Loading...

Italy after WWI
Quiz by Marie-Christine Castonguay
Customize this quiz to suit your class
Instantly translate to 100+ languages
Tag the questions with any skills you have. Your dashboard will track each student's mastery of each skill.
Give this quiz to my class
Multiple choice quiz on this reading: By 1900, the United States had claimed its place as a world power through the Spanish-American War. As the new century began, the country governed subject territories in Puerto Rico, Hawaii, Guam, the Wake Islands, and the Philippines. U.S. troops also occupied Cuba. U.S. businesses reached beyond the country's borders. During the first decade of the new century, the Coca-Cola Company, Quaker Oats, AT&T, the Standard Oil Company, Du Pont, General Electric, and Ford Motor Company seized the opportunity for international sales. After finding international markets, they built factories abroad, taking advantage of lower labor costs in foreign countries. Then they asked for U.S. protection of their investments and interests. Foreign countries invested heavily in Central America. U.S. investors focused on banana plantations and mining, as well as railroads, with little money in government bonds. By 1913, U.S. investments in Central America totaled about $93 million. British investment in Central America peaked at about $115 million in 1913. About $75 million of that total represented railroad holdings, mostly in Costa Rica and Guatemala. The other $40 million was in government bonds, which were worth little or nothing. The Roosevelt Corollary to the Monroe Doctrine From its earliest days, the United States claimed a special interest in the Western Hemisphere. The Monroe Doctrine, issued in 1823, warned European powers to keep their hands off Latin America. In 1902, Britain, Germany, and Italy mounted a naval blockade of Venezuela. They wanted to force the government to repay its debts. All the countries involved eventually agreed to settle the matter by arbitration. The United States stood back and did nothing, but U.S. citizens were clearly uneasy with the appearance of European military forces in "their" hemisphere. In 1904, President Theodore Roosevelt issued a corollary to the Monroe Doctrine, saying that the United States would act as a police officer to keep order in the region. He intended both to keep European military forces out of the hemisphere and to protect U.S. and European investors, exerting whatever pressure or control on Latin American governments that might be necessary to these ends. In 1905, the Dominican Republic owed $40 million in debts to European lenders. In order to prevent the European nations from using military force to collect their debts, Roosevelt used U.S. power. The United States basically took over collection of Dominican customs taxes, declared that $20 million of the debt was unjustified, and began repayment of the rest. Building a Canal The United States needed a canal through Central America, in order to save shipping time and costs. Colombia had the best location for a canal, and the United States negotiated a deal. It would pay Colombia $10 million for a three-mile-wide strip of land and would make annual rental payments of $250,000 yearly, beginning in 1912. Colombia's Senate turned down the deal, and Roosevelt exploded in rage, calling its members "foolish and homicidal corruptionists." Roosevelt considered seizing the land for the canal by military force but soon found an easier way. The province of Panama seceded from Colombia. A U.S. gunship stood off shore, protecting the Panamanian rebels. They formed a new republic under the protection of the United States. The new country of Panama and the United States agreed on a canal treaty within days. The new treaty had similar terms except that the Canal Zone would be five miles wide, instead of three, and the United States would guarantee and maintain the independence of Panama. Revolutions While Roosevelt welcomed the revolution that separated Panama from Colombia, he opposed most other revolutionary activity. So did his successors in office, William Howard Taft and Woodrow Wilson. The U.S. presidents sent troops to put down revolutions in Nicaragua and Haiti, using U.S. military forces to set up new governments in those countries and maintaining military occupations for years. U.S. military interventions were frequent throughout the hemisphere. Dollar Diplomacy President Taft preferred using "dollar diplomacy" to control Latin American countries. In Honduras, for example, U.S.-based banana companies virtually ran the government. Taft supported expanded U.S. investment in South and Central American countries, the Caribbean, and the Far East. He ordered Secretary of State Philander Chase Knox to protect U.S. investments, sending in military troops if necessary. On the World Stage As a world power, the United States did not limit its involvement to the Western Hemisphere. In 1905, President Roosevelt brought Russia and Japan to the negotiating table to end their war over control of Korea and Manchuria. Roosevelt agreed to Japanese annexation of Korea in return for Japan giving up any claim to China, Hawaii, and the Philippines. Roosevelt won the Nobel Peace Prize for settling this dispute. In 1906, Roosevelt's negotiating powers were tested again. This time, he mediated a dispute between the Alliance powersâGermany, Austria-Hungary, and Italyâwith the EntenteâFrance, Russia, and Britainâover control of Morocco. The United States backed France and ended the dispute. No longer an upstart, the United States had taken its place as a world power alongside its former colonial ruler.
Continental Drift Theory. From the discussion of the rock cycle, it has been pointed out that through Earth's external and internal processes. Earth's surface is constantly changing. However, this idea of a changing environment did not conform with the belief of earlier scientists. Rather, they thought that the geographic positions of ocean basins and continents have been static since the beginning of time. It was around the 1500s when Leonardo da Vinci, upon his discovery of fossil seashells found at the high mountains of Italy, first thought of the idea that the areas where mountains are located may have been oceans in the past. Through time, other fossils of marine organisms found far above the current sea level further supported the idea that mountains were uplifted and weathering wore them down. At around the 1800s, most scientists have accepted the idea that Earth's crust is undergoing large vertical movements or uplifting. There was also evidence of possible horizontal movements, but the scientists then were not convinced about it. Alfred Wegener showed evidence of horizontal or lateral movement of the continents in his continental drift theory. According to him, the continents have drifted around the world and have once formed a giant landmass or supercontinent called Pangaea. To support his theory, Alfred Wegener presented a set of geographical, biological, and climatic evidence.Wegener's geographical evidence included the jigsaw puzzle fit of the current continents. He pointed out that the coastlines of South America and Africa seem to fit together. He also pointed the presence of mountain ranges having similar rock types and age but separated by vast oceans, like that of the folded rocks of the Caledonian mountains. The same folded rocks run through West Africa, North America, Newfoundland, Ireland, Wales, Scotland, Greenland, and Norway, all of which are now separated by the Atlantic Ocean. A geographical evidence on the similar rock types in West Africa, North America, Greenland, and Europe is found. The biological evidence came in the discovery of similar plant and animal fossils in different continents separated by oceans. The animal fossils of Mesosaurus and Lystrosaurus indicate that they were not capable of crossing the oceans to reach the other continents. If they were, the fossils should have been more widely distributed Africa, Australia, India, and South America were too large to be carried by wind. This indicates that the areas where the fossils were found were closely linked. It has also been found out that the plant only grew in areas with subpolar climate, which would indicate that the landmasses were located near the South Pole.Lastly, for his climatic evidence, Wegener discovered that a glacial period occurred during the late Paleozoic era in Southern Africa, South America, Australia, and India. The initial explanation for this event was global cooling, but it was rejected because large tropical swamps with so much vegetation were found at the same time in the Northern Hemisphere. This further supported the idea that the supercontinent was indeed near the South Pole, and the continents in Northern Hemisphere were once near the equator. The glacial period also left glacial striations, or the scratches glaciers make as they move across on the underlying bedrock, on the aforementioned continents. For such an event to happen, the continents would have to be connected. SCIENCE PIONEER. Alfred Wegener (1880-1930). Alfred Wegener was a German polar researcher, geophysicist, and meteorologist. He was known for his work on the continental drift theory. In his effort to defend his work, he went to the Greenland ice sheet where he died.Even with all the compelling evidence, the continental drift theory hardly convinced the scientific community at that time because Wegener was unable to identify a credible mechanism that drives the continental drift. He was unable to clearly explain how the continents moved and how the larger continents broke through the ocean floor. Eventually, critics of the continental drift began to accept the theory when new evidence supporting the theory was discovered. The new evidence led to a more encompassing theory the theory of plate tectonics. This theory provided a more convincing explanation as to how the continents moved. The evidence that paved the way for the theory of plate tectonics was the idea of wandering poles. Scientists began studying volcanic rocks to determine the location of the magnetic poles. When volcanic rocks crystallize, the minerals with magnetic properties align themselves parallel to Earth's magnetic field at the time the minerals were formed. This finding allowed scientists to determine the polarity of Earth's magnetic field and the magnetic inclination that showed the location of the poles. Upon studying the paleomagnetism of the rocks, geophysicists found out that rocks from various locations point to different magnetic north poles, suggesting that the poles have wandered. Since movement of magnetic poles is very unlikely, scientists have accepted the idea that the continents are indeed moving. And if the continents are moving, scientists thought that maybe the ocean basins are moving too. They also discovered that some rocks showed magnetic reversals, which led them to believe that the magnetic north pole now was not always the magnetic north pole. Seafloor Spreading. After World War II, exploration on the ocean floor became the focus of many geologic studies. It was only then that the ocean ridge system was discovered. A geologist in Princeton University named Harry Hess, along with other scientists, studied this ocean ridge system and hypothesized that the oceanic crust was moving away from the ridge. His hypothesis, known as seafloor spreading, showed that the ocean floor is split along the ridge where the magma rises to form the new ocean floor.Because of this, rocks located near the ridge are younger than those that are located magnetic polarity of Earth is also preserved in those rocks. Withe ridge scientists were able to see the magnetic reversals in the ocean floor, and they were able to make use of information to determine that the ocean floor is moving at a rate of about 10 cm per year. Plate Tectonics. Confirmation of the seafloor spreading hypothesis proved that continents are not moving above the ocean floor. Rather, it is the fragments of the lithosphere. The lithosphere is the rigid layer that is composed of the uppermost mantle and the crust that carry the continents and the ocean basins along. These fragments