881–1940) played with the Kingston Frontenacs and the Queen's University team in Kingston, Ontario, and with the New York Athletic Club and the New York Wanderers in the AAHL, Harold Metcalfe Clarke (1885–1924) played with the Kingston Frontenacs, the University of Toronto, and with the New York Athletic Club, and Herbert Secord Clarke (1887–1938) played with the Kingston Frontenacs, the University of Toronto, and with the Cobalt Silver Kings of the National Hockey Association.

From 1904 until his death in 1924 Clarke was married to Theresa Gallagher.

End of life
Clarke became ill in the autumn of 1923 and died in Toronto early the next year. A headline in the Toronto Sunday World of 23 March 1924 read "Canada owes immeasurable debt to Dr. C.K. Clarke who helped to lift the shadow of misery and hopelessness from insane asylums". The Clarke Institute of Psychiatry in Toronto, Ontario, Canada was named in his honour.

title: Charles Kirk Clarke


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Seigmen

Seigmen (formed in 1989 in Tønsberg, Vestfold, Norway) is a Norwegian alternative rock band who came into prominence in the early 1990s. The band's name is derived from Norwegian sweets brand Laban Seigmenn. The band went from a hard-edged grunge-like style to a more dynamic sound with more ambient parts and use of synthesizers and various audio-effects.

History
The band was formed in Tønsberg, Norway, in 1989. Økshoff and Møklebust started a band with the name Klisne Seigmenn having their first gig at the “Julerock” (“Christmas rock”) event in Tønsberg on December 27, 1989. In 1990, Christensen, Ljung and Ronthi joined the band. They recorded several studio albums, including two with American producer Sylvia Massy in Los Angeles. After a farewell tour they split, relocated to Los Angeles and formed Zeromancer in January 2000.

Seigmen reunited during the UKA-festival in Trondheim on October 20, 2005, and decided in November 2005 to do even more reunion gigs in Norway: there were seven shows in February 2006. Having great success with the reunion tour, they did six more gigs at various festivals across Norway during summer 2006, mostly as the headlining act. Media reports that summer said that Seigmen did not rule out another reunion some time in the future. In early 2008 it was announced that Seigmen would again play live, which they did on June 21 the Oslo Opera House, as one of the shows celebrating the opening of the new Opera House in Oslo. Selling out the show quickly, a second concert was set up the day after. In 2013 they contributed to the book "Think like a rockstar" Tenk som en rockestjerne, by Ståle Økland. Seigmen released a new album Enola in 2015.

Members

 * Kim Ljung (bass guitar, vocals)
 * Alex Møklebust (main vocals)
 * Noralf Ronthi (percussion)
 * Marius Roth Christensen (guitar, vocals)
 * Sverre Økshoff (guitar)

Møklebust, Ljung and Ronthi formed the band Zeromancer in 2000. Ljung also has a solo project under the name Ljungblut.

Albums

 * Ameneon (1993)
 * Total (1994) Norway #19
 * Metropolis (1995) Norway #1
 * Metropolis - The Grandmaster Recordings (English language version of Metropolis) (1996) Norway #11
 * Radio Waves (1997) Norway #1
 * Enola (2015)
 * Resonans (2024)

Singles/EPs

 * Pluto (1992)
 * "Monsun" (1993)
 * "Hjernen er alene" (1994) Norway #5
 * "Döderlein" (1994) Norway #14
 * "Lament" (1994)
 * "Metropolis" (1995) Norway #4
 * "Slaver av solen" (1995) Norway #3
 * "The First Wave" (1997) Norway #12
 * "The Next Wave" (1997)
 * "The Opera For The Crying Machinery" (1997) [Rare and never released]
 * "Mørkets øy" (1997)
 * "Döderlein" (2006) (single from the live album Rockefeller)

Demos

 * Det finnes alltid en utvei.... (1990) [This came in only 45 copies, cassette tapes only. Very rare.]

DVDs

 * Rockefeller (live reunion album) (2006) Norway #8
 * Fra X til døden (2006) [Concert DVD recorded at UKA-05, in Dødens dal, Trondheim]
 * Seigmen - Seigmen I Operaen 2008 (2012) [Concert DVD *LTD - Signed by the band - Only a limited number of copies]

Compilations

 * Monument (1999) Norway #11

title: Seigmen


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Nathan Cobb

Nathan Augustus Cobb (30 June 1859 – 4 June 1932) is known as "the father of nematology in the United States".

He provided the foundations for nematode taxonomy and described over 1000 different nematode species. His technical innovations in nematological methods included fixation and preservation techniques; the Cobb metal mounting slide; improvements in photography and microscopic equipment; and the first device to use flotation to remove nematodes from soil. An individual with a variety of skills, he made significant contributions to a number of scientific disciplines and the USDA Nematology Laboratory, originally established with him as the director, continues today.

He was the father of Frjeda Blanchard, the geneticist who first demonstrated Mendelian inheritance in reptiles.

Books
This list can be accessed via the Biodiversity Heritage Library. The list is incomplete.

 * "A Nematode formula." (1890) Sydney : C. Potter
 * "Nematodes, mostly Australian and Fijian." (1893) Sydney : F. Cunninghame & Co., printers
 * "The sheep-fluke." (1897) Sydney : W. A. Gullick, gov't. printer
 * "Letters on the diseases of plants." (1897) Sydney : W. A. Gullick, gov't. printer
 * "Seed wheat: an investigation and discussion of the relative value as seed of large plump and small shrivelled grains." (1903) Sydney : W. A. Gullick, gov't. printer
 * "Letters on the diseases of plants. Second series." (1904) Sydney : W. A. Gullick, gov't. printer
 * "Methods of using the microscope, camera-lucida and solar projector for purposes of examination and the production of illustrations." (1905) Honolulu : Hawaiian Sugar Planters' Association
 * "Contributions to a science of nematology." (1914–35) Baltimore : Williams & Wilkins Co.

title: Nathan Cobb


text:
Kaimanawa

The New Zealand Māori word Kaimanawa relates to two separate things:

 * The Kaimanawa Range of mountains, in the North Island
 * Kaimanawa horses, a feral horse found in the area

title: Kaimanawa


text:
Petrićevac

Petrićevac is a part of the city of Banja Luka in Republika Srpska, entity of Bosnia and Herzegovina. Today, there are about 25,000 inhabitants in Petrićevac.

The place is the location of a Catholic church of Saint Anthony and a Franciscan monastery in the 20th century. There was also an Orthodox Church made by Ilija Rankić.

During World War II, the Orthodox church was destroyed in 1941 by the Ustaša fascist organization. Miroslav Filipović originated from the Catholic monastery before he went on to join the Ustaše during World War II, and commit numerous atrocities and war crimes over the Serbs in the region between 1942 and 1945. Filipović was defrocked after a February 1942 massacre of Serb civilians in the nearby villages (Drakulić and Motike).

During the war in Bosnia in 1995, as the part of persecution and ethnic cleansing of the non-Serb population of the city of Banja Luka and the surrounding settlements, the Catholic Church and the monastery experienced the same fate as the 16 mosques of the city of Banja Luka which were destroyed by the Serbs already in 1993 (List of 16 destroyed mosques in Banja Luka ). The Catholic Church and the monastery were destroyed in revenge by the Bosnian Serb Army, causing the death of one of the friars in the process. The reconstruction of the buildings started in 2003 after Pope John Paul II visited the site.

title: Petrićevac


text:
Fetal alcohol spectrum disorder

Fetal alcohol spectrum disorders (FASDs) are a group of conditions that can occur in a person who is exposed to alcohol during gestation. FASD affects 1 in 20 Americans, but is highly mis- and under-diagnosed.

