Tris Speaker Traded to the Indians What was Tris speaker traded for? After 1915, Red Sox president Joseph Lannin wanted Speaker to take a pay cut from about $15,000 (equal to $362,862 today) to about $9,000 ( Are there any other interesting aspects about this article? Speaker refused and offered $12,000 ($290,289 today). On April 8, 1916, Lannin traded Speaker to the Cleveland Indians. In Was Speaker happy with this? The angry Speaker held out until he received $10,000 (equal to $224,893 today) of the cash that Boston collected. With an annual salary of $40,000 what did he do after the trade? Speaker hit over .350 in nine of his eleven years with Cleveland. In 1916, he led the league in Any notable wins? In 1916, he led the league in hits, doubles, batting average, slugging percentage and on-base percentage. Cobb had won the previous nine consecutive AL batting titles; Did he take the Indians to the championship? Speaker outhit him with a .386 batting average compared to Cobb's .371. What were the terms of his contract? Lannin traded Speaker to the Cleveland Indians. In exchange, Boston received Sad Sam Jones, Fred Thomas and $50,000 ($1,124,465 today).
When di this occur?
When did the trade of Speaker to Cleveland Indians occur?
After 1915, Red Sox president Joseph Lannin wanted Speaker to take a pay cut from about $15,000 (equal to $362,862 today) to about $9,000 (equal to $217,717 today) because of the drop in his batting average; Speaker refused and offered $12,000 ($290,289 today). On April 8, 1916, Lannin traded Speaker to the Cleveland Indians. In exchange, Boston received Sad Sam Jones, Fred Thomas and $50,000 ($1,124,465 today). The angry Speaker held out until he received $10,000 (equal to $224,893 today) of the cash that Boston collected. With an annual salary of $40,000 (equal to $899,572 today), Speaker was the highest paid player in baseball. Speaker hit over .350 in nine of his eleven years with Cleveland. In 1916, he led the league in hits, doubles, batting average, slugging percentage and on-base percentage. Cobb had won the previous nine consecutive AL batting titles; Speaker outhit him with a .386 batting average compared to Cobb's .371.  The center field fence at Cleveland's Dunn Field was 460 feet from home plate until it was shortened to 420 feet in 1920. Even so, Speaker played so shallow in the outfield that he was able to execute six career unassisted double plays at second base, catching low line drives on the run and then beating baserunners to the bag. At least once he was credited as the pivot man in a routine double play. He was often shallow enough to catch pickoff throws at second base. At one point, Speaker's signature move was to come in behind second base on a bunt and make a tag play on a baserunner who had passed the bag.  While in Cleveland, Speaker participated in diverse activities off the baseball field. Speaker enrolled in an aviator training program in 1918. Though World War I ended less than two months after he enrolled, Speaker completed his training and served in the naval reserves for several years. He also owned a ranch in Texas and competed in roping events during the baseball offseason. CANNOTANSWER
After 1915,
Tristram Edgar Speaker (April 4, 1888 – December 8, 1958), nicknamed "The Gray Eagle", was an American professional baseball player. Considered one of the greatest offensive and defensive center fielders in the history of Major League Baseball (MLB), he compiled a career batting average of .345 (sixth all-time). His 792 career doubles represent an MLB career record. His 3,514 hits are fifth in the all-time hits list. Defensively, Speaker holds career records for assists, double plays, and unassisted double plays by an outfielder. His fielding glove was known as the place "where triples go to die."

After playing in the minor leagues in Texas and Arkansas, Speaker debuted with the Boston Red Sox in 1907. He became the regular center fielder by 1909 and led the Red Sox to World Series championships in 1912 and 1915. In 1915, Speaker's batting average dropped to .322 from .338 the previous season; he was traded to the Cleveland Indians when he refused to take a pay cut. As player-manager for Cleveland, he led the team to its first World Series title. In ten of his eleven seasons with Cleveland, he finished with a batting average greater than .350. Speaker resigned as Cleveland's manager in 1926 after he and Ty Cobb faced game fixing allegations; both men were later cleared. During his managerial stint in Cleveland, Speaker introduced the platoon system in the major leagues.