of the lithosphere are called plates. Underneath the lithosphere is a weaker region in the mantle known as asthenosphere that behaves like a fluid. Thus, the lithosphere floats above the asthenosphere, making it detached and free to move. This became the basis of the theory of plate tectonics. Now that it has been made clear that it is the plates which are moving, the question as to how they move remained. Sir Arthur Holmes proposed the driving force for this plate movement in 1919. He suggested that the movement in the mantle carries the plates along. It was previously discussed that Earth's interior is very hot due to the heat produced by radioactive decay. Convection takes place in the mantle, keeping the asthenosphere hot and weak. The convection currents produced in the asthenosphere are the ones carrying the lithospheric plates and making them move. However, convection currents are not enough. Mechanisms such as ridge push and slab pull aid the convection currents to slowly move the lithospheric plates. Ridge push occurs at mid ocean ridges which are higher in elevation than the surrounding trenches and abyssal plains. The new ocean floor from the ridge is hot and relatively thin. As it moves away from the ridge, it cools down and gets denser, heavier, and thicker. Below this cooling ocean floor is the asthenosphere, which is less dense. This area becomes a massive shear zone and the new ocean floor will effectively slide down the slope of the asthenosphere. When the plate collides with another plate with lesser density, the denser plate sinks and a subduction zone is formed. When the subducting plate sinks, it pulls on the rest of the plate behind it. These mechanisms explain the movement of the plates.Earth has seven major lithospheric plates that account for 94% of Earth's surface. These are the North American Plate, South American Plate, Pacific Plate, African Plate, Eurasian Plate, Indo-Australian Plate, and Antarctic Plate. These plates are constantly moving relative to the other plates. Thus, the interaction of plates occurs mostly along the boundaries. These movements are plotted using information from earthquakes and volcanic activities. There are three main types of plate boundaries: convergent, divergent, and transform boundaries Convergent boundaries are boundaries where two plates move towards each other A convergent boundary is also known as destructive margin since this is where the collision between two plates occhins. There are three types of convergence-oceanic oceanic, oceanic-continental, and continental-continental. Trenches are features of the ocean floor that are present in both oceanic-oceanic boundary and oceanic-continental boundary. Subduction occurs at the trenches, therefore, these are characterized as the deepest parts of Earth. A divergent boundary is the opposite of convergent boundary: two plates move away from each other. Divergent boundaries create new crust; thus, they are also known as constructive margins. The ocean ridge system is a divergent boundary where new ocean floor is produced as magma rises, pushing the older rocks aside.Transform boundary is also known as conservative plate margin since two plates just move past one another, neither creating nor destroying land. Earthquake epicenters are usually detected at transform boundaries because the rocks tend to break and not fold or sink, like in convergent boundaries. Evolution of the Ocean Basins. Both the movement of the plates and seafloor are responsible for the evolution of ocean basins. Along the divergent boundary where ocean ridge systems are found, magma is released and new ocean floor is created. Along convergent boundaries, the ocean floor is being destroyed. The evolution of the ocean basins started during the time when Pangaea was still present and was surrounded by the vast ocean or superocean known as Panthalassa, also called Paleo-Pacific or "old Pacific." Upon the initial break up of Pangaea into Laurasia and Gondwanaland, the Tethys Sea began to form. Then, the Eurasian and North about, forming the North Atlantic. The South Atlantic only started to form when the African Plate and South American Plate separated. The continued movement of the plates created the Himalayas at one side and separated the Pacific Ocean and Atlantic Ocean at the other side, which consequently formed the current ocean basins. Both the movement of the plates and seafloor are responsible for the evolution of ocean basins. Along the divergent boundary where ocean ridge systems are found, magma is released and new ocean floor is created. Along convergent boundaries, the ocean floor is being destroyed. The evolution of the ocean basins started during the time when Pangaea was still present and was surrounded by the vast ocean or superocean known as Panthalassa, also called Paleo-Pacific or "old Pacific." Upon the initial break up of Pangaea into Laurasia and Gondwanaland, the Tethys Sea began to form. Then, the Eurasian and North about, forming the North Atlantic. The South Atlantic only started to form when the African Plate and South American Plate separated. The continued movement of the plates created the Himalayas at one side and separated the Pacific Ocean and Atlantic Ocean at the other side, which consequently formed the current ocean basins.Continents do not immediately end at the point where the ocean meets the land. They may extend slightly into the oceans. The portion of the continent that is submerged is called continental margin. There are two types of continental margin: passive margin and active margin. A passive continental margin consists of a continental shelf, continental slope, and continental rise. It is not associated with plate boundaries; thus, there are very little tectonic activities. An active continental margin only has a continental shelf and a continental slope. It is associated with plate boundaries; thus, a main feature of this boundary is a trench. The different features of a continental margin are the following: 1. The continental shelf is the gently-sloping submerged portion of the continent. 2. The continental slope is the steep slope after the continental shelf. It is still part of the continent. 3. The continental rise is the gently-sloping area after the continental slope and before the ocean floor. 4. The trenches are the deepest parts of the ocean. These are narrow depressions caused by the subduction of the ocean floor along the convergent boundaries. 5. The mid-oceanic ridge is the mountain range system in the ocean. It is responsible for the production of new ocean floor. This is the region where new magma constantly emerges from. SCIENCE CAREER. A scientific illustrator uses art to inform and communicate complex details and concepts of science. He/She makes use of scientifically informed observations and research along with his/her technical art and aesthetic skills to make accurate representations. In Natural History, the scientific illustrators recreate how the extinct species look like by working with scientists and fossil records. Moreover, with the advances in technology, illustrators are now into 3D modelling, animation, and video making. Earth's History. All the processes that have been discussed require long periods of time to create a noticeable change on Earth's surface. You can just imagine how long it would take to create an oceanas vast as the Pacific Ocean if the ocean floor moves only at about 10 cm/year. It is then important to know the history of Earth to learn the complexities of its past and be able to use it to understand the present. Just like learning the history of a country that requires one to read a lot of books, learning the history of Earth involves studying a lot of rocks. Rocks, especially sedimentary rocks, contain a lot of information about Earth's past. It holds the key to most of the geologic processes that happened on Earth and the key to uncovering how life on Earth evolved. But these discoveries are worthless if there is no time perspective. Thus, one of the most important contributions of geologists to mankind is the geologic time scale, which holds a history that is exceedingly long.
MYTH The British helped the Jews displace the native Arab population of Palestine. FACT Herbert Samuel, a British Jew who served as the first High Commissioner of Palestine, placed restrictions on Jewish immigration âin the âinterests of the present populationâ and the âabsorptive capacityâ of the country.â1 The influx of Jewish settlers was said to force the Arab fellahin (native peasants) from their land. This was when less than a million people lived in an area that now supports more than nine million. The British limited the absorptive capacity of Palestine when, in 1921, Colonial Secretary Winston Churchill severed nearly four-fifths of Palestineâsome thirty-five thousand square milesâto create a new Arab entity, Transjordan. As a consolation prize for the Hejaz and Arabia (which are both now Saudi Arabia) going to the Saud family, Churchill rewarded Sharif Husseinâs son Abdullah for his contribution to the war against Turkey by installing him as Transjordanâs emir. The British went further and placed restrictions on Jewish land purchases in what remained of Palestine. By 1949, the British had allotted 87,500 acres of the 187,500 acres of cultivable land to Arabs and only 4,250 acres to Jews. This contradicted Article 6 of the Mandate which stated that âthe Administration of PalestineâŠshall encourage, in cooperation with the Jewish AgencyâŠclose settlement by Jews on the land, including State lands and waste lands not acquired for public purposes.â2 Ultimately, the British admitted that the argument about the countryâs absorptive capacity was specious. The Peel Commission said, âThe heavy immigration in the years 1933â36 would seem to show that the Jews have been able to enlarge the absorptive capacity of the country for Jews.â3 MYTH The British allowed Jews to flood Palestine while Arab immigration was tightly controlled. FACT The British response to Jewish immigration set a precedent of appeasing the Arabs, which was followed for the duration of the Mandate. The British restricted Jewish immigration while allowing Arabs to enter the country freely. Apparently, London did not feel that a flood of Arab immigrants would affect the countryâs âabsorptive capacity.â During World War I, the Jewish population in Palestine declined because of the war, famine, disease, and expulsion by the Turks. In 1915, approximately 83,000 Jews lived in Palestine among 590,000 Muslim and Christian Arabs. According to the 1922 census, the Jewish population was 83,000, while the Arabs numbered 643,000.4 Thus, the Arab population grew exponentially while that of the Jews stagnated. In the mid-1920s, Jewish immigration to Palestine increased primarily because of anti-Jewish economic legislation in Poland and Washingtonâs imposition of restrictive quotas.5 The record number of immigrants in 1935 (see table) was a response to the growing persecution of Jews in Nazi Germany. The British administration considered this number too large, however, so the Jewish Agency was informed that less than one-third of the quota it asked for would be approved in 1936.6 The British gave in further to Arab demands by announcing in the 1939 White Paper that an independent Arab state would be created within ten years and that Jewish immigration was to be limited to 75,000 for the next five years, after which it was to cease altogether. It also forbade land sales to Jews in 95% of the territory of Palestine. The Arabs, nevertheless, rejected the proposal. Jewish Immigration to Palestine7 1919 1,806 1931 4,075 1920 8,223 1932 12,533 1921 8,294 1933 37,337 1922 8,685 1934 45,267 1923 8,175 1935 66,472 1924 13,892 1936 29,595 1925 34,386 1937 10,629 1926 13,855 1938 14,675 1927 3,034 1939 31,195 1928 2,178 1940 10,643 1929 5,249 1941 4,592 1930 4,944 By contrast, throughout the Mandatory period, Arab immigration was unrestricted. In 1930, the Hope Simpson Commission, sent from London to investigate the 1929 Arab riots, said the British practice of ignoring the uncontrolled illegal Arab immigration from Egypt, Transjordan, and Syria had the effect of displacing the prospective Jewish immigrants.8 The British governor of the Sinai from 1922 to 1936 observed, âThis illegal immigration was not only going on from the Sinai, but also from Transjordan and Syria, and it is very difficult to make a case out for the misery of the Arabs if at the same time their compatriots from adjoining states could not be kept from going in to share that misery.