The several forms of the condition (in order of most severe to least severe) are: fetal alcohol syndrome (FAS), partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorder (ARND), and neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE). Other terms used are fetal alcohol effects (FAE), partial fetal alcohol effects (PFAE), alcohol-related birth defects (ARBD), and static encephalopathy, but these terms have fallen out of favor and are no longer considered part of the spectrum.

Not all infants exposed to alcohol in utero will have detectable FASD or pregnancy complications. The risk of FASD increases with amount consumed, the frequency of consumption, and longer duration of alcohol consumption during pregnancy, particularly binge drinking. The variance seen in outcomes of alcohol consumption during pregnancy is poorly understood. Diagnosis is based on an assessment of growth, facial features, central nervous system, and alcohol exposure by a multi-disciplinary team of professionals. The main criteria for diagnosis of FASD is nervous system damage and alcohol exposure, with FAS including congenital malformations of the lips and growth deficiency. FASD is often misdiagnosed as or comorbid with ADHD.

Almost all experts recommend that the mother abstain from alcohol use during pregnancy to prevent FASDs. As the woman may not become aware that she has conceived until several weeks into the pregnancy, it is also recommended to abstain while attempting to become pregnant. Although the condition has no known cure, treatment can improve outcomes. Treatment needs vary but include psychoactive medications, behavioral interventions, tailored accommodations, case management, and public resources.

Globally, one in 10 women drink alcohol during pregnancy, and the prevalence of having any FASD disorder is estimated to be at least 1 in 20. The rates of alcohol use, FAS, and FASD are likely to be underestimated, because of the difficulty in making the diagnosis and the reluctance of clinicians to label children and mothers. Some have argued that the FAS label stigmatizes alcohol use, while authorities point out that the risk is real. The condition has appeared in several works of fiction.

Signs and symptoms
The key signs of fetal alcohol syndrome (FAS) required for diagnosis include:
 * Growth deficiency or failure to thrive: slow fetal growth low birth weight or height, small head circumference (microcephaly)
 * Congenital malformations of lips: short palpebral fissure lengths, smooth philtrum, and thin upper lip.
 * Nervous system damage: Clinically significant structural neurological, or functional impairment

Popova et al. identified 428 ICD-10 conditions as co-occurring in individuals with FAS. Excluding conditions used in FAS diagnosis, co-occurring conditions with 50% prevalence or greater include:
 * Conduct disorder, behavioral problems, disruptive behavior, or impulsivity
 * Developmental language disorder
 * Hearing loss
 * Visual impairment, including blindness or astigmatism
 * Developmental delay, cognitive disorder, or mental deficiency
 * Premature birth
 * Substance dependence
 * Congenital malformation of retina
 * Congenital fusion of cervical vertebrae or cervical spin fusion
 * Attention deficit hyperactivity disorder or otherwise impaired attention
 * Small eye openings (blepharophimosis) and/or an abnormally increased distance between the eyes (hypertelorism)

Other FASD conditions are partial expressions of FAS where the central nervous system shows clinical deficits. In these other FASD conditions, an individual may be at greater risk for adverse outcomes because brain damage is present without associated visual cues of poor growth or the "FAS face" that might ordinarily trigger an FASD evaluation. Such individuals may be misdiagnosed with primary mental health disorders such as ADHD or oppositional defiance disorder without appreciation that brain damage is the underlying cause of these disorders, which requires a different treatment paradigm than typical mental health disorders. While other FASD conditions may not yet be included as an ICD or DSM-IV-TR diagnosis, they nonetheless pose significant impairment in functional behavior because of underlying brain damage. Many indications of fetal alcohol spectrum disorders are developmental. Therefore, although a child may appear 'normal' at birth, intellectual disabilities caused by alcohol before birth may not appear until the child begins school.

More broadly, alcohol use during pregnancy is also associated with:
 * Intellectual disability, both in overall IQ measurements and in many functional tests
 * Fetal mortality, such as spontaneous abortion (Miscarriage), stillbirth, and sudden infant death syndrome
 * Domestic violence and potential harm to the infant
 * Sleep and sucking problems as a baby
 * Heart: A heart murmur that frequently disappears by one year of age. Ventricular septal defect, atrial septal defect, tetralogy of Fallot, coarctation of the aorta, and/or cardiac rhythm dysfunction.
 * Bones: Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails.
 * Kidneys: Horseshoe, aplastic, dysplastic, or hypoplastic kidneys.
 * Eyes: Strabismus, optic nerve hypoplasia (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements).
 * Cleft lip with or without a cleft palate: Alcohol is known to be a folic acid antagonist, and a baby's palate and lip develop during the first trimester of the pregnancy (first 12 weeks). Heavy alcohol consumption and binge drinking during this time have been linked to orofacial cleft.
 * Occasional problems: ptosis of the eyelid, microphthalmia, webbed neck, short neck, radioulnar synostosis, spina bifida, and hydrocephalus.

Alcohol can also harm the fertility of women who are planning for pregnancy. Adverse effects of alcohol can lead to malnutrition, seizures, vomiting and dehydration. The mother can suffer from anxiety and depression which can result in child abuse/neglect. It has also been observed that when the pregnant mother withdraws from alcohol, its effects are visible on the infant as well. The baby remains in an irritated mood, cries frequently, doesn't sleep properly, weakening of sucking ability and increased hunger.

In 2019, a study found that individuals with FASD have a higher risk of hypertension independent of race/ethnicity and obesity.

Prenatal Alcohol Exposure (PAE)
Fetal alcohol spectrum disorders are caused by alcohol exposure during gestational development. If an individual was not exposed to alcohol before birth, they will not get FASD. However, not all infants exposed to alcohol in utero will have detectable FAS, FASD, or pregnancy complications.

How Much Alcohol Is Safe?
None. Drinking any quantity during pregnancy, the risk of giving birth to a child with FASD is about 15%, and to a child with FAS about 1.5%. Drinking large quantities, defined as 2 standard drinks a day, or 6 standard drinks in a short time, carries a 4.3% risk of a FAS birth (i.e. one of every 23 heavy-drinking pregnant women will deliver a child with FAS). Furthermore, alcohol-related congenital abnormalities occur at an incidence of roughly one out of 67 women who drink alcohol during pregnancy. Among those mothers who have a substance use disorder, an estimated one-third of their children have FAS.

There are protective and risk factors to the impact of prenatal alcohol exposure:

 * Amount consumed, the frequency of consumption, and longer duration of alcohol consumption during pregnancy.
 * Blood alcohol concentration has been identified as a relevant factor.
 * All forms of alcohol, such as beer, wine, and liquor, pose similar risk.
 * Binge drinking increases the chances and severity of FASD to such an extent that Svetlana Popova has stated that "binge drinking is the direct cause of FAS or FASD".

Evidence regarding the effects of low levels of alcohol consumption during pregnancy is inconsistent and contradictory: many studies find no significant effect, but some find beneficial associations, and others find detrimental associations, even on the same outcomes. Summarizing studies by country shows some similarity in results, due to using the same data source.