Speaker played with the Washington Senators in 1927 and the Philadelphia Athletics in 1928, then became a minor league manager and part owner. He later held several roles for the Cleveland Indians. Late in life, Speaker led a short-lived indoor baseball league, ran a wholesale liquor business, worked in sales and chaired Cleveland's boxing commission. He was inducted into the Baseball Hall of Fame in 1937. He was named 27th  in the Sporting News 100 Greatest Baseball Players (1999) and was also included in the Major League Baseball All-Century Team.

Early life
Speaker was born on April 4, 1888, in Hubbard, Texas, to Archie and Nancy Poer Speaker. As a youth, Speaker broke his arm after he fell from a horse; the injury forced him to become left-handed. In 1905, Speaker played a year of college baseball for Fort Worth Polytechnic Institute. Newspaper reports have held that Speaker suffered a football injury and nearly had his arm amputated around this time; biographer Timothy Gay characterizes this as "a story that the macho Speaker never ." He worked on a ranch before beginning his professional baseball career.

Speaker's abilities drew the interest of Doak Roberts, owner of the Cleburne Railroaders of the Texas League, in . After losing several games as a pitcher, Speaker converted to outfielder to replace a Cleburne player who had been struck in the head with a pitch. He batted .318 for the Railroaders. Speaker's mother opposed his participation in the major leagues, saying that they reminded her of slavery. Though she relented, for several years Mrs. Speaker questioned why her son had not stayed home and entered the cattle or oil businesses.

He performed well for the Texas League's Houston Buffaloes in 1907, but his mother stated that she would never allow him to go to the Boston Americans. Roberts sold the youngster to the Americans for $750 or $800 (equal to $ or $ today). Speaker played in seven games for the Americans in , with three hits in 19 at-bats for a .158 average. In 1908, Boston Americans owner John I. Taylor changed the team's name to the Boston Red Sox after the bright socks in the team's uniform. That year, the club traded Speaker to the Little Rock Travelers of the Southern League in exchange for use of their facilities for spring training. Speaker batted .350 for the Travelers and his contract was repurchased by the Red Sox. He logged a .224 batting average in 116 at-bats.

Major league career

Early years

Speaker became the regular starting center fielder for Boston in 1909 and light-hitting Denny Sullivan was sold to the Cleveland Naps. Speaker hit .309 in 143 games as the team finished third in the pennant race. Defensively, Speaker was involved in 12 double plays, leading the league's outfielders, and had a .973 fielding percentage, third among outfielders. In  the Red Sox signed left fielder Duffy Lewis. Speaker, Lewis and Harry Hooper formed Boston's "Million-Dollar Outfield", one of the finest outfield trios in baseball history. Speaker was the star of the Million-Dollar Outfield. He ran fast enough that he could stand very close to second base, effectively giving the team a fifth infielder, but he still caught the balls hit to center field.  In 1910 and 1911, Boston finished fourth in the American League standings.

Speaker's best season came in 1912. He played every game and led the American League (AL) in doubles (53) and home runs (10). He set career highs with 222 hits, 136 runs, 580 at-bats, and 52 stolen bases. Speaker's stolen base tally was a team record until Tommy Harper stole 54 bases in 1973. He batted .383 and his .567 slugging percentage was the highest of his dead-ball days.  Speaker set a major league single-season record with three hitting streaks of 20 or more games (30, 23, and 22). He also became the first major leaguer to hit 50 doubles and steal 50 bases in the same season. In August, Speaker's mother unsuccessfully attempted to convince him to quit baseball and come home. In Fenway Park's first game, Speaker drove in the winning run in the 11th inning, giving Boston the 7–6 win.

The 1912 Red Sox won the AL pennant, finishing 14 games ahead of the Washington Senators and 15 games ahead of the Philadelphia Athletics. In the 1912 World Series, Speaker led the Red Sox to their second World Series title by defeating John McGraw's New York Giants. After the second game was called on account of darkness and ended in a tie, the series went to eight games. The Red Sox won the final game after Fred Snodgrass dropped an easy fly ball and later failed to go after a Speaker pop foul. After the pop foul, Speaker tied the game with a single. The Red Sox won the game in the bottom of the tenth inning. He finished the series with a .300 batting average, nine hits and four runs scored. Speaker was named the AL Most Valuable Player (MVP) for 1912. Though he did not lead the league in any offensive categories in 1913, Speaker finished fourth in AL MVP voting.