â9 The Peel Commission reported in 1937 that the âshortfall of land isâŠdue less to the amount of land acquired by Jews than to the increase in the Arab population.â10 MYTH The British changed their policy to allow Holocaust survivors to settle in Palestine. FACT The gates of Palestine remained closed for the duration of the war, stranding hundreds of thousands of Jews in Europe, many of whom became victims of Hitlerâs âFinal Solution.â After the war, the British refused to allow the survivors of the Nazi nightmare to find sanctuary in Palestine. On June 6, 1946, President Truman urged the British government to relieve the suffering of the Jews confined to displaced persons camps in Europe by immediately accepting 100,000 Jewish immigrants. Britainâs foreign minister Ernest Bevin replied sarcastically that the United States wanted displaced Jews to immigrate to Palestine âbecause they did not want too many of them in New York.â11 Some Jews reached Palestine, many smuggled in on dilapidated ships organized by the Haganah. Between August 1945 and the establishment of the State of Israel in May 1948, sixty-five âillegalâ immigrant ships, carrying 69,878 people, arrived from European shores. In August 1946, however, the British began to intern those they caught in camps on Cyprus. Approximately 50,000 people were detained in the camps, and 28,000 remained imprisoned when Israel declared independence.12 MYTH As the Jewish population grew, the plight of the Palestinian Arabs worsened. FACT In July 1921, Hasan Shukri, the mayor of Haifa and president of the Muslim National Associations, sent a telegram to the British government in reaction to a delegation of Palestinians that went to London to try to stop the implementation of the Balfour Declaration. Shukri wrote: We are certain that without Jewish immigration and financial assistance there will be no future development of our country as may be judged from the fact that the towns inhabited in part by Jews such as Jerusalem, Jaffa, Haifa, and Tiberias are making steady progress while Nablus, Acre, and Nazareth where no Jews reside are steadily declining.13 The Jewish population increased by 470,000 between World War I and World War II, while the non-Jewish population rose by 588,000.14 The permanent Arab population increased by 120% between 1922 and 1947.15 This rapid growth of the Arab population was a result of several factors. One was immigration from neighboring statesâconstituting 37% of the total immigration to pre-state Israelâby Arabs who wanted to take advantage of the higher standard of living the Jews had made possible.16 The Arab population also grew because of the improved living conditions created by the Jews as they drained malarial swamps and brought improved sanitation and health care to the region. Thus, for example, the Muslim infant mortality rate fell from 201 per thousand in 1925 to 94 per thousand in 1945, and life expectancy rose from 37 years in 1926 to 49 in 1943.17 The Arab population increased the most in cities where large Jewish populations had created new economic opportunities. From 1922â1947, the non-Jewish population increased by 290% in Haifa, 131% in Jerusalem, and 158% in Jaffa. The growth in Arab towns was more modest: 42% in Nablus, 78% in Jenin, and 37% in Bethlehem.18 MYTH Jews stole Arab land. FACT Despite the growth in their population, the Arabs continued to assert they were being displaced. From the beginning of World War I, however, part of Palestineâs land was owned by absentee landlords who lived in Cairo, Damascus, and Beirut. About 80% of the Palestinian Arabs were debt-ridden peasants, semi-nomads, and Bedouins.19 Jews went out of their way to avoid purchasing land in areas where Arabs might be displaced. They sought land that was largely uncultivated, swampy, cheap, andâmost importantâwithout tenants. In 1920, Labor Zionist leader David Ben-Gurion expressed his concern about the Arab fellahin, whom he viewed as âthe most important asset of the native population.â He insisted that âunder no circumstances must we touch land belonging to fellahs or worked by them.â Instead, he advocated helping liberate them from their oppressors. âOnly if a fellah leaves his place of settlement,â Ben-Gurion added, âshould we offer to buy his land, at an appropriate price.â20 Jews only began to purchase cultivated land after buying all the uncultivated territory. Many Arabs were willing to sell because of the migration to coastal towns and because they needed money to invest in the citrus industry.21 When John Hope Simpson arrived in Palestine in May 1930, he observed, âThey [the Jews] paid high prices for the land and, in addition, they paid to certain of the occupants of those lands a considerable amount of money which they were not legally bound to pay.â22 In 1931, Lewis French conducted a survey of landlessness for the British government and offered new plots to any Arabs who had been âdispossessed.â British officials received more than 3,000 applications, of which 80% were ruled invalid by the governmentâs legal adviser because the applicants were not landless Arabs. This left only about 600 landless Arabs, 100 of whom accepted the government land offer.23 In April 1936, a new outbreak of Arab attacks on Jews was instigated by local Palestinian leaders who were later joined by Arab volunteers led by a Syrian guerrilla named Fawzi al-Qawuqji, the commander of the Arab Liberation Army. By November, when the British finally sent a new commission headed by Lord Peel to investigate, 89 Jews had been killed and more than 300 wounded.24 The Peel Commissionâs report found that Arab complaints about Jewish land acquisition were baseless. It pointed out that âmuch of the land now carrying orange groves was sand dunes or swamp and uncultivated when it was purchasedâŠThere was at the time of the earlier sales little evidence that the owners possessed either the resources or training needed to develop the land.â25 Moreover, the Commission found the shortage was âdue less to the amount of land acquired by Jews than to the increase in the Arab population.â The report concluded that the presence of Jews in Palestine, along with the work of the British administration, had resulted in higher wages, an improved standard of living, and ample employment opportunities.26 It is made quite clear to all, both by the map drawn up by the Simpson Commission and by another compiled by the Peel Commission, that the Arabs are as prodigal in selling their land as they are in useless wailing and weeping (emphasis in the original). âTransjordanâs king Abdullah27 Even at the height of the Arab revolt in 1938 (which began in April 1936 with the murder of two Jews by Arabs and the subsequent murder of two Arab workers by members of the Jewish underground28), the British high commissioner to Palestine believed the Arab landowners were complaining about sales to Jews to drive up prices for lands they wished to sell. Many Arab landowners had been so terrorized by Arab rebels they decided to leave Palestine and sell their property to the Jews.29 The Jews paid exorbitant prices to wealthy landowners for small tracts of arid land. âIn 1944, Jews paid between $1,000 and $1,100 per acre in Palestine, mostly for arid or semiarid land; in the same year, rich black soil in Iowa was selling for about $110 per acre.â30 By 1947, Jewish holdings in Palestine amounted to about 463,000 acres. Approximately 45,000 were acquired from the mandatory government, 30,000 were bought from various churches, and 387,500 were purchased from Arabs. Analyses of land purchases from 1880 to 1948 show that 73% of Jewish plots were purchased from large landowners, not poor fellahin.31 Many leaders of the Arab nationalist movement, including members of the Muslim Supreme Council, and the mayors of Gaza, Jerusalem, and s sold land to the Jews. Asâad el-Shuqeiri, a Muslim religious scholar and father of Palestine Liberation Organization chairman Ahmed Shuqeiri, took Jewish money for his land. Even King Abdullah leased land to the Jews.32 MYTH The British helped the Palestinians to live peacefully with the Jews. FACT In 1921, Haj Amin el-Husseini first began to organize fedayeen (âone who sacrifices himselfâ) to terrorize Jews. El-Husseini hoped to duplicate the success of Kemal AtatĂŒrk in Turkey by driving the Jews out of Palestine just as Kemal had driven the invading Greeks from his country.33 Arab radicals gained influence because the British administration was unwilling to take effective action against them until they began a revolt against British rule. Colonel Richard Meinertzhagen, former head of British military intelligence in Cairo, and later chief political officer for Palestine and Syria, wrote in his diary that British officials âincline towards the exclusion of Zionism in Palestine.â The British encouraged the Palestinians to attack the Jews. According to Meinertzhagen, Col. Bertie Harry Waters-Taylor (financial adviser to the military administration in Palestine 1919â23) met with el-Husseini in 1920, a few days before Easter, and told him that âhe had a great opportunity at Easter to show the worldâŠthat Zionism was unpopular not only with the Palestine administration but in Whitehall.â He added that âif disturbances of sufficient violence occurred in Jerusalem at Easter, both General [Louis] Bols [chief administrator in Palestine, 1919â20] and General [Edmund] Allenby [commander of the Egyptian force, 1917â19, then high commissioner of Egypt] would advocate the abandonment of the Jewish Home. Waters-Taylor explained that freedom could only be attained through violence.â34 El-Husseini took the colonelâs advice and instigated a riot. The British withdrew their troops and the Jewish police from Jerusalem, allowing the Arab mob to attack Jews and loot their shops. Because of el-Husseiniâs overt role in instigating the pogrom, the British decided to arrest him. He escaped, however, and was sentenced to ten years in absentia. A year later, some British Arabists convinced High Commissioner Herbert Samuel to pardon el-Husseini and to appoint him Mufti (a cleric in charge of Jerusalemâs Islamic holy places). By contrast, Vladimir Jabotinsky and several followers, who had formed a Jewish defense organization during the unrest, were sentenced to 15 years. They were released a few months later.35 Samuel met with el-Husseini on April 11, 1921, and was assured âthat the influences of his family and himself would be devoted to tranquility.â Three weeks later, riots in Jaffa and elsewhere left forty-three Jews dead.36 El-Husseini consolidated his power and took control of all Muslim religious funds in Palestine. He used his authority to gain control over the mosques, the schools, and the courts. No Arab could reach an influential position without being loyal to the Mufti. His power was so absolute that âno Muslim in Palestine could be born or die without being beholden to Haj Amin.â37 The Muftiâs henchmen also ensured he would have no opposition by systematically killing Palestinians who discussed cooperation with the Jews from rival clans. As the spokesman for Palestinian Arabs, el-Husseini did not ask that Britain grant them independence. On the contrary, in a letter to Churchill in 1921, he demanded that Palestine be reunited with Syria and Transjordan.38 The Arabs found rioting an effective political tool because of the lax British response toward violence against Jews. In handling each riot, the British prevented Jews from protecting themselves but made little effort to prevent the Arabs from attacking them. After each outbreak, a British commission of inquiry would try to establish the cause of the violence. The conclusion was always the same: The Arabs feared being displaced by the Jews. To stop the rioting, the commissions would recommend that restrictions be placed on Jewish immigration. Thus, the Arabs learned they could always stop the influx of Jews by staging riots. This cycle began after a series of riots in May 1921. After failing to protect the Jewish community from Arab mobs, the British appointed the Haycraft Commission to investigate the cause of the violence. Although the panel concluded the Arabs had been the aggressors, it rationalized the cause of the attack: âThe fundamental cause of the riots was a feeling among the Arabs of discontent with, and hostility to, the Jews, due to political and economic causes, and connected with Jewish immigration, and with their conception of Zionist policy.