Limitations to Research
The definition of low alcohol consumption varies significantly among studies and often fails to incorporate all aspects of timing, dose, and duration. Recall bias and socioeconomic and psychosocial factors have been controlled for in most studies, but it is likely that residual confounding due to missing factors and variation in methods still exists and is larger than any observed effects. Because alcohol is a known teratogen, it is considered unethical to do randomized controlled trials on pregnant women to determine the precise level of alcohol toxicity, so studies mainly rely on observational evidence. Small amounts of alcohol may not cause an abnormal appearance, however, small amounts of alcohol consumption while pregnant may cause behavioral problems and also increases the risk of miscarriage. Quasi-experimental studies provide moderately strong evidence that prenatal alcohol exposure causes detrimental cognitive outcomes, and some evidence of reduced birthweight, although no study was fully rated at low risk of bias and quantity of studies was limited.

The variance seen in outcomes of alcohol consumption during pregnancy is poorly understood. Aggravating factors may include advanced maternal age, smoking, poor diet, genetics, and social risk factors.

Paternal Alcohol Use
Fathers who consume alcohol prior to conception may contribute to FAS through long term epigenetic modification of the father's sperm.

Prevention and Stigma
Almost all experts recommend that the mother abstain from alcohol use during pregnancy to prevent FASDs.

However, the most current advocacy perspectives encourage people and systems to approach FASD with interventions and support for individuals who are already living with FASD. Focusing on prevention often only further stigmatizes individuals with FASD and their birth parents. Advocates say, if you are supporting people currently living with FASD then you are spreading the awareness needed for successful prevention efforts; "Intervention is Prevention".

The US national advocacy organization, FASD United, has examined prevention messaging through perspectives of individuals with FASD and researchers, and shared public awareness content to combat shame and stigma perpetuated by prevention focuses.

Pregnant people may not become aware that she has conceived until several weeks into the pregnancy, so it is recommended to abstain from alcohol while attempting to become pregnant. There are also many social determinants of health that impacts the effects of PAE:

 * Genetics
 * Poverty/Access to nutritious food
 * Malnutrition
 * Poor social support networks
 * Lack of personal autonomy
 * Access to healthcare
 * Generational and sociocultural traumas
 * Access to mental health care and treatment

US Surgeon General Advisory
These two recommendations have been made by the Surgeon General of the United States, the Centers for Disease Control, the American College of Obstetricians and Gynecologists, the American Academy of Pediatrics, the World Health Organization, the United Kingdom's National Institute for Health and Clinical Excellence, and many others.[excessive citations] In the United States, federal legislation has required that warning labels be placed on all alcoholic beverage containers since 1988 under the Alcoholic Beverage Labeling Act.

Women can experience serious symptoms that accompany alcohol withdrawal during pregnancy. According to the World Health Organization, these symptoms can be treated during pregnancy with brief use of benzodiazepine tranquilizers. Currently, the FDA has approved three medications—naltrexone, acamprosate, and disulfiram—for the treatment of alcohol use disorder (AUD). However, there is insufficient data regarding the safety of these medications for pregnant women.

 * Naltrexone is a nonselective opioid antagonist that is used to treat AUD and opioid use disorder. The long-term effects of naltrexone on the fetus are currently unknown. Animal studies show that naltrexone administered during pregnancy increases the incidence of early fetal loss; however, there are insufficient data available to identify the extent to which this is a risk in pregnant women.
 * Acamprosate functions as both an antagonist of NMDA and glutamate and an agonist at GABAA receptors, although its molecular mechanism is not completely understood. Acamprosate has been shown to be effective at preventing alcohol relapse during abstinence. Animal data, however, suggests that acamprosate can have possible teratogenic effects on fetuses.
 * Disulfiram prevents relapse by blocking the metabolism of acetaldehyde after consumption of alcohol which leads to headache, nausea, and vomiting. Some evidence suggests that disulfiram use during the first trimester is associated with an increased risk of congenital malformations such as reduction defects and cleft palate. Additionally, the effects of disulfiram can involve hypertension which can be harmful to both the pregnant woman and the fetus.

American Psychiatric Association guidelines recommend that medications not be used to treat alcohol use disorder in pregnant women except in cases of acute alcohol withdrawals or other co-existing conditions. Instead, behavioral interventions are usually preferred as treatments for pregnant women with AUD. Medications should only be used for pregnant women after carefully considering potential risks and harms of the medications versus the benefits of alcohol cessation.

Mechanism
After the pregnant person consumes alcohol, the alcohol crosses through the placenta and umbilical cord to the developing fetus. Alcohol metabolizes slowly in the fetus and remains for a long time when compared to an adult. A human fetus appears to be at triple risk from maternal alcohol consumption:
 * 1) The placenta allows free entry of ethanol and toxic metabolites like acetaldehyde into the fetal compartment. The so-called placental barrier is practically absent with respect to ethanol.
 * 2) The developing fetal nervous system appears particularly sensitive to ethanol toxicity. The latter interferes with proliferation, differentiation, neuronal migration, axonic outgrowth, integration, and fine-tuning of the synaptic network. In short, all major processes in the developing central nervous system appear compromised.
 * 3) Fetal tissues are quite different from adult tissues in function and purpose. For example, the main detoxicating organ in adults is the liver, whereas the fetal liver is incapable of detoxifying ethanol, as the ADH and ALDH enzymes have not yet been brought to expression at this early stage. Up to term, fetal tissues do not have significant capacity for the detoxification of ethanol, and the fetus remains exposed to ethanol in the amniotic fluid for periods far longer than the decay time of ethanol in the maternal circulation. The lack of significant quantities of ADH and ALDH means that fetal tissues have much lower quantities of antioxidant enzymes, like SOD, glutathione transferases, and glutathione peroxidases, resulting in antioxidant protection being much less effective.

Although alcohol is known to be a teratogen (causing birth defects), the exact biological mechanisms for the development of FAS or FASD are unknown. However, clinical and animal studies have identified a broad spectrum of pathways through which maternal alcohol can negatively affect the outcome of a pregnancy. Clear conclusions with universal validity are difficult to draw, since different ethnic groups show considerable genetic polymorphism for the hepatic enzymes responsible for ethanol detoxification. Genetic examinations have revealed a continuum of long-lasting molecular effects that are not only timing specific but are also dosage specific; with even moderate amounts being able to cause alterations. Additionally, ethanol may alter fetal development by interfering with retinoic acid signaling as acetaldehyde can compete with retinaldehyde and prevents its oxidation to retinoic acid.

Developmental stages
Different body systems in the infant grow, mature and develop at specific times during gestation. The effect of consumption of alcohol differs during each of these developmental stages:
 * From conception and to the third week, the most susceptible systems and organs are the brain, spinal cord, and heart. The effects of alcohol consumption early in the pregnancy can result in defects to these systems and organs.
 * During the third week, alcohol can also damage the central nervous system of the fetus.
 * During the fourth week of gestation, the limbs are being formed and it is at this point that alcohol can affect the development of arms, legs, fingers and toes. The eyes and ears also form during the fourth week and are more susceptible to the effects of alcohol.
 * By the sixth week of gestation, the teeth and palate are forming and alcohol consumption at this time will affect these structures. Alcohol use in this window is responsible for many of the facial characteristics of fetal alcohol syndrome.
 * During the twelfth week, frequent alcohol exposure can negatively impact the brain development which affects cognitive, learning and behavioral skills before birth.
 * By the 20th week of gestation the formation of organs and organ systems is well-developed. The infant is still susceptible to the damaging effects of alcohol.
 * Ethanol exposure in the second trimester reduces nutrition levels and can affect the functioning of the endocrine system in both fetus and mother. This is because blood flow via umbilical artery to fetal brain is reduced.