Speaker batted .338 and tied his career high of 12 double plays as an outfielder in . He hit .322 in . The Red Sox beat the Philadelphia Phillies in the 1915 World Series. The Red Sox were led by pitcher Babe Ruth, who was playing in his first full season. Ruth won 18 games and hit a team-high four home runs. Speaker got five hits, including a triple, in 17 at-bats during the series. He scored twice but did not drive in any runs.

Traded to the Indians

After 1915, Red Sox president Joseph Lannin wanted Speaker to take a pay cut from about $15,000 (equal to $ today) to about $9,000 (equal to $ today) because of the drop in his batting average; Speaker refused and offered $12,000 ($ today). On April 8, 1916, Lannin traded Speaker to the Cleveland Indians. In exchange, Boston received Sad Sam Jones, Fred Thomas and $50,000 ($ today). The angry Speaker held out until he received $10,000 (equal to $ today) of the cash that Boston collected.

For many years, this was considered the worst trade in Red Sox history, and was thought to be far more damaging to the Red Sox than the sale of Babe Ruth more than four years later. In his book about the Red Sox-Yankees rivalry, Emperors and Idiots, Mike Vaccaro recalled that for some time, "Red Sox fans shook their head(s) in fury" when recalling the trade. Vaccaro recalled that no one knew in the winter of 1919-20 that Ruth would blossom into a superstar. In contrast, Speaker had established himself as "indisputably the best player in the American League" by 1916.

With an annual salary of $40,000 (equal to $ today), Speaker was the highest paid player in baseball. Speaker hit over .350 in nine of his eleven years with Cleveland. In , he led the league in hits, doubles, batting average, slugging percentage and on-base percentage. Cobb had won the previous nine consecutive AL batting titles; Speaker outhit him with a .386 batting average compared to Cobb's .371.

The center field fence at Cleveland's Dunn Field was  from home plate until it was shortened to  in 1920. Even so, Speaker played so shallow in the outfield that he was able to execute six career unassisted double plays at second base, catching low line drives on the run and then beating baserunners to the bag. At least once he was credited as the pivot man in a routine double play. He was often shallow enough to catch pickoff throws at second base. At one point, Speaker's signature move was to come in behind second base on a bunt and make a tag play on a baserunner who had passed the bag.

While in Cleveland, Speaker participated in diverse activities off the baseball field. Speaker enrolled in an aviator training program in 1918. Though World War I ended less than two months after he enrolled, Speaker completed his training and served in the naval reserves for several years. He also owned a ranch in Texas and competed in roping events during the baseball offseason.

Stint as player-manager
From the day that Speaker arrived in Cleveland, he was effectively assistant manager to Lee Fohl, who rarely made an important move without consulting him. George Uhle recalled an incident from 1919 during his rookie year with the Indians. Speaker often signaled to Fohl when he thought that a pitcher should be brought in from the bullpen. One day, Fohl misread Speaker's signal and brought in a different pitcher than Speaker had intended. To avoid the appearance of overruling his manager, Speaker let the change stand. Pitcher Fritz Coumbe lost the game, Fohl resigned that night and Speaker became manager. Uhle said that Speaker felt bad for contributing to Fohl's departure.

Speaker guided the 1920 Indians to their first World Series win. In a crucial late season game against the second-place White Sox, Speaker caught a hard line drive hit to deep right-center field by Shoeless Joe Jackson, ending the game. On a dead run, Speaker leaped with both feet off the ground, snaring the ball before crashing into a concrete wall. As he lay unconscious from the impact, Speaker still held the baseball. In the 1920 World Series against Brooklyn, Speaker hit an RBI triple in the deciding game, which the Indians won 3–0. Cleveland's 1920 season was also significant due to the death of Ray Chapman on August 17. Chapman died after being hit in the head by a pitch from Carl Mays. Chapman had been asked about retirement before the season, and he said that he wanted to help Speaker earn Cleveland's first World Series victory before thinking of retirement.

During that championship season, Speaker is credited with introducing the platoon system, which attempted to match right-handed batters against left-handed pitchers and vice versa. Sportswriter John B. Sheridan was among the critics of the system, saying, "The specialist in baseball is no good and won't go very far... The whole effect of the system will be to make the players affected half men... It is farewell, a long farewell to all that player's chance of greatness... It destroys young ball players by destroying their most precious quality – confidence in their ability to hit any pitcher, left or right, alive, dead, or waiting to be born." Baseball Magazine was supportive, pointing out that Speaker had results that backed up his system.