â39 One consequence of the violence was the institution of a temporary ban on Jewish immigration. The Arab fear of being âdisplacedâ or âdominatedâ was an excuse for their attacks on Jewish settlers. Note, too, that these riots were not inspired by nationalistic fervorânationalists would have rebelled against their British overlordsâthey were motivated by economics, the radical Islamic views of the Mufti, and misunderstanding. In 1929, Arab provocateurs convinced the masses that the Jews had designs on the Temple Mount (a tactic still used today to incite violence). A Jewish religious observance at the Western Wall, which forms a part of the Temple Mount, served as a pretext for rioting by Arabs against Jews, which spilled out of Jerusalem into other villages and towns, including Safed and Hebron. Again, the British administration made no effort to prevent the violence, and, after it began, the British did nothing to protect the Jewish population. After six days of mayhem, the British finally brought troops in to quell the disturbance. By this time, most of Hebronâs Jews had fled or been killed. In all, 133 Jews were killed and 399 wounded in the pogroms.40 After the riots, the British ordered an investigation, resulting in the Passfield White Paper. It said the âimmigration, land purchase and settlement policies of the Zionist Organization were already or were likely to become, prejudicial to Arab interests. It understood the mandatory governmentâs obligation to the non-Jewish community to mean that Palestineâs resources must be primarily reserved for the growing Arab economy.â41 This meant it was necessary to restrict Jewish immigration and land purchases. MYTH The Mufti was not a Nazi collaborator. FACT In 1941, Haj Amin al-Husseini, the Mufti of Jerusalem, fled to Germany and met with Adolf Hitler, Heinrich Himmler, Joachim Von Ribbentrop, and other Nazi leaders. He wanted to persuade them to extend the Nazisâ anti-Jewish program to the Arab world. The Mufti sent Hitler fifteen drafts of declarations he wanted Germany and Italy to make concerning the Middle East. One called on the two countries to declare the illegality of the Jewish home in Palestine. He also asked the Axis powers to âaccord to Palestine and to other Arab countries the right to solve the problem of the Jewish elements in Palestine and other Arab countries in accordance with the interest of the Arabs, and by the same method that the question is now being settled in the Axis countries.â42 In November 1941, the Mufti met with Hitler, who told him the Jews were his foremost enemy. The Nazi dictator rebuffed the Muftiâs requests for a declaration in support of the Arabs, however, telling him the time was not right. The Mufti offered Hitler his âthanks for the sympathy which he had always shown for the Arab and especially Palestinian cause, and to which he had given clear expression in his public speeches.â He added, âThe Arabs were Germanyâs natural friends because they had the same enemies as had Germany, namelyâŠthe Jews.â Hitler told the Mufti he opposed the creation of a Jewish state and that Germanyâs objective was destroying the Jewish element in the Arab sphere.43 In 1945, Yugoslavia sought to indict the Mufti as a war criminal for his role in recruiting twenty thousand Muslim volunteers for the SS, who participated in the killing of Jews in Croatia and Hungary. He escaped French detention in 1946, however, and continued his fight against the Jews from Cairo and later Beirut where he died in 1974. MYTH The bombing of the King David Hotel was part of a deliberate terror campaign against civilians. FACT British troops seized the Jewish Agency compound on June 29, 1946, and confiscated large quantities of documents. At about the same time, more than 2,500 Jews from all over Palestine were arrested. A week later, news of a massacre of 40 Jews in a pogrom in Poland reminded the Jews of Palestine how Britainâs restrictive immigration policy had condemned thousands to death. In response to the British provocations, and a desire to demonstrate that the Jewsâ spirit could not be broken, the United Resistance Movement planned to bomb the King David Hotel, which housed the British military command and the Criminal Investigation Division in addition to hotel guests. The Haganah pulled out of the plot and left it up to the Irgun. Irgun leader Menachem Begin stressed his desire to avoid civilian casualties and the plan was to warn the British so they would evacuate the building before it was blown up. Three telephone calls were placed on July 22, 1946, one to the hotel, another to the French Consulate, and a third to the Palestine Post warning that explosives in the King David Hotel would soon be detonated. The call to the hotel was received and ignored. Begin quotes one British official who supposedly refused to evacuate the building, saying, âWe donât take orders from the Jews.â44 As a result, when the bombs exploded, the casualty toll was high: 91 killed and 45 injured. Among the casualties were 15 Jews. Few people in the main part of the hotel were injured.45 For decades, the British denied they had been warned. In 1979, however, a member of the British Parliament provided the testimony of a British officer who heard other officers in the King David Hotel bar joking about a Zionist threat to the headquarters. The officer who overheard the conversation immediately left the hotel and survived.46 In contrast to Arab attacks against Jews, which Arab leaders hailed as heroic actions, the Jewish National Council denounced the bombing of the King David.47 1 Aharon Cohen, Israel and the Arab World, (NY: Funk and Wagnalls, 1970), p. 172
The Revolt of the Northern Earls (1569) Most people in the North remained loyal to the Catholic noble families who controlled the north and their Catholic faith. When Elizabeth came to power, she promoted ânew menâ (Protestants) from the gentry and the powerful Catholic nobles lost their power and influence. This led them to organise the most serious rebellion of Elizabethâs reign in 1569. Why did the Northern Earlâs revolt? The Earls had lost their power when Elizabeth became Queen (and wanted it back). They wanted Catholicism restored in England (and felt that ordinary Catholics would support it). Elizabeth was refusing to marry or to name an heir, causing uncertainty about Englandâs future. Mary Queen of Scots (if freed from prison) could replace Elizabeth and solve all these problems Who were the key players in the Revolt? Earl of Northumberland âą A Catholic who had held an important position under Mary I. âą He lost a lot of influence under Elizabeth (as she favoured Protestant gentry) âą Elizabeth also took the rights to a valuable copper mine found on his lands Earl of Westmorland âą From a rich Catholic family in the north Also the Duke of Norfolkâs brother in law Duke of Norfolk âą Englandâs most senior Protestant noble, but he had very close links to old northern Catholic families, & was sympathetic to them & greedy for power. âą He hated William Cecil & Robert Dudley, Earl of Leicester (Elizabethâs favourite) who were Protestant and from the gentry âą He planned to marry Mary QS, but later backed down and urged the earls to call off the rebellion. Mary also supported the plan to marry him What role did religion play? (7/10 â but only because it was linked to power) âą Most northerners held onto their Catholic beliefs & although Elizabeth didnât persecute them, they knew that she wanted their religion to gradually die out, so they supported the revolt. âą In 1561 Elizabeth hired a strict Protestant as archbishop of Durham to promote Protestantism in the north, but he was unpopular & turned many northerners against the Protestant religion. What role did politics/power play? (9/10 â this was the most important cause of the revolt) âą The Northern Earls lost a lot of their power/influence (even jobs/money under Elizabeth) âą Northumberland was jealous of new Protestant families being given top jobs in the North âą William Cecil & Robert Dudley were not from ancient noble families, but were very close to the Queen, so the northern Earls resented them getting top jobs in her Government âą Elizabeth also confiscated large areas of land & the profits from their copper mines âą It is possible, that had Elizabeth allowed the Catholic Northern Earls to keep their jobs, money and influence at court, they may have âtoleratedâ her as a Protestant Queen (greedy/selfish). What role did Mary Queen of Scots and the Succession play? âą Elizabeth was refusing to name an heir and it was becoming clear that she would not marry âą If Mary Queen of Scots married the Duke of Norfolk, England would have an heir and England would be Catholic again. The country would be stable without people competing for power. âą However, some of Elizabethâs courtiers got worried that it might not work and that it might lead to charges of treason (punishable by death) âą So by September 1569, Robert Dudley (Earl of Leicester) decided to tell Elizabeth about the plot. By this time it was much more serious than simply marrying Norfolk to Mary. âą Mary QS had secretly asked Spain to send troops to help the rebellion & overthrow Elizabeth Plan for the Revolt of the Northern Earls (1569) âą The Earls of Northumberland & Westmorland will raise rebel troops from their lands in the north and take control of Durham. âą The rebels will then march south towards London to join with the Duke of Norfolk âą 1000s of Spanish troops will land in England to support the rebel forces âą The Duke of Norfolk & rebel forces will seize control of Government & overthrow Elizabeth âą Mary Queen of Scots is to be freed, ready to marry the Duke of Norfolk Key Events of the Revolt âą Once Elizabeth knew of the plot, Norfolk was arrested and sent to the Tower of London âą The Northern Earls were worried they would be executed for their involvement and in a desperate attempt to avoid punishment, pushed ahead with the revolt âą They raised an army of ordinary Catholics and took control of Durham cathedral âą Catholic mass was celebrated across the north for 2 weeks. âą They then headed south, to try and free Mary âą Mary QSs was moved south to Coventry on the orders of Elizabeth, so she couldnât escape âą The rebellion failed as Spanish troops never arrived âą Elizabethâs friend (Earl of Sussex) had raised an army of 7,000 men to defend her throne. Results: âą The rebellion was a serious threat to Elizabeth âą She executed 450 rebels in the north âą Northumberland was executed in 1572 & his head was put on a spike on the city gate âą The Privy Council called for the Duke of Norfolkâs execution too, but Elizabeth released him. âą Mary Queen of Scots was kept in prison for the next 14 years. âą The failed plot also led the Pope to take action against Elizabeth âą In 1570 he excommunicated Elizabeth from the Catholic Church âą He also issued a Papal Bull (order) calling on all loyal Catholics to overthrow her hoping it would encourage another rebellion. âą In 1571 Elizabeth called parliament to pass an Act making it treason to claim that she was not the rightful Queen and to bring in/print papal bulls in England. The Significance of the Revolt of the Northern Earls âą It was the first and most serious rebellion by English Catholics against Elizabeth âą Treason laws were made much harsher âą It ended the influence of the powerful Catholic Earls in the North âą It led to harsher treatment of Catholics, e.g. 1572 Elizabeth sent the Earl of Huntingdon (strict Protestant) to the north to carry out laws against Catholics (and suppress Catholicism). âą Although Elizabethâs brutal revenge on the rebels show how serious a threat it was, most Catholics in the north stayed loyal, but the Popeâs Papal Bull now put their loyalty in doubt There was little support for the revolt among the rest of the Catholic nobility and ordinary people. When faced with a choice between Elizabeth and their religion, most Catholics chose to support the Queen. 