Diagnosis
Fetal alcohol spectrum disorders encompass a range of physical and neurodevelopmental problems which can result from prenatal alcohol exposure. Diagnosis is based on the signs and symptoms in the person and evidence of alcohol use. These diagnoses of fetal alcohol spectrum disorders are currently recognized:
 * Fetal alcohol syndrome (FAS)
 * Partial fetal alcohol syndrome (pFAS) refers to individuals with a known, or highly suspected, history of prenatal alcohol exposure who have alcohol-related physical and neurodevelopmental deficits that do not meet the full criteria for FAS.
 * Alcohol-related neurodevelopmental disorder (ARND)
 * Neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE)

As of 2016, the Swedish Agency for Health Technology Assessment and Assessment of Social Services accepts only FAS as a diagnosis, seeing the evidence as inconclusive with respect to other types. The agency feels it is unclear if identifying a FASD-related condition benefits the diagnosed individual.

Classification
Presently, four FASD diagnostic systems that diagnose FAS and other FASD conditions have been developed in North America:
 * The Institute of Medicine's guidelines for FAS, the first system to standardize diagnoses of individuals with prenatal alcohol exposure;
 * The University of Washington's "The 4-Digit Diagnostic Code", which ranks the four key features of FASD on a Likert scale of one to four and yields 256 descriptive codes that can be categorized into 22 distinct clinical categories, ranging from FAS to no findings;
 * The Centers for Disease Control's "Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis", which established consensus on the diagnosis FAS in the U.S. but deferred addressing other FASD conditions; and
 * Canadian guidelines for FASD diagnoses, which established criteria for diagnosing FASD in Canada and harmonized most differences between the IOM and University of Washington's systems.

Each diagnostic system requires an assessment of four key features: growth, facial features, central nervous system, and alcohol exposure. To determine any FASD condition, a multi-disciplinary evaluation is necessary to assess each of the four key features for assessment. Generally, a trained physician will determine growth deficiency and FAS facial features. While a qualified physician may also assess central nervous system structural abnormalities and/or neurological problems, usually central nervous system damage is determined through psychological, speech-language, and occupational therapy assessments to ascertain clinically significant impairments in three or more of the Ten Brain Domains. Prenatal alcohol exposure risk may be assessed by a qualified physician, psychologist, social worker, or chemical health counselor. These professionals work together as a team to assess and interpret data of each key feature for assessment and develop an integrative, multi-disciplinary report to diagnose FAS (or other FASD conditions) in an individual.

A positive finding on all four features is required for a diagnosis of FAS, and the four diagnostic systems essentially agree on criteria for fetal alcohol syndrome (FAS). However, there are differences among systems when full criteria for FAS are not met. Prenatal alcohol exposure and central nervous system damage are the critical elements of the spectrum of FASD, and a positive finding in these two features is sufficient for an FASD diagnosis in all FASD systems. But different researchers and systems may use a wide variety of terminology to describe an individual's FASD condition, as the nomenclature is still evolving. Most individuals with deficits resulting from prenatal alcohol exposure do not express all features of FAS and fall into other FASD conditions. The Canadian guidelines recommend the assessment and descriptive approach of the "4-Digit Diagnostic Code" for each key feature of FASD and the terminology of the IOM in diagnostic categories, excepting ARBD.

Fetal alcohol syndrome
The most severe condition is called Fetal Alcohol Syndrome (FAS), which refers to individuals who have a specific set of birth defects and neurodevelopmental disorders characteristic of the diagnosis. The following criteria must be fully met for an FAS diagnosis:

 * 1) Prenatal or postnatal height or weight (or both) at or below the 10th percentile
 * 2) All three FAS facial features present
 * 3) Clinically significant structural, neurological, or functional impairment of the central nervous system
 * 4) Confirmed or Unknown prenatal alcohol exposure

FAS is the only expression of FASD that has garnered consensus among experts to become an official ICD-9 and ICD-10 diagnosis.

Partial FAS
Partial FAS (pFAS) was previously known as atypical FAS in the 1997 edition of the "4-Digit Diagnostic Code". People with pFAS have a confirmed history of prenatal alcohol exposure, but may lack growth deficiency or the complete facial stigmata. Central nervous system damage is present at the same level as FAS. These individuals have the same functional disabilities but "look" less like FAS.

The following criteria must be fully met for a diagnosis of Partial FAS:

 * 1) Two or three FAS facial features present
 * 2) Clinically significant structural, neurological, or functional impairment in three or more of the Ten Brain Domains
 * 3) Confirmed prenatal alcohol exposure

Growth or height may range from normal to deficient.

Alcohol-related neurodevelopmental disorder
Alcohol-related neurodevelopmental disorder (ARND) is the specific diagnosis of the non-dysmorphic type of FASD, where a majority of the symptoms are witnessed. The diagnosis was initially suggested by the Institute of Medicine to replace the terms FAE (fetal alcohol effects). It focuses on central nervous system damage, rather than growth deficiency or FAS facial features. The Canadian guidelines also use this diagnosis and the same criteria. While the "4-Digit Diagnostic Code" includes these criteria for three of its diagnostic categories, it refers to this condition as static encephalopathy. The behavioral effects of ARND are not necessarily unique to alcohol however, so use of the term must be within the context of confirmed prenatal alcohol exposure. ARND may be gaining acceptance over the terms FAE and ARBD to describe FASD conditions with central nervous system abnormalities or behavioral or cognitive abnormalities or both due to prenatal alcohol exposure without regard to growth deficiency or FAS facial features.

The following criteria must be fully met for a diagnosis of ARND or static encephalopathy:

 * 1) Minimal or no FAS facial features present
 * 2) Clinically significant structural, neurological, or functional impairment in three or more of the Ten Brain Domains
 * 3) Confirmed prenatal alcohol exposure

Growth or height may range from normal to minimally deficient.

Neurobehavioral disorder associated with prenatal alcohol exposure
Neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE) is the spectrum-wide term for the psychiatric, behavioral, and neurological symptoms of all FASDs. It was introduced into the DSM-V as a "condition for further study" and as a specified condition under, "other specified neurodevelopmental disorders" as a way to better study the behavioral aspects of all FASD disorders.

Growth
In terms of FASD, growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements. Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the population. Prenatal or postnatal presentation of growth deficits can occur, but are most often postnatal.

Criteria for FASD are least specific in the Institute of Medicine (IOM) diagnostic system ("low birth weight..., decelerating weight not due to nutrition..., [or] disproportional low weight to height" p. 4 of executive summary), while the CDC use the 10th percentile as a cut-off to determine growth deficiency. The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile. Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and pFAS, but not ARND or static encephalopathy.

The "4-Digit Diagnostic Code" from 2004 ranks growth deficiency as follows:
 * Severe: Height and weight at or below the 3rd percentile.
 * Moderate: Either height or weight at or below the 3rd percentile, but not both.
 * Mild: Either height or weight or both between the 3rd and 10th percentiles.
 * None: Height and weight both above the 10th percentile.