The 1921 Indians remained in a tight pennant race all year, finishing  games behind the Yankees. The Indians did not seriously contend for the pennant from 1922 through 1925. Speaker led the league in doubles eight times, including every year between 1920 and 1923. He led the league's outfielders in fielding percentage in 1921 and 1922. On May 17, 1925, Speaker became the fifth member of the 3,000 hit club when he hit a single off pitcher Tom Zachary of the Washington Senators. Only Napoleon Lajoie had previously accomplished the feat as a member of the Indians.

AL President Ban Johnson asked Speaker and Detroit manager Cobb to resign their posts after a scandal broke in . Pitcher Dutch Leonard claimed that Speaker and Cobb fixed at least one game between Cleveland and Detroit. In a newspaper column published shortly before the hearings were to begin, Billy Evans characterized the accusations as "purely a matter of personal revenge" for Leonard. The pitcher was said to be upset with Cobb and Speaker after a trade ended with Leonard in the minor leagues. When Leonard refused to appear at the January 5, 1927, hearings to discuss his accusations, Commissioner Landis cleared both Speaker and Cobb of any wrongdoing. Both were reinstated to their original teams, but each team declared its manager free to sign elsewhere. Speaker did not return to big league managing and he finished his MLB managerial career with a 617–520 record.

At the time of his 1926 resignation, news reports described Speaker as permanently retiring from baseball to pursue business ventures. However, Speaker signed to play with the Washington Senators for . Cobb joined the Philadelphia Athletics. Speaker joined Cobb in Philadelphia for the  season; he played part time and finished with a .267 average. Prior to that season, Speaker had not hit for a batting average below .300 since 1908.

Speaker's major league playing career ended after 1928. He retired with 792 doubles, an all-time career record. Defensively, Speaker holds the all-time career records for assists as an outfielder and double plays as an outfielder. He remains the last batter to hit 200 triples in a career.

Later life

In  Speaker replaced Walter Johnson as the manager of the Newark Bears of the International League. In two seasons with Newark, he also appeared as a player in 59 games. When Speaker resigned during his second season, the Bears were in seventh place after a sixth-place finish in 1929. In January 1933 he became a part owner and manager of the Kansas City Blues. By May, Speaker had been replaced as manager but remained secretary of the club. By 1936, he had sold his share of the team. In 1937, Speaker was voted into the Baseball Hall of Fame during its second year of balloting. He was honored at the hall's first induction ceremony in 1939.

After his playing and managing days, Speaker was an entrepreneur and salesman. By 1937, Speaker had opened a wholesale liquor business and worked as a state sales representative for a steel company. He chaired Cleveland's boxing commission between 1936 and 1943. Newspaper coverage credited Speaker with several key reforms to boxing in Cleveland, including the recruitment of new officials and protections against fight fixing. Under Speaker, fight payouts went directly to boxers rather than managers. Speaker sorted out a scheduling conflict for a 1940 boxing match in Cleveland involving former middleweight champion Teddy Yarosz. Yarosz defeated Jimmy Reeves in ten rounds and the fight attracted over 8,300 spectators.

In 1937, Speaker sustained a 16-foot fall while working on a flower box near a second-story window at his home. Upon admission to the hospital, he underwent facial surgery. He was described as having "better than an even chance to live" and was suffering from a skull fracture, a broken arm and possible internal injuries. He ultimately recovered.

In 1939, Speaker was president of the National Professional Indoor Baseball League. The league had teams in New York, Brooklyn, Philadelphia, Boston, Cleveland, Chicago, Cincinnati and St. Louis. The league shut down operations due to poor attendance only two months after its formation. Speaker was one of the founders of Cleveland's Society for Crippled Children and he helped to promote the society's rehabilitation center, Camp Cheerful. Speaker served as vice president of the society, ran fundraising campaigns and received a distinguished service award from the organization. He became seriously ill with pneumonia in 1942. Speaker ultimately recovered, but Gay characterized Speaker's condition as "touch-and-go for several days".