1569, was the last time English Catholics tried to remove Elizabeth by force. The future plots against her were always uncovered by Cecil & Walsingham, before they had a chance to get any public support. Despite this, the Northern Revolt & Papal Bull changed Elizabethâs attitude towards Catholics who were now seen as potential traitors. From 1570, Elizabeth became less tolerant of recusants (people refusing to attend her church) & took increasingly tough measures against Catholics. The Ridolfi, Throckmorton & Babington plots âą In the 1870s-80s, there were 3 Catholic plots to assassinate Elizabeth & replace her with Mary. âą The plots were supported by France, Spain, the Pope and some Catholic nobles. âą They reinforced the form Mary & from Catholics at home and abroad. Also the threat from Spain. The Ridolfi Plot (1571) âą Ridolfi was an Italian banker living in England and a spy for the Pope. âą He organised a plot to murder Eliz, marry Mary QS to the Duke of Norfolk & make her Queen. âą The Pope & King Philip supported the plot & Philip told the Duke of Alba in the Netherlands to prepare 10,000 troops (but to only invade AFTER the English had overthrown Elizabeth). âą The plot failed because Sir William Cecil intercepted coded letters & Norfolk was executed. âą Mary was kept under closer watch. âą Ridolfi was abroad when the plot was discovered and never returned to England. 1574: Catholic Priests and Priest Holes âą From 1574 Catholic priests were smuggled into England to keep the religion alive. âą They stayed with rich Catholic families, so Catholic families were kept under surveillance. âą Catholic homes were raided â to find âpriest holesâ where Catholic priests were hiding. âą Catholic priests who were found could be hung, drawn and quartered (although not all were) âą In 1581, Parliament also passed 2 new tougher laws against Catholics: âą Recusants would be fined ÂŁ20 (which would bankrupt most families) âą Trying to convert people to Catholicism was now treason (punishable by death) The Throckmorton Plot (1583) âą It aimed to assassinate Elizabeth and replace her with Mary. The French Duke of Guise (Maryâs cousin) would invade England with an army, funded by King Philip (Pope also supported it). âą An Englishman, Throckmorton carried messages between Mary & Catholic plotters abroad. âą Sir Walsingham (Secretary of State) uncovered the plot after his agents found the plans for the plot in Throckmortonâs house. Throckmorton confessed under torture and was executed. Significance: âą The plots showed that Maryâs presence in England posed a serious threat âą It also showed that France & Spain were a serious threat (& could invade) âą Throckmortonâs papers showed a list of Catholic supporters in England, so the threat from English Catholics was also real âą 1,000s of Catholics were imprisoned or kept under surveillance/house arrest âą In 1585 another Act was passed to make helping Catholic priests punishable by death. âą The Bond of Association was signed by the English nobles & gentry & forced them to promise to execute anyone who tried to overthrow the Queen. Weaknesses of the Plots The plots lacked public support & were uncovered by informers & spies before they had the chance to work King Philip was reluctant to destroy his alliance with Elizabeth (France was still a bigger rival) so is support for the plots was half-hearted, he rarely followed through on his promises to help the plotters or send an army The Babington Plot (1586) In 1586, Walsingham used his spy network to PROVE that Mary supported the Babington plot. His evidence persuaded Elizabeth to put Mary on trial & execute her for treason. âą This was a plot to murder Elizabeth and put Mary on the throne âą France would invade England with 60,000 men and Spain would also send an army âą Babington was passing coded letters between Mary & her supporters in England & Europe. âą But all of her letters were being intercepted and read by Walsingham. âą Walsingham used his spies to follow every stage of the plot & had the letters decoded âą One of Maryâs letters approved plans to murder the Queen and free Mary from prison âą They also contained the names of 6 Catholics who planned to kill Elizabeth âą They were arrested, hung, drawn and quartered for treason. âą Mary had been implicated in plots before, but Elizabeth was always reluctant to execute her âą But the proof found by Walsingham finally persuaded her to put Mary on trial âą In October 1586, Mary was found guilty & was sentenced to death âą But Elizabeth still hesitated, and did not sign the death warrant until February 1587. Significance 1) This plot was very significant because by 1585 England was effectively at war with Spain since Elizabeth had sent her army to help the Dutch Protestants fight the Spanish 2) This meant that Elizabethâ situation was more dangerous than during previous plots. 3) Elizabethâs government also became more determined to crush Catholicism 4) 1000s of recusants were arrested & 31 priests were executed 5) Maryâs execution removed the Catholic threat at home 6) English Catholics had no one to rally around, & lost hope of overthrowing Elizabeth 7) But Maryâs death increased the threat of a foreign invasion as England was at war with Spain and King Philip had been preparing an attack on England since 1585 8) Maryâs death made Philip even more determined to invade, Mary had left her claim to the English throne to King Philip upon her death Why was Mary Queen of Scots finally executed? 1 âą A new Act in 1585 stated that in the event of Elizabethâs assassination, Mary could be executed as long as she had been proved guilty & Walsingham had provided hard proof. 2 âą Another reason was that by 1587, it was clear that Philip was planning to invade England âą There were rumours that Spanish ships had landed in Wales & that Mary had escaped. This convinced Elizabeth that Mary had to be executed if she wanted to keep her throne. Walsinghamâs Spy Network: âą Walsingham (Secretary of State from 1573) had a network of spies all over England & abroad. He had spies in every English town, some were normal people paid to spy on neighbours. âą He also had agents and spies in Spain, France, Germany and Italy âą He hired mathematicians to crack written codes and people to open/seal letters secretly âą He also pressured captured Catholic priests to spy on others for him in return for a pardon. âą He used double agents to infiltrate Catholic networks - to help him discover traitors âą But he only used torture against Catholic priests caught in England in the most serious cases âą But 130 priests and 60 of their supporters were still executed during Elizabethâs reign. Why did Relations with Spain get worse (1569-1588) âą England had tried to stay on good terms with Spain, because Eliz wanted to avoid an expensive war that could lead to her being overthrown (English Catholics could support it) âą But by the 1570s, Elizabeth wanted to have an empire of her own. âą She also needed to make more money to defend her country and throne (by improving trade) âą This religious, political and economic rivalry led to growing tensions between England & Spain Political and Religious Rivalry 1) Land abroad, gave countries wealth/power. By the 1580s, Eliz wanted an empire to rival Spainâs (especially as Spain had supported the Catholic plots against Eliz â even if it was half-hearted) 2) Religion was another cause of conflict. Philip opposed Elizabethâs religious settlement 1559 3) Luckily for Elizabeth, in the 1550s Spain & France were competing to be the greatest European power and both wanted England as an ally against the other. 4) But from 1567, Spanish ships were sailing to the Netherlands with money for the Albaâs army 5) This alarmed English Protestants and Elizabethâs Privy Council who put more and more pressure on her to send an army to help the Dutch Protestant rebels (in the Netherlands). Economic (commercial) Rivalry: The New World, privateers and Sir Francis Drake âą Under Elizabeth, English merchants wanted to make big profits in the New World (Americas). âą However, trading in the New World was difficult because of Spainâs power 1) Spain controlled most of the New World where there were huge profits to be made and anyone who wanted to trade there needed a licence from Spain (which it would not give): 2) But the Americas had valuable crops like tobacco, sugar, and also silver and gold 3) Elizabeth secretly encouraged privateers to trade illegally & raid Spanish ports & ships 4) At first Elizabeth denied responsibility for their actions, which delaye war with Spain Sir Francis Drake: Elizabeth sends Drake to rob Spanish colonies and ships (which infuriates Spain) 1) Spainâs support for the Ridolfi plot (1571) made her more willing to support Drake âą In 1572 Eliz hired Drake to sail to the New World & steal ÂŁ40,000 of Spanish silver âą In 1577 she sent Drake back again with a secret mission to rob Spainâs colonies/ships âą Drake brought back ÂŁ400,000 of Spanish treasure & claimed an area of California in Elizabethâs name (New Albion). He gave a lot of this money to Elizabeth âą He boosted Englandâs finances at a time of growing concern over Spainâs threat âą He became famous as the first Englishman to circumnavigate the globe. âą Eliz knighted Drake as a reward, which infuriated Philip (as he saw Drake as a pirate) âą Drakeâs actions & his claim to California made it clear that England did not accept Spainâs domination of the New World. Elizabethâs Support for the Dutch Rebels led to War with Spain (1585-88) âą By the 1580s, tension between England & Spain had reached boiling point âą At first, Eliz refused to send her army to help the Dutch rebels, because she wanted to avoid a war with Spain. So she tried to get the Spanish to leave the Netherlands in other INDIRECT ways: 1) By allowing Drake (& other English privateers) to attack and rob Spanish ships and colonies 2) By encouraging others (the French heir/mercenaries) to fight the Spanish in the Netherlands âą In the 1570s, Elizabeth promised to marry the heir to the French throne (the Duke of Alencon) so that he would take an army to fight the Spanish in the Netherlands The Spanish Fury (1576) and the Pacification of Ghent (1576) âą By 1576, the Spanish Govt in the Netherlands was bankrupt (the war was expensive) âą After months without pay, Spainâs soldiers violently robbed Dutch towns in the âSpanish Furyâ Spanish troops rebelling and robbing cities in the Netherlands in 1576. This united the Dutch Protestants & Catholics against Spain. They drew up the âPacification of Ghentâ (demanding that): âą Spanish troops leave the Netherlands âą Spain allows the Dutch to rule themselves âą The persecution of Dutch Protestants stops What did Elizabeth do? âą Elizabeth sent ÂŁ100,000 to help the Dutch rebels âą In 1577 King Philipâs brother, Don Juan agreed to the rebels demands (but this was a trick) as just 6 months later Philip sent an even bigger army to attack the Dutch. âą Elizabeth then hired a mercenary army of 6000 English & Scottish volunteers to help the Dutch. âą But her plan backfired because the mercenaries destroyed Dutch Catholic churches, which caused the Catholics to make peace with Spain. âą In 1578, her Privy Council urged Eliz to send her official army to help the Dutch, but she refused. The Dutch were disappointed & turned to France for help. The French Duke of Alencon arrived with an army to fight the Spanish, but by 1579 Spain had taken control again. âą In 1580 Spain got even stronger after Philip won control of Portugal & its empire. âą So Elizabeth gave the Duke of Alencon ÂŁ70,000 to help him fight the Spanish âą In 1582, Alencon took his army the Netherlands but failed to defeat Spain. âą Elizabethâs foreign policy in the Netherlands had failed & she had only managed to annoy Spain 1585: Why did Eliz finally decide to send her army to the Netherlands? (she lost her 2 main allies) âą 1584 the Duke of Alencon died (so he could no longer fight the Spanish in the Netherlands) âą 1 month later, William of Orange, the leader of the Dutch Protestant rebels was assassinated. âą In 1585, Spain signed the Treaty of Joinville with France, agreeing to stamp out Protestantism in France/Europe meaning France & Spain were now allies against Protestantism âą Elizabeth now felt she had no choice but to send her official army to the Netherlands âą She signed the Treaty of Nonsuch with the Dutch rebels which promised them military help 1585: Robert Dudleyâs campaign in the Netherlands was unsuccessful She sent 7,400 man army to the Netherlands led by Dudley. But he accepted the title of âGovernor Generalâ. Eliz was angry as it suggested that she had deposed King Philip so she told Dudley to resign this position. His army was defeated by the bigger Spanish Army as Eliz had not provided him with enough money to win. In 1587 Dudley resigned and returned to England. At the same time, Eliz had sent Drake to raid Spanish colonies in the New World to disrupt King Philipâs flow of money. Philip was furious and told the Pope he planned to invade England at the end of 1585. Drake singes the King of Spainâs beard 1587 âą In 1587 Elizabeth ordered Drake to attack Spainâs most important port Cadiz âą He destroyed 30 ships in 3 days â known as the âSingeing of the King of Spainâs Beardâ âą He also stole lots of wood, meaning the Armada did not have quality barrels for food/water âą Drakeâs disruption delayed the Armada by a year (& meant that its food rotted in 1588). âą This bought England more time to prepare for war. The Spanish Armada (1588) The Plan âą By 1588, the Spanish Armada was ready to invade England âą It had 130 ships with 8000 sailors & 18,000 soldiers âą The Duke of Medina Sidonia would lead the Armada, but he had little experience at sea and didnât want the job âą The Armada would collect Parmaâs army from France & sail to England under the protection of the Armadaâs warships âą Parma would march to London to depose Elizabeth & impose a Catholic government in England. 1) The Armada reached the English Channel The Armada set out in May 1588, but was delayed for a few weeks by bad weather In July the Armada was near England & signal fires were lit to warn Elizabeth English ships set sail to meet the Armada The Armada sailed up the channel in a crescent (half moon) formation, to use the large armed galleons to protect the weaker supply and army ships The English navy carried out a few minor raids, but did not inflict much damage Only 2 Spanish ships were lost (by accident) 2) The English attack the Spanish at Calais (with fire ships) and at Gravelines The Armada sailed up the English channel & anchored at Calais to wait for Parmaâs army But Parmaâs men didn't reach the coast in time (news had reached them too late) At midnight, the English sent 8 fireships into the Spanish ships causing panic They cut their anchors, broke formation & headed for the open sea (without Parma) The Spanish ships sailed to Gravelines, but bad weather stopped them returning to Calais The English attacked and the battle lasted many hours (5 Spanish ships were sunk) The rest were forced to sail away from France towards Scotland The English ships followed them to make sure they didnât come back to collect Parmaâs army 3) The Armadaâs Journey back to Spain around Ireland was a disaster The Spanish called off the attack and returned to Spain around Scotland & Ireland Bad storms sank many ships and wrecked more on the Irish coast Many sailors died from starvation & disease â less than half the men made it back to Spain How did England defeat the Spanish Armada? !) Faster Ships âą Years before the battle, England had started building smaller, faster ships (galleons) that could fire canon balls quicker & further than Spanish ships âą Spanish ships were huge and slow to change direction. 2) Bad Planning & Communication (Spanish) âą Philipâs plan to join with the Duke of Parmaâs army in France was risky. âą Parma had lots of small ships which took 48 hours to load, man and set sail. âą It took too long (a week) for word to reach Parma that Medina was in the English Channel, by which time Medina had set sail to Calais. âą Parma was not ready to set sail & the English were already ready to attack (leaving Medina with very little back up when anchored in France). 2) English Tactics were more effective âą Spanish ships aimed to come alongside the English ones, jump on board & fight the enemy. But the English ships were faster & kept a safe distance. âą They chased the Armada down the Channel, with heavy cannon fire, which forced the Spanish to arrive in France before Parmaâs army was ready âą As the Armada was waiting, the English sent fireships into the Spanish fleet. âą This caused the Armada to panic, cut their anchors & sail away to the north âą When the Spanish ships regrouped, the English attacked them in the Battle of Gravelines & the Armada was forced to sail north, chased by faster ships. 5) Bad Weather âą Strong winds made it impossible for the Armada to return & pick up Parmaâs army and storms wrecked or sunk Spanish ships as they tried to return home along the Scottish-Irish coasts. 2) Spanish Supplies âą The Armada was not well supplied with food/weapons. Drakeâs attack on Cadiz port in 1587 had destroyed food barrels. Delays in setting sail meant that by the time the English attacked the Armada it had been at sea for 10 weeks and had rotting food. 1000s died from starvation/disease. The consequences of the English victory? âą Victory over the Spanish Armada gave Elizabeth a great propaganda victory âą A new portrait was made, and a medal was made to commemorate her victory, it said âGod blew and they were scatteredâ. âą Elizabeth claimed that God was on the side of Protestantism âą This led to a feeling of English pride and encouraged the Dutch rebels to renew their fight against the Spanish âą The defeat of the Armada showed the strength of the English navy and gave England the confidence to trade and explore more widely at sea âą Although Philip did not give up and continued the war for the rest of Elizabethâs reign, the defeat had cost Spain dearly, both financially and in terms of its power âą The Armada marked the start of a long decline in Spainâs power and fortunes. âą English ships were sent on voyages of discovery and set up valuable new trade routes âą By the end of Elizabethâs reign, the navy was also trying to set up a new colony in Virginia âą The English victory boosted Elizabethâs popularity & strengthened the Protestant cause
Create questions based on the following text Not long ago, I grabbed breakfast at a hotel in southern Spain. The only cereal available was a local version of frosted corn flakes, so I readied myself to enjoy a bowl of my childhood favorite. But my sweet indulgence wasn't what I'd expected: The cereal milk was heated â apparently standard in this part of Spain â and my poor frosted flakes immediately turned to mush. Not so grrrrrrreat. Soggy flakes or not, I find breakfast to be a fun part of my travel day, especially because the experience varies so much from one country's breakfast table to the next. The farther north you go in Europe, the heartier the breakfasts. The heaviest is the traditional British "fry." Also known as a "Plate of Cardiac Arrest," the fry is a fundamental part of the bed-and-breakfast experience, and is generally included in your room price. A standard fry comes with cereal or porridge, a fried egg, Canadian-style bacon or sausage (and sometimes mackerel or haggis), a grilled tomato, sautĂ©ed mushrooms, baked beans, and fried bread or toast. This protein-stuffed meal can tide me over until dinner. You'll quickly figure out which parts of the fry you like. Your host will likely ask you up front which breakfast items you actually like, rather than serve you the whole shebang and risk having to throw out uneaten food. The Scandinavian breakfasts buffet is the perennial favorite for the "most food on the table" award. It pays to take advantage of breakfast smorgasbords when you can. For about $20 (a cheap meal in these parts), you can dig into an all-you-can-eat extravaganza of fresh bread, cheeses, yogurt, cereal, boiled eggs, herring, cold cuts, and coffee or tea. In place of cereal and milk, Scandinavians like to pour thick yogurt over their granola. Throughout the Netherlands, Belgium, Germany, Austria, Switzerland, and most points east of there, expect a more modest buffet â but still plenty of options (rolls, bread, jam, cold cuts, cheeses, fruit, yogurt, and cereal). In these countries, there's a good chance of finding hard-boiled eggs, but scrambled or fried eggs are relatively rare. In Poland, track down jajecznica, the local wake-up call of eggs scrambled with kielbasa sausage, served with a side of potato pancakes. The breakfast of choice in Russia is oladi, pancakes perfectly fried to be crisp on the outside but soft in the middle, then topped with sour cream, honey, or berries. Germans have an endearing habit of greeting others in the breakfast room with a slow and dour "Morgen" ("Morning" â short for "good morning"), though they have plenty to be happy about. Breakfast is usually included, and offers hearty fuel for the day: ham, eggs, cheese, bread, rolls, and pots of coffee. In Switzerland, don't miss an opportunity to try Bircher Muesli, a healthful mix of oats, nuts, yogurt, and fruit that tastes far more delicious than it looks. If breakfast is optional, take a walk to the nearest bakery â every German, Austrian, and Swiss town has at least a few bakeries offering a world of enticing varieties of bread and pastries, baked fresh every morning. As you move south and west (France, Italy, Spain, and Portugal), skimpier "continental" breakfasts are the norm. You'll mostly likely get a roll with marmalade or jam, occasionally a slice of ham or cheese, and coffee or tea. The good news? These little breakfasts compel you to sample regional favorites: In Spain, look for chocolate con churros (fritters served with a thick, warm chocolate drink), pan con tomate (a toasted baguette rubbed with fresh garlic and ripe tomato), or a tortilla española (a hearty slice of potato omelet). Italian breakfasts are particularly tiny, but the delicious red orange juice you get is made from Sicilian blood oranges. And you can buy a delightful toasted sandwich from a corner bar anywhere, anytime in Italy to make up for the minuscule breakfast. In France, locals just grab a warm croissant and coffee on the way to work. Queue up with the French and consider the yummy options: croissants studded with raisins, packed with crushed almonds, or filled with chocolate or cream. If you expect breakfast to be too sparse, plan ahead to supplement it with a piece of fruit and a wrapped chunk of cheese from a local market. Being a juice man, I keep a liter box of OJ in my room for a morning eye-opener. Coffee drinkers know that breakfast is the only cheap time to caffeinate yourself. Some hotels will serve you a bottomless cup of a rich brew only with breakfast. After that, the cups acquire bottoms and refills will cost you. Juice is generally available at breakfast, but in Mediterranean countries, you have to askâŠand you'll probably be charged. In many countries, breakfast is included in your hotel bill, though if you make prior arrangements with the hotelier, you may be able to skip breakfast and pay a lower price for the room. If breakfast costs extra, it's often optional, and you can usually save money and gain atmosphere by buying coffee and a roll or croissant at the cafĂ© down the street or by brunching picnic-style in the park. When deciding whether to request breakfast, consider your timing; if you need to get an early start, skip the breakfast â few hotel breakfasts are worth waiting around for. Come to the European breakfast table with an adventurous spirit. I'm a big-breakfast traditionalist at home, but when I feel the urge for an American breakfast in Europe, I beat it to death with a hard roll.