In the initial studies that described FAS, growth deficiency was a requirement for inclusion in the studies; thus, all the original people with FAS had growth deficiency as an artifact of sampling characteristics used to establish criteria for the syndrome. That is, growth deficiency is a key feature of FASD because growth deficiency was a criterion for inclusion in the study that defined FAS. Growth deficiency may be less critical for understanding the disabilities of FASD than the neurobehavioral sequelae to the brain damage. Canadian guidelines updated in 2016 deleted growth as a diagnostic criterion.

Facial features
Several characteristic craniofacial abnormalities are often visible in individuals with FAS. The presence of FAS facial features indicates brain damage, although brain damage may also exist in their absence. FAS facial features (and most other visible, but non-diagnostic, deformities) are believed to be caused mainly during the 10th to 20th week of gestation.

Refinements in diagnostic criteria since 1975 have yielded three distinctive and diagnostically significant facial features which distinguish FAS from other disorders with partially overlapping characteristics. The three FAS facial features are:
 * A smooth philtrum: The divot or groove between the nose and upper lip flattens with increased prenatal alcohol exposure.
 * Thin vermilion: The upper lip thins with increased prenatal alcohol exposure.
 * Small palpebral fissures: Eye width decreases with increased prenatal alcohol exposure.

Measurement of FAS facial features uses criteria developed by the University of Washington. The lip and philtrum are measured by a trained physician with the Lip-Philtrum Guide, a five-point Likert scale with representative photographs of lip and philtrum combinations ranging from normal (ranked 1) to severe (ranked 5). Palpebral fissure length (PFL) is measured in millimeters with either calipers or a clear ruler and then compared to a PFL growth chart, also developed by the University of Washington.

Ranking FAS facial features is complicated because the three separate facial features can be affected independently by prenatal alcohol. A summary of the criteria follows:
 * Severe: All three facial features ranked independently as severe (lip ranked at 4 or 5, philtrum ranked at 4 or 5, and PFL two or more standard deviations below average).
 * Moderate: Two facial features ranked as severe and one feature ranked as moderate (lip or philtrum ranked at 3, or PFL between one and two standard deviations below average).
 * Mild: A mild ranking of FAS facial features covers a broad range of facial feature combinations:
 * Two facial features ranked severe and one ranked within normal limits,
 * One facial feature ranked severe and two ranked moderate, or
 * One facial feature ranked severe, one ranked moderate and one ranked within normal limits.
 * None: All three facial features ranked within normal limits.

Central nervous system
Central nervous system (CNS) damage is the primary feature of any FASD diagnosis. Prenatal alcohol exposure, which is classified as a teratogen, can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother. While functional abnormalities are the behavioral and cognitive expressions of the FASD disability, CNS damage can be assessed in three areas: structural, neurological, and functional impairments.

All four diagnostic systems allow for assessment of CNS damage in these areas, but criteria vary. The IOM system requires structural or neurological impairment for a diagnosis of FAS, but also allows a "complex pattern" of functional anomalies for diagnosing PFAS and ARND. The "4-Digit Diagnostic Code" and CDC guidelines allow for a positive CNS finding in any of the three areas for any FASD diagnosis, but functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnosis of FAS, PFAS, and ARND. The "4-Digit Diagnostic Code" also allows for an FASD diagnosis when only two functional domains are measured at two standard deviations or worse. The "4-Digit Diagnostic Code" further elaborates the degree of CNS damage according to four ranks:
 * Definite: Structural impairments or neurological impairments for FAS or static encephalopathy.
 * Probable: Significant dysfunction of two standard deviations or worse in three or more functional domains.
 * Possible: Mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by judgment of the clinical evaluation team that CNS damage cannot be dismissed.
 * Unlikely: No evidence of CNS damage.

Structural
Structural abnormalities of the brain are observable, physical damage to the brain or brain structures caused by prenatal alcohol exposure. Structural impairments may include microcephaly (small head size) of two or more standard deviations below the average, or other abnormalities in brain structure (e.g., agenesis of the corpus callosum, cerebellar hypoplasia).

Microcephaly is determined by comparing head circumference (often called occipitofrontal circumference, or OFC) to appropriate OFC growth charts. Other structural impairments must be observed through medical imaging techniques by a trained physician. Because imaging procedures are expensive and relatively inaccessible to most people, diagnosis of FAS is not frequently made via structural impairments, except for microcephaly.

Evidence of a CNS structural impairment due to prenatal alcohol exposure will result in a diagnosis of FAS, and neurological and functional impairments are highly likely.

During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells, which can create structural deformities or deficits within the brain. During the third trimester, damage can be caused to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information, all of which can create neurological and functional CNS impairments as well.

As of 2002, there were 25 reports of autopsies on infants known to have FAS. The first was in 1973, on an infant who died shortly after birth. The examination revealed extensive brain damage, including microcephaly, migration anomalies, corpus callosum dysgenesis, and a massive neuroglial, leptomeningeal heterotopia covering the left hemisphere.

In 1977, Clarren described a second infant whose mother was a binge drinker. The infant died ten days after birth. The autopsy showed severe hydrocephalus, abnormal neuronal migration, and a small corpus callosum. FAS has also been linked to brainstem and cerebellar changes, agenesis of the corpus callosum and anterior commissure, neuronal migration errors, absent olfactory bulbs, meningomyelocele, and porencephaly.

Neurological
When structural impairments are not observable or do not exist, neurological impairments are assessed. In the context of FASD, neurological impairments are caused by prenatal alcohol exposure which causes general neurological damage to the central nervous system (CNS), the peripheral nervous system, or the autonomic nervous system. A determination of a neurological problem must be made by a trained physician, and must not be due to a postnatal insult, such as meningitis, concussion, traumatic brain injury, etc.

All four diagnostic systems show virtual agreement on their criteria for CNS damage at the neurological level, and evidence of a CNS neurological impairment due to prenatal alcohol exposure will result in a diagnosis of FAS or pFAS, and functional impairments are highly likely.

Neurological problems are expressed as either hard signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or soft signs. Soft signs are broader, nonspecific neurological impairments, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, clumsiness, and poor eye–hand coordination. Many soft signs have norm-referenced criteria, while others are determined through clinical judgment. "Clinical judgment" is only as good as the clinician, and soft signs should be assessed by either a pediatric neurologist, a pediatric neuropsychologist, or both.

Functional
When structural or neurological impairments are not observed, all four diagnostic systems allow CNS damage due to prenatal alcohol exposure to be assessed in terms of functional impairments. Functional impairments are deficits, problems, delays, or abnormalities due to prenatal alcohol exposure (rather than hereditary causes or postnatal insults) in observable and measurable domains related to daily functioning, often referred to as developmental disabilities. There is no consensus on a specific pattern of functional impairments due to prenatal alcohol exposure and only CDC guidelines label developmental delays as such, so criteria (and FASD diagnoses) vary somewhat across diagnostic systems.