In 1947, Speaker returned to baseball as "ambassador of good will" for Bill Veeck and the Cleveland Indians. He remained in advisory, coaching or scouting roles for the Indians until his death in 1958. In an article in the July 1952 issue of SPORT, Speaker recounted how Veeck hired him in 1947 to be a coaching consultant to Larry Doby, the first black player in the AL and the second in the major leagues. Before the Indians had signed Doby, he was the star second baseman of the Newark Eagles of the Negro leagues.  A SPORT photograph that accompanied the article shows Speaker mentoring five members of the Indians: Luke Easter, Jim Hegan, Ray Boone, Al Rosen and Doby. Speaker was inducted into the Texas Sports Hall of Fame in 1951. Texas was the first state to establish a state sports hall of fame and Speaker was in its inaugural induction class.

Death
Speaker died of a heart attack on December 8, 1958, at the age of 70, at Lake Whitney, Texas. He collapsed as he and a friend were pulling their boat into the dock after a fishing trip.  It was his second heart attack in four years. Speaker was buried at Fairview Cemetery in Hubbard, Texas.

After Speaker's death, Cobb said, "Terribly depressed. I never let him know how much I admired him when we were playing against each other... It was only after we finally became teammates and then retired that I could tell Tris Speaker of the underlying respect I had for him." Lajoie said, "He was one of the greatest fellows I ever knew, both as a baseball player and as a gentleman." Former Boston teammate Duffy Lewis said, "He was a team player. As great a hitter as he was, he wasn't looking out for his own average ... Speaker was the bell cow of our outfield. Harry Hooper and I would watch him and know how to play the hitters."

Legacy

Immediately after Speaker's death, the baseball field at the city park in Cleburne, Texas, was renamed in honor of Speaker. In 1961, the Tris Speaker Memorial Award was created by the Baseball Writers' Association of America to honor players or officials who make outstanding contributions to baseball. In 1999, he ranked number 27 on the Sporting News''' list of the 100 Greatest Baseball Players. He was named to the Major League Baseball All-Century Team. Speaker is mentioned in the poem "Line-Up for Yesterday"'' by Ogden Nash.

In 2008, former baseball players' union chief Marvin Miller, trying to defend the recently retired catcher Mike Piazza against claims that he should not be elected to the Hall of Fame because of association with the use of steroids, on the basis that the Hall of Fame has various unsavory people in it, opined that Speaker should be removed from the Hall of Fame because of alleged membership in the Ku Klux Klan. Miller said, "Some of the early people inducted in the Hall were members of the Ku Klux Klan: Tris Speaker, Cap Anson, and some people suspect Ty Cobb as well. I think that by and large, the players, and certainly the ones I knew, are good people. But the Hall is full of villains." Miller's comment about Anson has no basis, other than speculating that he could have been a Klansman since he was a racist during his playing career, which ended in 1897, although he was umpiring games with black players by 1901, including featuring the all-black Columbia Giants.  Miller, age 91 at the time the 2008 article appeared, is the earliest source for declaring that it is factual that Anson was a member of the Klan, based purely on an Internet search of sources that try to link Anson to the Klan.  By contrast, Speaker-Cobb-Rogers Hornsby biographer Charles C. Alexander, a Klan expert in his general history writings, told fellow baseball author Marty Appel, apparently referring to the 1920s (Anson died in 1922), “As I’ve suggested in the biographies, it’s possible that they [Speaker, Cobb and Hornsby] were briefly in the Klan, which was very strong in Texas and especially in Fort Worth and Dallas.  The Klan went all out to recruit prominent people in all fields, provided they were native born, Protestant and white.”

Baseball historian Bill James does not dispute this claim in apparently referring to Speaker and possibly Cobb, but says that the Klan had toned down its racist overtures during the 1920s and pulled in hundreds of thousands of men, including Hugo Black. James adds that Speaker was a staunch supporter of Doby when he broke the American League color barrier, working long hours with the former second baseman on how to play the outfield.