Not long ago, I grabbed breakfast at a hotel in southern Spain. The only cereal available was a local version of frosted corn flakes, so I readied myself to enjoy a bowl of my childhood favorite. But my sweet indulgence wasn't what I'd expected: The cereal milk was heated â apparently standard in this part of Spain â and my poor frosted flakes immediately turned to mush. Not so grrrrrrreat. Soggy flakes or not, I find breakfast to be a fun part of my travel day, especially because the experience varies so much from one country's breakfast table to the next. The farther north you go in Europe, the heartier the breakfasts. The heaviest is the traditional British "fry." Also known as a "Plate of Cardiac Arrest," the fry is a fundamental part of the bed-and-breakfast experience, and is generally included in your room price. A standard fry comes with cereal or porridge, a fried egg, Canadian-style bacon or sausage (and sometimes mackerel or haggis), a grilled tomato, sautĂ©ed mushrooms, baked beans, and fried bread or toast. This protein-stuffed meal can tide me over until dinner. You'll quickly figure out which parts of the fry you like. Your host will likely ask you up front which breakfast items you actually like, rather than serve you the whole shebang and risk having to throw out uneaten food. The Scandinavian breakfasts buffet is the perennial favorite for the "most food on the table" award. It pays to take advantage of breakfast smorgasbords when you can. For about $20 (a cheap meal in these parts), you can dig into an all-you-can-eat extravaganza of fresh bread, cheeses, yogurt, cereal, boiled eggs, herring, cold cuts, and coffee or tea. In place of cereal and milk, Scandinavians like to pour thick yogurt over their granola. Throughout the Netherlands, Belgium, Germany, Austria, Switzerland, and most points east of there, expect a more modest buffet â but still plenty of options (rolls, bread, jam, cold cuts, cheeses, fruit, yogurt, and cereal). In these countries, there's a good chance of finding hard-boiled eggs, but scrambled or fried eggs are relatively rare. In Poland, track down jajecznica, the local wake-up call of eggs scrambled with kielbasa sausage, served with a side of potato pancakes. The breakfast of choice in Russia is oladi, pancakes perfectly fried to be crisp on the outside but soft in the middle, then topped with sour cream, honey, or berries. Germans have an endearing habit of greeting others in the breakfast room with a slow and dour "Morgen" ("Morning" â short for "good morning"), though they have plenty to be happy about. Breakfast is usually included, and offers hearty fuel for the day: ham, eggs, cheese, bread, rolls, and pots of coffee. In Switzerland, don't miss an opportunity to try Bircher Muesli, a healthful mix of oats, nuts, yogurt, and fruit that tastes far more delicious than it looks. If breakfast is optional, take a walk to the nearest bakery â every German, Austrian, and Swiss town has at least a few bakeries offering a world of enticing varieties of bread and pastries, baked fresh every morning. As you move south and west (France, Italy, Spain, and Portugal), skimpier "continental" breakfasts are the norm. You'll mostly likely get a roll with marmalade or jam, occasionally a slice of ham or cheese, and coffee or tea. The good news? These little breakfasts compel you to sample regional favorites: In Spain, look for chocolate con churros (fritters served with a thick, warm chocolate drink), pan con tomate (a toasted baguette rubbed with fresh garlic and ripe tomato), or a tortilla española (a hearty slice of potato omelet). Italian breakfasts are particularly tiny, but the delicious red orange juice you get is made from Sicilian blood oranges. And you can buy a delightful toasted sandwich from a corner bar anywhere, anytime in Italy to make up for the minuscule breakfast. In France, locals just grab a warm croissant and coffee on the way to work. Queue up with the French and consider the yummy options: croissants studded with raisins, packed with crushed almonds, or filled with chocolate or cream. If you expect breakfast to be too sparse, plan ahead to supplement it with a piece of fruit and a wrapped chunk of cheese from a local market. Being a juice man, I keep a liter box of OJ in my room for a morning eye-opener. Coffee drinkers know that breakfast is the only cheap time to caffeinate yourself. Some hotels will serve you a bottomless cup of a rich brew only with breakfast. After that, the cups acquire bottoms and refills will cost you. Juice is generally available at breakfast, but in Mediterranean countries, you have to askâŠand you'll probably be charged. In many countries, breakfast is included in your hotel bill, though if you make prior arrangements with the hotelier, you may be able to skip breakfast and pay a lower price for the room. If breakfast costs extra, it's often optional, and you can usually save money and gain atmosphere by buying coffee and a roll or croissant at the cafĂ© down the street or by brunching picnic-style in the park. When deciding whether to request breakfast, consider your timing; if you need to get an early start, skip the breakfast â few hotel breakfasts are worth waiting around for. Come to the European breakfast table with an adventurous spirit. I'm a big-breakfast traditionalist at home, but when I feel the urge for an American breakfast in Europe, I beat it to death with a hard roll. Can you make 5 questions based on the text
Received: 26 November 2019 Revised: 10 January 2020 Accepted: 19 January 2020 DOI: 10.1111/obr.13005 PEDIATRICS/PHYSIOLOGY Adipokines: A gear shift in puberty DesirĂ©e Nieuwenhuis | NatĂ lia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-α alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- α and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-α 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-α, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-α and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. The majority of the studies examining boys with obesity indicate an early onset of puberty, while not all reported an earlier onset of puberty. In detail, high leptin, TNF-α, and IL-6 levels combined with low adiponectin levels stimulate the activation of the HPG axis in girls and boys with obesity, and 5, 45, 50, 51 REFERENCES 1. Kumar S, Kelly AS. Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. May- o Clin Proc. 2017;92(2):251-265. 2. Reinehr T, Roth CL. Is there a causal relationship between obesity and puberty? The Lancet Child & adolescent health. 2019;3(1):44-54. 3. WorldHealthOrganization. Facts and figures on childhood obesity. 2017. 4. Guglielmi V, Sbraccia P. Obesity phenotypes: depot-differences in adipose tissue and their clinical implications. Eat Weight Disord. 2018; 23(1):3-14. 5. Gomez-Hernandez A, Beneit N, Diaz-Castroverde S. Escribano O. Dif- ferential role of adipose tissues in obesity and related metabolic and vas- cular complications. 2016;2016:1-15, 1216783. 6. Zwick RK, Guerrero-Juarez CF, Horsley V, Plikus MV. Anatomical, physiological, and functional diversity of adipose tissue. Cell Metab. 2018;27(1):68-83. 7. Gulyaeva O, Dempersmier J, Sul HS. Genetic and epigenetic control of adipose development. Biochimica et Biophysica Acta (BBA)â Molecular and Cell Biology of Lipids. 2019;1864:3-12. 8. Khan M, Joseph F. Adipose tissue and adipokines: the association with and application of adipokines in obesity. Forensic Sci. 2014;2014: 711-724, 328592. 9. Alotaibi MF. Physiology of puberty in boys and girls and pathological disorders affecting its onset. J Adolesc. 2019;71:63-71. 10. Cousminer DL, Stergiakouli E, Berry DJ, et al. Genome-wide associa- tion study of sexual maturation in males and females highlights a role for body mass and menarche loci in male puberty. Hum Mol Genet. 2014;23(16):4452-4464. 11. Ahmed ML, Ong KK, Dunger DB. Childhood obesity and the timing of puberty. Trends in endocrinology and metabolism: TEM. 2009;20(5): 237-242. 12. Biro FM, Pajak A, Wolff MS, et al. Age of menarche in a longitudinal US cohort. J Pediatr Adolesc Gynecol. 2018;31(4):339-345. 13. Currie C, Ahluwalia N, Godeau E, Nic Gabhainn S, Due P, Currie DB. Is obesity at individual and national level associated with lower age at menarche? Evidence from 34 countries in the Health Behaviour in School-aged Children Study. The Journal of adolescent health: official publication of the Society for Adolescent Medicine. 2012;50(6): 621-626. 14. De Leonibus C, Marcovecchio ML, Chiavaroli V, de Giorgis T, Chiarelli F, Mohn A. Timing of puberty and physical growth in obese children: a longitudinal study in boys and girls. Pediatr Obes. 2014; 9(4):292-299. 15. Flom JD, Cohn BA, Tehranifar P, et al. Earlier age at menarche in girls with rapid early life growth: cohort and within sibling analyses. Ann Epidemiol. 2017;27(3):187-93.e2. 16. Glass NA, Torner JC, Letuchy EM, et al. The relationship between greater prepubertal adiposity, subsequent age of maturation, and bone strength during adolescence. Journal of bone and mineral research: the official journal of the American Society for Bone and Min- eral Research. 2016;31(7):1455-1465. 17. Holmgren A, Niklasson A, Nierop AF, et al. Pubertal height gain is inversely related to peak BMI in childhood. Pediatr Res. 2017;81(3): 448-454. 18. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman- Giddens ME. Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics. 2001;108(2):347-353. 19. Kelly Y, Zilanawala A, Sacker A, Hiatt R, Viner R. Early puberty in 11-year-old girls: Millennium Cohort Study findings. Arch Dis Child. 2017;102(3):232-237. 20. Lazzeri G, Tosti C, Pammolli A, et al. Overweight and lower age at menarche: evidence from the Italian HBSC cross-sectional survey. BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including âonset of puberty and adiposity/obesityâ, âonset of pubertyâ, âchildren with obesityâ, âadipose tissueâ, âchildhood obesityâ, âadiposityâ, âobesityâ, âadipokine(s)â, âHPG axisâ, âadipokines ovary/ova- riesâ, or âadipokines testesâ, either alone or in combination. Selection criteria used were English language, longitudinal or cross-sectional studies assessing the onset of puberty, including menarche, thelarche, spermarche, or voice break, combined with high BMI or obesity/adiposity, and articles assessing or reviewing adipokines and its effects on the reproductive system. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 9 of 10 21. Lian Q, Mao Y, Luo S, et al. Puberty timing associated with obesity and central obesity in Chinese Han girls. BMC Pediatr. 2019; 19(1):1-7. 22. Deng Y, Liang J, Zong Y, et al. Timing of spermarche and menarche among urban students in Guangzhou, China: trends from 2005 to 2012 and association with Obesity. Sci Rep. 2018;8(1):263-270. 23. Li W, Liu Q. Association of prepubertal obesity with pubertal devel- opment in Chinese girls and boys: a longitudinal study. 2018;30: e23195. 24. Mendle J, Beltz AM, Carter R, Dorn LD. Understanding puberty and its measurement: ideas for research in a new generation. Journal of research on adolescence: the official journal of the Society for Research on Adolescence. 