The four diagnostic systems list various CNS domains that can qualify for functional impairment that can determine an FASD diagnosis:
 * Evidence of a complex pattern of behavior or cognitive abnormalities inconsistent with developmental level in the following CNS domains – Sufficient for a pFAS or ARND diagnosis using IOM guidelines
 * Learning disabilities, academic achievement, impulse control, social perception, communication, abstraction, math skills, memory, attention, judgment
 * Performance at two or more standard deviations on standardized testing in three or more of the following CNS domains – Sufficient for an FAS, pFAS or static encephalopathy diagnosis using 4-Digit Diagnostic Code
 * Executive functioning, memory, cognition, social/adaptive skills, academic achievement, language, motor skills, attention, activity level
 * General cognitive deficits (e.g., IQ) at or below the 3rd percentile on standardized testing – Sufficient for an FAS diagnosis using CDC guidelines
 * Performance at or below the 16th percentile on standardized testing in three or more of the following CNS domains – Sufficient for an FAS diagnosis using CDC guidelines
 * Cognition, executive functioning, motor functioning, attention and hyperactive problems, social skills, sensory processing disorder, social communication, memory, difficulties responding to common parenting practices
 * Performance at two or more standard deviations on standardized testing in three or more of the following CNS domains – Sufficient for an FAS diagnosis using Canadian guidelines
 * Cognition, communication, academic achievement, memory, executive functioning, adaptive behavior, motor skills, social skills, social communication

Ten brain domains
A recent effort to standardize assessment of functional CNS damage has been suggested by an experienced FASD diagnostic team in Minnesota. The proposed framework attempts to harmonize IOM, 4-Digit Diagnostic Code, CDC, and Canadian guidelines for measuring CNS damage vis-à-vis FASD evaluations and diagnosis. The standardized approach is referred to as the Ten Brain Domains and encompasses aspects of all four diagnostic systems' recommendations for assessing CNS damage due to prenatal alcohol exposure. The framework provides clear definitions of brain dysfunction, specifies empirical data needed for accurate diagnosis, and defines intervention considerations that address the complex nature of FASD with the intention to avoid common secondary disabilities.

The proposed Ten Brain Domains include:
 * Achievement
 * Adaptive behavior
 * Attention
 * Cognition
 * Executive functioning
 * Language
 * Memory
 * Motor skills
 * Multisensory integration or soft neurological problems
 * Social communication

The Fetal Alcohol Diagnostic Program (FADP) uses unpublished Minnesota state criteria of performance at 1.5 or more standard deviations on standardized testing in three or more of the Ten Brain Domains to determine CNS damage. However, the Ten Brain Domains are easily incorporated into any of the four diagnostic systems' CNS damage criteria, as the framework only proposes the domains, rather than the cut-off criteria for FASD.

Alcohol exposure
Prenatal alcohol exposure is determined by interview of the biological mother or other family members knowledgeable of the mother's alcohol use during the pregnancy (if available), prenatal health records (if available), and review of available birth records, court records (if applicable), chemical dependency treatment records (if applicable), chemical biomarkers, or other reliable sources.

Exposure level is assessed as confirmed exposure, unknown exposure, and confirmed absence of exposure by the IOM, CDC and Canadian diagnostic systems. The "4-Digit Diagnostic Code" further distinguishes confirmed exposure as High Risk and Some Risk:
 * Confirmed exposure: The CDC guidelines are silent on using information on amount, frequency, and timing of prenatal alcohol use for diagnostic purposes. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30-day period. "The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as high risk and some risk. It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg female drinking six to eight beers in one sitting.
 * High Risk: Confirmed use of alcohol during pregnancy known to be at high blood alcohol levels (100 mg/dL or greater) delivered at least weekly in early pregnancy.
 * Some Risk: Confirmed use of alcohol during pregnancy with use less than High Risk or unknown usage patterns.
 * Unknown Risk: Unknown use of alcohol during pregnancy. For many adopted or adults and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. Many are reluctant to admit to drinking or to provide an accurate report of the quantity they drank. In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.
 * No Risk: Confirmed absence of prenatal alcohol exposure. Confirmed absence of exposure would apply to planned pregnancies in which no alcohol was used or pregnancies of women who do not use alcohol or report no use during the pregnancy. This designation is relatively rare, as most people presenting for an FASD evaluation are at least suspected to have had a prenatal alcohol exposure due to presence of other key features of FASD.

Biomarkers
Evidence is insufficient for the use of chemical biomarkers to detect prenatal alcohol exposure. Biomarkers being studied include fatty acid ethyl esters (FAEE) detected in the meconium (first feces of an infant) and hair. FAEE may be present if chronic alcohol exposure occurs during the second and third trimester since this is when the meconium begins to form. Concentrations of FAEE can be influence by medication use, diet, and individual genetic variations in FAEE metabolism however.

Differential diagnosis
The CDC reviewed nine syndromes that have overlapping features with FAS; however, none of these syndromes include all three FAS facial features, and none are the result of prenatal alcohol exposure:
 * Aarskog syndrome
 * Williams syndrome
 * Noonan syndrome
 * Dubowitz syndrome
 * Brachman-DeLange syndrome
 * Toluene syndrome
 * Fetal hydantoin syndrome
 * Fetal valproate syndrome
 * Maternal PKU fetal effects

Other disorders that have overlapping behavioral symptoms and/or that might be comorbid to fetal alcohol spectrum disorder might include:
 * Attention deficit hyperactive disorder
 * Autism spectrum disorder
 * Reactive attachment disorder
 * Oppositional defiant disorder
 * Sensory integration dysfunction
 * Bipolar disorder
 * Depression

Most people with an FASD have most often been misdiagnosed with ADHD due to the large overlap between their behavioral deficits.

Treatment
Although the condition has no available cure, treatment can improve outcomes. Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual, there is no one treatment type that works for everyone.

Between 2017 and 2019 researchers made a breakthrough when they discovered a possible cure using neural stem cells (NSCs); they propose that if applied to a newborn, the damage can be reversed and prevent any lasting effects in the future.

Medications
Psychoactive drugs are frequently tried as many FASD symptoms are mistaken for or overlap with other disorders, most notably ADHD. Medications are used to specifically treat symptoms of FASDs and not FAS entirely. Some of the medications used are antidepressants, stimulants, neuroleptics and anti-anxiety drugs.

Behavioral interventions
Early intervention from birth to age 3 has been shown to improve the development of a child born with FASD. Interventions may include parent–child interaction therapy, efforts to modify child behavior, and drugs. Behavioral interventions are based on the learning theory, which is the basis for many parenting and professional strategies and interventions. Along with ordinary parenting styles, such strategies are frequently used by default for treating those with FAS, as the diagnoses oppositional defiance disorder (ODD), conduct disorder, reactive attachment disorder (RAD) often overlap with FAS (along with ADHD), and these are sometimes thought to benefit from behavioral interventions. Frequently, a person's poor academic achievement results in special education services, which also utilizes principles of learning theory, behavior modification, and outcome-based education.

Children with FAS benefit from behavioral and functional training, social skill training and tutoring. Support groups and talk therapy not only help the children suffering from FAS, but also help the parents and siblings of these children.

Developmental framework
Many books and handouts on FAS recommend a developmental approach, based on developmental psychology, even though most do not specify it as such and provide little theoretical background. Optimal human development generally occurs in identifiable stages (e.g., Jean Piaget's theory of cognitive development, Erik Erikson's stages of psychosocial development, John Bowlby's attachment framework, and other developmental stage theories). FAS interferes with normal development, which may cause stages to be delayed, skipped, or immaturely developed. Over time, an unaffected child can negotiate the increasing demands of life by progressing through stages of development normally, but not so for a child with FAS.