Regular season statistics

Managerial record

See also

 Boston Red Sox Hall of Fame
 List of Major League Baseball players to hit for the cycle
 List of Major League Baseball batting champions
 List of Major League Baseball annual doubles leaders
 List of Major League Baseball doubles records
 List of Major League Baseball hit records
 List of Major League Baseball annual home run leaders
 List of Major League Baseball career stolen bases leaders
 List of Major League Baseball player-managers
 List of Major League Baseball career triples leaders
 List of Major League Baseball career runs scored leaders
 List of Major League Baseball career runs batted in leaders
 List of Major League Baseball career hits leaders
 List of Major League Baseball career doubles leaders
 List of Major League Baseball career total bases leaders
 List of Major League Baseball triples records

Notes

References

Further reading
 
 Tris Speaker at the Encyclopedia of Cleveland History

External links

1888 births
1958 deaths
American League batting champions
American League home run champions
Baseball players from Texas
Boston Americans players
Boston Red Sox players
Cleburne Railroaders players
Cleveland Indians coaches
Cleveland Indians managers
Cleveland Indians players
Houston Buffaloes players
Kansas City Blues (baseball) managers
Little Rock Travelers players
Major League Baseball player-managers
Major League Baseball center fielders
Minor league baseball managers
National Baseball Hall of Fame inductees
Newark Bears (IL) players
People from Hubbard, Texas
Philadelphia Athletics players
Texas Wesleyan Rams baseball players
Washington Senators (1901–1960) players
Sp
Baseball coaches from Texas
The average directional movement index (ADX) was developed in 1978 by J. Welles Wilder as an indicator of trend strength in a series of prices of a financial instrument. ADX has become a widely used indicator for technical analysts, and is provided as a standard in collections of indicators offered by various trading platforms.

Calculations
The ADX is a combination of two other indicators developed by Wilder, the positive directional indicator (abbreviated +DI) and negative directional indicator (-DI). 
The ADX combines them and smooths the result with a smoothed moving average.

To calculate +DI and -DI, one needs price data consisting of high, low, and closing prices each period (typically each day). One first calculates the directional movement (+DM and -DM):

UpMove = today's high − yesterday's high
DownMove = yesterday's low − today's low
if UpMove > DownMove and UpMove > 0, then +DM = UpMove, else +DM = 0
if DownMove > UpMove and DownMove > 0, then -DM = DownMove, else -DM = 0

After selecting the number of periods (Wilder used 14 days originally), +DI and -DI are:

+DI = 100 times the smoothed moving average of (+DM) divided by average true range
-DI = 100 times the smoothed moving average of (-DM) divided by average true range

The smoothed moving average is calculated over the number of periods selected, and the average true range is a smoothed average of the true ranges. Then:

ADX = 100 times the smoothed moving average of the absolute value of (+DI − -DI) divided by (+DI + -DI)

Variations of this calculation typically involve using different types of moving averages, such as an exponential moving average, a weighted moving average or an adaptive moving average.

Interpretation
The ADX does not indicate trend direction or momentum, only trend strength. It is a lagging indicator; that is, a trend must have established itself before the ADX will generate a signal that a trend is under way. ADX will range between 0 and 100. Generally, ADX readings below 20 indicate trend weakness, and readings above 40 indicate trend strength. An extremely strong trend is indicated by readings above 50. Alternative interpretations have also been proposed and accepted among technical analysts.  For example it has been shown how ADX is a reliable coincident indicator of classical chart pattern development, whereby ADX readings below 20 occur just prior to pattern breakouts.  The value of the ADX is proportional to the slope of the trend. The slope of the ADX line is proportional to the acceleration of the price movement (changing trend slope). If the trend is a constant slope then the ADX value tends to flatten out.

Timing

Various market timing methods have been devised using ADX. One of these methods is discussed by Alexander Elder in his book Trading for a Living.  One of the best buy signals is when ADX turns up when below both Directional Lines  and +DI is above -DI.  You would sell when ADX turns back down.

References 

Technical indicators Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst. The amount of urine produced can be nearly 20 liters per day. Reduction of fluid has little effect on the concentration of the urine. Complications may include dehydration or seizures.

There are four types of DI, each with a different set of causes. Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone). This can be due to injury to the hypothalamus or pituitary gland or genetics. Nephrogenic DI (NDI) occurs when the kidneys do not respond properly to vasopressin. Dipsogenic DI is a result of excessive fluid intake due to damage to the hypothalamic thirst mechanism. It occurs more often in those with certain psychiatric disorders or on certain medications. Gestational DI occurs only during pregnancy. Diagnosis is often based on urine tests, blood tests and the fluid deprivation test. Diabetes insipidus is unrelated to diabetes mellitus and the conditions have a distinct mechanism, though both can result in the production of large amounts of urine.