2019;29(1):82-95. 25. Pagani S, Meazza C, Gertosio C, Bozzola E, Bozzola M. Growth hor- mone receptor gene expression in puberty. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2015;47:581-584. 26. Abreu AP, Kaiser UB. Pubertal development and regulation. Lancet Diabetes Endocrinol. 2016;4(3):254-264. 27. Aguirre RS, Eugster EA. Central precocious puberty: from genetics to treatment. Best Pract Res Clin Endocrinol Metab. 2018;32(4): 343-354. 28. Sultan C, Gaspari L, Maimoun L, Kalfa N, Paris F. Disorders of puberty. Best Pract Res Clin Obstet Gynaecol. 2018;48:62-89. 29. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH path- way in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. 30. Dahl SK, Amstalden M, Coolen L, Fitzgerald M, Lehman M. Dynorphin immunoreactive fibers contact GnRH neurons in the human hypothal- amus. Reprod Sci. 2009;16(8):781-787. 31. Navarro VM, Gottsch ML, Chavkin C, Okamura H, Clifton DK, Steiner RA. Regulation of gonadotropin-releasing hormone secretion by kisspeptin/dynorphin/neurokinin B neurons in the arcuate nucleus of the mouse. J Neurosci. 2009;29(38):11859-11866. 32. Zhai L, Liu J, Zhao J, et al. Association of obesity with onset of puberty and sex hormones in chinese girls: a 4-year longitudinal study. PLoS ONE. 2015;10(8):1-12, e0134656. 33. Cizza G, Dorn LD, Lotsikas A, Sereika S, Rotenstein D, Chrousos GP. Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: potential implications of a preliminary study. Horm Metab Res. 2001;33(3):138-143. 34. Cousminer DL, WidĂ©n E, Palmert MR. The genetics of pubertal timing in the general population: recent advances and evidence for sex-spec- ificity. Curr Opin Endocrinol Diabetes Obes. 2016;23(1):57-65. 35. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child. 1969;44(235):291-303. 36. Lacroix AE, Whitten R. Physiology. Treasure Island (FL): Menarche. StatPearls. StatPearls Publishing; 2018. 37. McDowell MA, Brody DJ, Hughes JP. Has Age at Menarche Chan- ged? Results from the National Health and Nutrition Examination Sur- vey (NHANES) 1999â2004. J Adolesc Health. 2007;40(3):227-231. 38. de Muinich Keizer SM, Mul D. Trends in pubertal development in Europe. Hum Reprod Update. 2001;7(3):287-291. 39. Talma H, Schönbeck Y, van Dommelen P, Bakker B, van Buuren S, Hirasing RA. Trends in menarcheal age between 1955 and 2009 in the Netherlands. PLoS ONE. 2013;8:e60056-e60056. 40. Kaplan HS, Lancaster JB. An evolutionary and ecological analysis of human fertility, mating patterns, and parental investment. Off- spring: Human fertility behavior in biodemographic perspective. 2003;1: 170-223. 41. Mitan LA. Menstrual dysfunction in anorexia nervosa. J Pediatr Adolesc Gynecol. 2004;17(2):81-85. 42. Xu H, Li P-H, Barrow TM, et al. Obesity as an effect modifier of the association between menstrual abnormalities and hypertension in young adult women: Results from Project ELEFANT. PLoS ONE. 2018; 13(11):e0207929-e0207929. 43. Tauqeer Z, Gomez G, Stanford FC. Obesity in women: insights for the clinician. J Womens Health (Larchmt). 2018;27(4):444-457. 44. de Ridder CM, Thijssen JH, Bruning PF, Van den Brande JL, Zonderland ML, Erich WB. Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. J Clin Endocrinol Metab. 1992;75(2): 442-446. 45. Lassek W, Gaulin S. Brief communication: menarche is related to fat distribution. Am J Phys Anthropol. 2007;133(4):1147-1151. 46. Loomba-Albrecht LA, Styne DM. Effect of puberty on body composi- tion. Curr Opin Endocrinol Diabetes Obes. 2009;16:10-15. 47. Simonneaux V, Bahougne T. A multi-oscillatory circadian system times female reproduction. Front Endocrinol. 2015;6:1-15. 48. Marques P, Skorupskaite K, George JT, Anderson RA. Physiology of GNRH and gonadotropin secretion. In: Feingold KR, Anawalt B, Boyce A, et al., eds. Endotext. Endotext.org: South Dartmouth (MA); 2000. 49. Barcellos Gemelli IF, Farias EDS, Souza OF. Age at menarche and its association with excess weight and body fat percentage in girls in the Southwestern Region of the Brazilian Amazon. J Pediatr Adolesc Gynecol. 2016;29(5):482-488. 50. Aksglaede L, Juul A, Olsen LW, Sorensen TI. Age at puberty and the emerging obesity epidemic. PLoS ONE. 2009;4:1-6, e8450. 51. Ribeiro J, Santos P, Duarte J, Mota J. Association between over- weight and early sexual maturation in Portuguese boys and girls. Ann Hum Biol. 2006;33(1):55-63. 52. Budak E, Fernandez Sanchez M, Bellver J, Cervero A, Simon C, Pellicer A. Interactions of the hormones leptin, ghrelin, adiponectin, resistin, and PYY3-36 with the reproductive system. Fertil Steril. 2006;85(6):1563-1581. 53. Castellano JM, Tena-Sempere M. Metabolic control of female puberty: potential therapeutic targets. Expert Opin Ther Targets. 2016; 20(10):1181-1193. 54. Venancio JC, Margatho LO, Rorato R, et al. Short-term high-fat diet increases leptin activation of CART neurons and advances puberty in female mice. Endocrinology. 2017;158(11):3929-3942. 55. l'Allemand D, Schmidt S, Rousson V, Brabant G, Gasser T, Gruters A. Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche. Eur J Endocrinol. 2002;146(4):537-543. 56. Böttner A, Jr K, MĂŒller G, et al. Gender Differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels. J Clin Endocrinol Metabol. 2004;89(8):4053- 4061. 57. Unanue N, Bazaes R, Iñiguez G, Cortes F, Avila A, Mericq V. Adre- narche in Prader-Willi syndrome appears not related to insulin sensi- tivity and serum adiponectin. Horm Res. 2007;67(3):152-158. 58. Michalakis K, Mintziori G, Kaprara A, Tarlatzis BC, Goulis DG. The complex interaction between obesity, metabolic syndrome and repro- ductive axis: a narrative review. Metabolism: clinical and experimental. 2013;62(4):457-478. 59. Machinal-Quelin F, Dieudonne MN, Pecquery R, Leneveu MC, Giudicelli Y. Direct in vitro effects of androgens and estrogens on ob gene expression and leptin secretion in human adipose tissue. Endo- crine. 2002;18(2):179-184. 60. Dobrzyn K, Smolinska N, Kiezun M. Adiponectin: A new regulator of female reproductive system. Int J Endocrinol. 2018;2018:1-12, 7965071. 61. Martin LJ. Implications of adiponectin in linking metabolism to testic- ular function. Endocrine. 2014;46(1):16-28. 62. Mathew H, Castracane VD, Mantzoros C. Adipose tissue and repro- ductive health. Metabolism: clinical and experimental. 2018;86:18-32. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 10 of 10 NIEUWENHUIS ET AL. 63. Sitticharoon C, Sukharomana M, Likitmaskul S, Churintaraphan M, Maikaew P. Corrigendum to: Increased high molecular weight adiponectin, but decreased total adiponectin and kisspeptin, in central precocious puberty compared with aged-matched prepubertal girls. Reprod Fertil Dev. 2017;29:2506-2517. 64. Das UN. Is obesity an inflammatory condition? Nutrition. 2001; 17(11-12):953-966. 65. Comninos AN, Jayasena CN, Dhillo WS. The relationship between gut and adipose hormones, and reproduction. Hum Reprod Update. 2014; 20(2):153-174. 66. Singh A, Choubey M, Bora P, Krishna A. Adiponectin and chemerin: contrary adipokines in regulating reproduction and metabolic disor- ders. Reproductive sciences (Thousand Oaks, Calif). 2018;25:1462- 1473. 67. Tsatsanis C, Dermitzaki E, Avgoustinaki P, Malliaraki N, Mytaras V, Margioris AN. The impact of adipose tissue-derived factors on the hypothalamic-pituitary-gonadal (HPG) axis. Hormones (Athens). 2015; 14:549-562. 68. Kang MJ, Oh YJ, Shim YS, Baek JW, Yang S. Hwang IT. The usefulness of circulating levels of leptin, kisspeptin, and neurokinin B in obese girls with precocious puberty. 2018;34:627-630. 69. Lee J, Song J, Hootman JM, et al. Obesity and other modifiable fac- tors for physical inactivity measured by accelerometer in adults with knee osteoarthritis: data from the osteoarthritis initiative (OAI). Arthritis Care Res (Hoboken). 2012;53-61. 70. Bramswig J, Dubbers A. Disorders of pubertal development. Deutsches Arzteblatt international. 2009;106:295-303. quiz 04 71. Elias CF, Purohit D. Leptin signaling and circuits in puberty and fertil- ity. Cell Mol Life Sci. 2013;70(5):841-862. 72. Riumallo J, Durnin JV. Changes in body composition in adolescent boys. Eur J Clin Nutr. 1988;42(2):107-112. 73. Siervogel RM, Demerath EW, Schubert C, et al. Puberty and body composition. Horm Res. 2003;60(Suppl 1):36-45. 74. Zhang J. Gong M. Andrologia: Review of the role of leptin in the regu- lation of male reproductive function; 2018. 75. Kauffman AS, Gottsch ML, Roa J, et al. Sexual differentiation of Kiss1 gene expression in the brain of the rat. Endocrinology. 2007;148(4): 1774-1783. 76. Zeydabadi Nejad S, Ramezani Tehrani F, Zadeh-Vakili A. The role of kisspeptin in female reproduction. Int J Endocrinol Metab. 2017;15:1- 11, e44337. 77. Sorensen K, Aksglaede L, Petersen JH, Juul A. Recent changes in pubertal timing in healthy Danish boys: associations with body mass index. J Clin Endocrinol Metab. 2010;95(1):263-270. 78. Juul A, Magnusdottir S, Scheike T, Prytz S, Skakkebaek NE. Age at voice break in Danish boys: effects of pre-pubertal body mass index and secular trend. Int J Androl. 2007;30(6):537-542. 79. Lee JM, Wasserman R, Kaciroti N, et al. Timing of puberty in overweight versus obese boys. Pediatrics. 2016;137(2):137-146, e20150164. 80. He F, Guan P, Liu Q, Crabtree D, Peng L, Wang H. The relationship between obesity and body compositions with respect to the timing of puberty in Chongqing adolescents: a cross-sectional study. BMC Pub- lic Health. 2017;17:664-673. 81. Ishikawa T, Fujioka H, Ishimura T, Takenaka A, Fujisawa M. Expres- sion of leptin and leptin receptor in the testis of fertile and infertile patients. Andrologia. 2007;39(1):22-27. 82. Martins AD, Moreira AC, Sa R, et al. Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta. 1852;2015: 1824-1832. 83. Morash BA, Willkinson D, Ur E, Wilkinson M. Resistin expression and regulation in mouse pituitary. FEBS Lett. 2002;526(1-3):26-30. 84. Cabrera SM, Bright GM, Frane JW, Blethen SL, Lee PA. Age of thelarche and menarche in contemporary US females: a cross- sectional analysis. Journal of pediatric endocrinology & metabolism: JPEM. 2014;27(1-2):47-51. 85. Herman-Giddens ME, Steffes J, Harris D, et al. Secondary sexual characteristics in boys: data from the Pediatric Research in Office Settings Network. Pediatrics. 2012;130(5):e1058-e1068. 86. WHO. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995;854:1-452. 87. Akin I, Tolg R, Hochadel M, et al. No evidence of âobesity paradoxâ after treatment with drug-eluting stents in a routine clinical practice: results from the prospective multicenter German DES.DE (German Drug-Eluting Stent) Registry. JACC Cardiovasc Interv. 2012;5(2): 162-169. 88. Marcovecchio ML, Chiarelli F. Obesity and growth during childhood and puberty. World Rev Nutr Diet. 2013;106:135-141. How to cite this article: Nieuwenhuis D, Pujol-Gualdo N, Arnoldussen IAC, Kiliaan AJ. Adipokines: A gear shift in puberty. Obesity Reviews. 2020;21:e13005. https://doi.org/ 10.1111/obr.13005 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are gover
Italy