By knowing what developmental stages and tasks children follow, treatment and interventions for FAS can be tailored to helping a person meet developmental tasks and demands successfully. If a person is delayed in the adaptive behavior domain, for instance, then interventions would be recommended to target specific delays through additional education and practice (e.g., practiced instruction on tying shoelaces), giving reminders, or making accommodations (e.g., using slip-on shoes) to support the desired functioning level. This approach is an advance over behavioral interventions, because it takes the person's developmental context into account while developing interventions.

Advocacy model
The advocacy model takes the point of view that someone is needed to actively mediate between the environment and the person with FAS. Advocacy activities are conducted by an advocate (for example, a family member, friend, or case manager) and fall into three basic categories. An advocate for FAS: (1) interprets FAS and the disabilities that arise from it and explains it to the environment in which the person operates, (2) engenders change or accommodation on behalf of the person, and (3) assists the person in developing and reaching attainable goals.

The advocacy model is often recommended, for example, when developing an individualized education program (IEP) for the person's progress at school.

An understanding of the developmental framework would presumably inform and enhance the advocacy model, but advocacy also implies interventions at a systems level as well, such as educating schools, social workers, and so forth on best practices for FAS. However, several organizations devoted to FAS also use the advocacy model at a community practice level as well.

Treating FAS at the public health and public policy level promotes FAS prevention and diversion of public resources to assist those with FAS. It is related to the advocacy model but promoted at a systems level (rather than with the individual or family), such as developing community education and supports, state or province level prevention efforts (e.g., screening for maternal alcohol use during OB/GYN or prenatal medical care visits), or national awareness programs. Several organizations and state agencies in the U.S. are dedicated to this type of intervention.

Epidemiology
Globally, one in 10 women drink alcohol during pregnancy. Out of this population, 20% binge drink and have four or more alcoholic drinks per single occasion. The use of alcohol during pregnancy occurs at different rates across the world, potentially due to various cultural differences and legislation. The five countries with the highest prevalence of alcohol use during pregnancy are Ireland (60%), Belarus (47%), Denmark (46%), the UK (41%), and the Russian Federation (37%).

In a recent count, the prevalence of having any FASD disorder was 1 person out of 20, but some people estimate it could be as high as 1 in 7. The rates of FAS and FASD are likely to be underestimated, because of the difficulty in making the diagnosis and the reluctance of clinicians to label children and mothers.

Australia
FASD among Australian youth is more common in indigenous Australians. The only states that have registered birth defects in Australian youth are Western Australia, New South Wales, Victoria and South Australia. In Australia, only 12% of Australian health professionals are aware of the diagnostics and symptoms of FASD. In Western Australia, the rate of births resulting in FASD is 0.02 per 1,000 births for non-Indigenous Australians, however among indigenous births the rate is 2.76 per 1,000 births. In Victoria, there have been no registered FASD related births for indigenous Australians, but the rate for the general population in Victoria is 0.01–0.03 per 1000 births. There have been no dedicated FASD clinics within Western Australia, but there are also no nationally supported diagnostic criteria anywhere in Australia. Passive surveillance is a prevention technique used within Australia to assist in monitoring and establishing detectable defects during pregnancy and childhood.

Canada
A 2015 review article estimated the overall costs to Canada from FASD at $9.7 billion (including from crime, healthcare, education, etc.).

South Africa
In South Africa, some populations have rates as high as 9%.

United States
In the United States, alcohol use at some point during pregnancy is common and appears to be rising in prevalence. In 2006-2010, an estimated 7.6% of pregnant women used alcohol, while 1.4% of pregnant women reported binge drinking during their pregnancy. The highest prevalence estimates of reported alcohol use during pregnancy were among women who are aged 35–44 years (14.3%), white (8.3%), college graduates (10.0%), or employed (9.6%). In 2015, about 10% of pregnant women drank alcohol in the past month, and 20% to 30% drank at some point during the pregnancy. Of pregnant American women, 3.6% met criteria for an alcohol use disorder in a 2001 epidemiological study. As of 2016, the US Centers for Disease Control estimated 3 million women in the United States are at risk of having a baby with FASD.

FASD is estimated to affect between 1-2% and 5% of people in the United States and Western Europe. FAS is believed to occur in between 0.2 and 9 per 1,000 live births in the United States. Using medical and other records, CDC studies have identified 0.2 to 1.5 infants with FAS for every 1,000 live births in certain areas of the United States. A more recent CDC study of 2010 data analyzed medical and other records and found FAS in 0.3 out of 1,000 children from 7 to 9 years of age.

The lifetime cost per child with FAS in the United States was estimated at $2 million (for an overall cost across the country of over $4 billion) by the CDC in 2002.

FASD United is the US national advocacy organization for FASD and houses resources, education, and community engagements for individuals, families, professionals, organizations, agencies, and policymakers who care about FASD.

Before designation
Some hold that ancient sources describe the negative effects of alcohol during pregnancy, identifying admonitions from ancient Greek, Roman, the Talmud, and the Bible. For example, Plato writes in his fourth-century B.C. Laws (6.775): "Drinking to excess is a practice that is nowhere seemly ... nor yet safe. ... It behooves both bride and bridegroom to be sober ... in order to ensure, as far as possible, in every case that the child that is begotten may be sprung from the loins of sober parents." The sixth-century AD Talmud (Kethuboth 60b) cautions, "One who drinks intoxicating liquor will have ungainly children." However, ancient sources rarely if ever distinguish maternal alcohol consumption from paternal, and are more concerned with conception than pregnancy. The sources can often be viewed as expressing heredity, that children are likely to turn out like their (alcoholic) parents, rather than presenting the modern viewpoint that alcohol itself has an impact.

In 1725, in the midst of the Gin Craze, British physicians petitioned the House of Commons on the effects of strong drink when consumed by pregnant women saying that such drinking is "too often the cause of weak, feeble, and distempered children, who must be, instead of an advantage and strength, a charge to their country". There are many other such historical references during that period. Gin specifically was implicated as affecting children's health and causing stillbirth and infant mortality, as depicted in William Hogarth's Gin Lane. In contrast, Hogarth's Beer Street shows commerce and happiness, suggesting that the alcohol in beer was not known to have deleterious effects at this time.

In Gaelic Scotland, according to Martin Martin, the mother and nurse were not allowed to consume ale during pregnancy and breastfeeding.

In the 19th century, Benjamin Rush and Thomas Trotter lobbied against alcohol consumption during pregnancy to avoid dependence and mental deficiency in children. The teetotalism and temperance movements popularized these and other claims, including the teratogenic effects of alcohol on animal embryos, but they were often sensationalized, so much so that any finding that alcohol was harmful was largely denounced as propaganda. A prominent observation of possible links between maternal alcohol use and fetal damage was made in 1899 by Dr. William Sullivan, a Liverpool prison physician who noted higher rates of stillbirth for 120 alcoholic female prisoners than their sober female relatives. He suggested the causal agent to be alcohol use. This contradicted the predominating belief at the time that heredity caused intellectual disability, poverty, and criminal behavior, which contemporary studies on the subjects usually concluded. A case study by Henry H. Goddard of the Kallikak family—popular in the early 1900s—represents this earlier perspective, though later researchers have suggested that the Kallikaks almost certainly had FAS. General studies and discussions on alcoholism throughout the mid-1900s were typically based on a heredity argument. Researchers were often temperance advocates and funded by like-minded organizations such as the Anti-Saloon League, so clinicians viewed all such research with heavy skepticism. The temperance movement effectively shut down serious research into the subject for nearly 50 years after Prohibition.