Treatment involves drinking sufficient fluids to prevent dehydration. Other treatments depend on the type. In central and gestational DI, treatment is with desmopressin. Nephrogenic DI may be treated by addressing the underlying cause or by the use of a thiazide, aspirin or ibuprofen. The number of new cases of diabetes insipidus each year is 3 in 100,000. Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally. Nephrogenic DI can begin at any age. The term "diabetes" is derived from the Greek word meaning siphon.

Signs and symptoms
Excessive urination and extreme thirst and increased fluid intake (especially for cold water and sometimes ice or ice water) are typical for DI. The symptoms of excessive urination and extreme thirst are similar to what is seen in untreated diabetes mellitus, with the distinction that the urine does not contain glucose. Blurred vision is a rarity. Signs of dehydration may also appear in some individuals, since the body cannot conserve much (if any) of the water it takes in.

Extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain and growth, as well. They may present with fever, vomiting or diarrhea. Adults with untreated DI may remain healthy for decades as long as enough water is consumed to offset the urinary losses. However, there is a continuous risk of dehydration and loss of potassium that may lead to hypokalemia.

Cause
The several forms of diabetes insipidus are:

Central

Central DI has many possible causes. According to the literature, the principal causes of central DI and their oft-cited approximate frequencies are as follows:
 Idiopathic – 30%
 Malignant or benign tumors of the brain or pituitary – 25%
 Cranial surgery – 20%
 Head trauma – 16%

Nephrogenic

Nephrogenic diabetes insipidus is due to the inability of the kidney to respond normally to vasopressin.

Dipsogenic
Dipsogenic DI or primary polydipsia results from excessive intake of fluids as opposed to deficiency of arginine vasopressin. It may be due to a defect or damage to the thirst mechanism, located in the hypothalamus, or due to mental illness. Treatment with desmopressin may lead to water intoxication.

Gestational
Gestational DI occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placenta, which breaks down antidiuretic hormone (ADH). Gestational DI is thought to occur with excessive production and/or impaired clearance of vasopressinase.

Most cases of gestational DI can be treated with desmopressin (DDAVP), but not vasopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used.

Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsia, HELLP syndrome and acute fatty liver of pregnancy. These cause DI by impairing hepatic clearance of circulating vasopressinase. It is important to consider these diseases if a woman presents with diabetes insipidus in pregnancy, because their treatments require delivery of the baby before the disease will improve. Failure to treat these diseases promptly can lead to maternal or perinatal mortality.

Pathophysiology
Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium. In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels.

The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.

Neurogenic/central DI results from a lack of ADH; occasionally it can present with decreased thirst as regulation of thirst and ADH production occur in close proximity in the hypothalamus. It is encountered as a result of hypoxic encephalopathy, neurosurgery, autoimmunity or cancer, or sometimes without an underlying cause (idiopathic).

The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules; specifically, it acts on proteins called aquaporins and more specifically aquaporin 2 in the following cascade. When released, ADH binds to V2 G-protein coupled receptors within the distal convoluted tubules, increasing cyclic AMP, which couples with protein kinase A, stimulating translocation of the aquaporin 2 channel stored in the cytoplasm of the distal convoluted tubules and collecting ducts into the apical membrane. These transcribed channels allow water into the collecting duct cells. The increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine.

Nephrogenic DI results from lack of aquaporin channels in the distal collecting duct (decreased surface expression and transcription). It is seen in lithium toxicity, hypercalcemia, hypokalemia, or release of ureteral obstruction. Therefore, a lack of ADH prevents water reabsorption and the osmolarity of the blood increases. With increased osmolarity, the osmoreceptors in the hypothalamus detect this change and stimulate thirst. With increased thirst, the person now experiences a polydipsia and polyuria cycle. 

Hereditary forms of diabetes insipidus account for less than 10% of the cases of diabetes insipidus seen in clinical practice.

Diagnosis
To distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level (hypernatremia as dehydration develops). Urinalysis demonstrates a dilute urine with a low specific gravity. Urine osmolarity and electrolyte levels are typically low.

A fluid deprivation test is another way of distinguishing DI from other causes of excessive urination. If there is no change in fluid loss, giving desmopressin can determine if DI is caused by:
 a defect in ADH production
 a defect in the kidneys' response to ADH

This test measures the changes in body weight, urine output, and urine composition when fluids are withheld to induce dehydration. The body's normal response to dehydration is to conserve water by concentrating the urine. Those with DI continue to urinate large amounts of dilute urine in spite of water deprivation. In primary polydipsia, the urine osmolality should increase and stabilize at above 280 mOsm/kg with fluid restriction, while a stabilization at a lower level indicates diabetes insipidus. Stabilization in this test means, more specifically, when the increase in urine osmolality is less than 30 Osm/kg per hour for at least three hours. Sometimes measuring blood levels of ADH toward the end of this test is also necessary, but is more time consuming to perform.

To distinguish between the main forms, desmopressin stimulation is also used; desmopressin can be taken by injection, a nasal spray, or a tablet. While taking desmopressin, a person should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in the central nervous system. If desmopressin reduces urine output and increases urine osmolarity, the hypothalamic production of ADH is deficient, and the kidney responds normally to exogenous vasopressin (desmopressin). If the DI is due to kidney pathology, desmopressin does not change either urine output or osmolarity (since the endogenous vasopressin levels are already high).

Whilst diabetes insipidus usually occurs with polydipsia, it can also rarely occur not only in the absence of polydipsia but in the presence of its opposite, adipsia (or hypodipsia). "Adipsic diabetes insipidus" is recognised as a marked absence of thirst even in response to hyperosmolality. In some cases of adipsic DI, the person may also fail to respond to desmopressin.

If central DI is suspected, testing of other hormones of the pituitary, as well as magnetic resonance imaging, particularly a pituitary MRI, is necessary to discover if a disease process (such as a prolactinoma, or histiocytosis, syphilis, tuberculosis or other tumor or granuloma) is affecting pituitary function. Most people with this form have either experienced past head trauma or have stopped ADH production for an unknown reason.

Treatment
Treatment involves drinking sufficient fluids to prevent dehydration. Other treatments depend on the type. In central and gestational DI treatment is with desmopressin. Nephrogenic DI may be treated by addressing the underlying cause or the use of a thiazide, aspirin, or ibuprofen.

Central
Central DI and gestational DI respond to desmopressin which is given as intranasal or oral tablets. Carbamazepine, an anticonvulsive medication, has also had some success in this type of DI. Also, gestational DI tends to abate on its own four to six weeks following labor, though some women may develop it again in subsequent pregnancies. In dipsogenic DI, desmopressin is not usually an option.

Nephrogenic
Desmopressin will be ineffective in nephrogenic DI which is treated by reversing the underlying cause (if possible) and replacing the free water deficit. A thiazide diuretic, such as chlorthalidone or hydrochlorothiazide, can be used to create mild hypovolemia which encourages salt and water uptake in proximal tubule and thus improve nephrogenic diabetes insipidus. Amiloride has additional benefit of blocking Na uptake. Thiazide diuretics are sometimes combined with amiloride to prevent hypokalemia caused by the thiazides. It seems paradoxical to treat an extreme diuresis with a diuretic, and the exact mechanism of action is unknown but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering the glomerular filtration rate and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained.

Lithium-induced nephrogenic DI may be effectively managed with the administration of amiloride, a potassium-sparing diuretic often used in conjunction with thiazide or loop diuretics. Clinicians have been aware of lithium toxicity for many years, and traditionally have administered thiazide diuretics for lithium-induced polyuria and nephrogenic diabetes insipidus. However, amiloride has recently been shown to be a successful treatment for this condition.

Etymology 
The word "diabetes" ( or ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs) which literally means "a passer through; a siphon". Ancient Greek physician Aretaeus of Cappadocia (fl. in the first century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". The word "diabetes" is first recorded in English, in the form "diabete", in a medical text written around 1425.

"Insipidus" comes from Latin language insipidus (tasteless), from Latin: in- "not" + sapidus "tasty" from sapere "have a taste" — the full meaning is "lacking flavor or zest; not tasty". Application of this name to DI arose from the fact that diabetes insipidus does not cause glycosuria (excretion of glucose into the urine).

References

External links 

 

Endocrine diseases
Nephrology
Rare diseases
Thirst
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