From the 1960s to the 1980s, alcohol was commonly used as a tocolytic, a method to stop preterm labor (born at less than 37 weeks gestation). The method originated with Dr. Fritz Fuchs, the chairman of the department of obstetrics and gynecology at Cornell University Medical College. Doctors recommended a small amount of alcohol to calm the uterus during contractions in early pregnancy or Braxton Hicks contractions. In later stages of pregnancy, the alcohol was administered intravenously and often in large amounts. "Women experienced similar effects as occur with oral ingestion, including intoxication, nausea and vomiting, and potential alcohol poisoning, followed by hangovers when the alcohol was discontinued." Vomiting put the mother at a high risk for aspiration and was "a brutal procedure for all involved". Because the alcohol was being given intravenously, the doctor could continue giving the treatment to the mother long after she had passed out, resulting in her being more intoxicated than would otherwise be possible. Such heavy intoxication was highly likely to contribute to FASD. In a 2015 review, ethanol was found to be no better than placebo (sugar water) in suppressing preterm birth and neonatal mortality. Not only was ethanol worse than other beta-mimetic drugs (tocolytic agents) at postponing birth, it also led to a higher rate of low birthweight babies, babies with breathing problems at birth, and neonatal death.

Western Medicine Defines Syndrome
In France in 1957, Jacqueline Rouquette had described 100 children whose parents were alcoholics in a thesis, which was not published. "She gave a good description in certain cases of the facies" according to her mentor, Paul Lemoine. In 1968, Paul Lemoine of Nantes, himself published a study in a French medical journal about children with distinctive features whose mothers were alcoholics.

Independently, in the U.S., Christy Ulleland at University of Washington Medical School conducted an 18-month study in 1968–1969 documenting the risk of maternal alcohol consumption among the offspring of 11 alcoholic mothers. This study is arguably is the true source of the modern understanding. The infants were studied by dysmorphologists Kenneth Lyons Jones and David Weyhe Smith, colleagues of Ulleland at University of Washington, who identified a pattern of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficiency and developmental delay" in eight children. The pattern of malformations indicated that the damage was prenatal. They named these defects "fetal alcohol syndrome". News of the discovery shocked some, while others were skeptical of the findings. While many syndromes are eponymous, i.e. named after the physician first reporting the association of symptoms, Smith named FAS after the causal agent of the symptoms. He reasoned that doing so would encourage prevention, believing that if people knew maternal alcohol consumption caused the syndrome, then abstinence during pregnancy would follow from patient education and public awareness. At the time, nobody was aware of the full range of possible birth defects from FAS or its rate of prevalence.

In 1978, within nine years of the Washington discovery, animal studies, including non-human monkey studies carried out at the University of Washington Primate Center by Sterling Clarren, had confirmed that alcohol was a teratogen. By 1978, 245 cases of FAS had been reported by medical researchers, and the syndrome began to be described as the most frequent known cause of intellectual disability. In 1979, the Washington and Nantes findings were confirmed by a research group in Gothenburg, Sweden. Researchers in France, Sweden, and the United States were struck by how similar these children looked, though they were not related, and how they behaved in the same unfocused and hyperactive manner.

"Spectrum" rather than Syndrome
Over time, subsequent research and clinical experience suggested that a range of effects could arise from prenatal alcohol exposure. The term fetal alcohol effects (FAE) was used for alcohol-related neurodevelopmental disorder and alcohol-related birth defects. It was initially used in research studies to describe humans and animals in whom teratogenic effects were seen after confirmed prenatal alcohol exposure (or unknown exposure for humans), but without obvious physical anomalies. Smith (1981) described FAE as an "extremely important concept" to highlight the debilitating effects of brain damage, regardless of the growth or facial features. This term fell out of favor with clinicians in the 1990s because it was often regarded by the public as a less severe disability than FAS, when in fact its effects could be just as detrimental. In 1996 the replacement terms ARBD and ARND were introduced. In 2002, the US Congress mandated that the CDC develop diagnostic guidelines for FAS and in 2004 a definition of a term that already had been used by some in the nineties, the Fetal Alcohol Spectrum Disorder (FASD) was adopted, > to include FAS as well as other conditions resulting from prenatal alcohol exposure. Currently, FAS is the only expression of prenatal alcohol exposure defined by the International Statistical Classification of Diseases and Related Health Problems and assigned ICD-9 and diagnoses.

Alcohol-related birth defects (ARBD), formerly known as possible fetal alcohol effect (PFAE), was a term proposed as an alternative to FAE and PFAE. The IOM presents ARBD as a list of congenital anomalies that are linked to maternal alcohol use but have no key features of FASD. PFAE and ARBD have fallen out of favor because these anomalies are not necessarily specific to maternal alcohol consumption and are not criteria for diagnosis of FASD.

In 2013, the American Psychiatric Association introduced neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE).

Criminalization
Criminalization of substance use during pregnancy because of harm to the fetus or child is fiercely debated. Elizabeth Armstrong has questioned the zero-tolerance approach taken towards alcohol consumption during pregnancy, describing it as a moral panic. While heavy alcohol consumption during pregnancy is known to be damaging to the unborn child, the effects of low intakes remain debatable, particularly in the absence of randomized controlled trials (c.f. ). The UK's abstinence recommendation was not chosen based on scientific evidence, but rather because it was simple advice that would ensure no one underestimated the risk. Tennessee's 2014 fetal assault law (which expired in 2016) was criticized for not addressing alcohol use. The law criminalized opioid use during pregnancy and resulted in women avoiding professional medical care for fear of prosecution. A wide variety of professional organizations oppose criminalization. Minnesota, North Dakota, Oklahoma, South Dakota, and Wisconsin have statutory authorization for the involuntary civil commitment of women who abuse alcohol during pregnancy.

2016 CDC controversy
In 2016, a CDC press release and infographic entitled "More than 3 million US women at risk for alcohol-exposed pregnancy" caused controversy. The CDC release contained the message "The risk is real. Why take the chance?". Darlena Cunha of Times Magazine interpreted the infographic as telling all women of child bearing age not to drink at all, in case they might accidentally fall pregnant, and called them "scare tactics" and "shaming recommendations". Julie Beck said that the infographic insinuated that "your womb is a Schrodinger's box and you shouldn't pour alcohol into it unless you've peeked in there to be 100 percent sure the coast is clear". The CDC later clarified that the infographic was not intended to make any new guidelines or recommendations for women who are pre-pregnant, but rather to encourage conversations about alcohol with health professionals. Nonetheless, half of the pregnancies in developed countries and over 80% in developing countries are unplanned. Many women don't realize they are pregnant during the early stages and continue drinking when pregnant. This controversy led the US national advocacy organization, FASD United, to examine the stigma related to prevention messaging (see Prevention and Stigma).

In fiction
In Aldous Huxley's 1932 novel Brave New World (where all fetuses are gestated in vitro in a factory), lower caste fetuses are created by receiving alcohol transfusions (Bokanovsky Process) to reduce intelligence and height, thus conditioning them for simple, menial tasks. Connections between alcohol and incubating embryos are made multiple times in the novel.

The main character of the 2009 film Defendor is implied to have the condition.

Tony Loneman, a character in Tommy Orange's 2018 novel There There, was born with fetal alcohol syndrome, which he calls "the Drome".

title: Fetal alcohol spectrum disorder