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Year 7 and 8 French - present tense recap SCR
Quiz by Lindsay Simpson
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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 ⢠A Catholic who had held an important position under Mary I. ⢠He lost a lot of influence under Elizabeth (as she favoured Protestant gentry) ⢠Elizabeth also took the rights to a valuable copper mine found on his lands Earl of Westmorland ⢠From a rich Catholic family in the north Also the Duke of Norfolkâs brother in law Duke of Norfolk ⢠Englandâs most senior Protestant noble, but he had very close links to old northern Catholic families, & was sympathetic to them & greedy for power. ⢠He hated William Cecil & Robert Dudley, Earl of Leicester (Elizabethâs favourite) who were Protestant and from the gentry ⢠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) ⢠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. ⢠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) ⢠The Northern Earls lost a lot of their power/influence (even jobs/money under Elizabeth) ⢠Northumberland was jealous of new Protestant families being given top jobs in the North ⢠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 ⢠Elizabeth also confiscated large areas of land & the profits from their copper mines ⢠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? ⢠Elizabeth was refusing to name an heir and it was becoming clear that she would not marry ⢠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. ⢠However, some of Elizabethâs courtiers got worried that it might not work and that it might lead to charges of treason (punishable by death) ⢠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. ⢠Mary QS had secretly asked Spain to send troops to help the rebellion & overthrow Elizabeth Plan for the Revolt of the Northern Earls (1569) ⢠The Earls of Northumberland & Westmorland will raise rebel troops from their lands in the north and take control of Durham. ⢠The rebels will then march south towards London to join with the Duke of Norfolk ⢠1000s of Spanish troops will land in England to support the rebel forces ⢠The Duke of Norfolk & rebel forces will seize control of Government & overthrow Elizabeth ⢠Mary Queen of Scots is to be freed, ready to marry the Duke of Norfolk Key Events of the Revolt ⢠Once Elizabeth knew of the plot, Norfolk was arrested and sent to the Tower of London ⢠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 ⢠They raised an army of ordinary Catholics and took control of Durham cathedral ⢠Catholic mass was celebrated across the north for 2 weeks. ⢠They then headed south, to try and free Mary ⢠Mary QSs was moved south to Coventry on the orders of Elizabeth, so she couldnât escape ⢠The rebellion failed as Spanish troops never arrived ⢠Elizabethâs friend (Earl of Sussex) had raised an army of 7,000 men to defend her throne. Results: ⢠The rebellion was a serious threat to Elizabeth ⢠She executed 450 rebels in the north ⢠Northumberland was executed in 1572 & his head was put on a spike on the city gate ⢠The Privy Council called for the Duke of Norfolkâs execution too, but Elizabeth released him. ⢠Mary Queen of Scots was kept in prison for the next 14 years. ⢠The failed plot also led the Pope to take action against Elizabeth ⢠In 1570 he excommunicated Elizabeth from the Catholic Church ⢠He also issued a Papal Bull (order) calling on all loyal Catholics to overthrow her hoping it would encourage another rebellion. ⢠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 ⢠It was the first and most serious rebellion by English Catholics against Elizabeth ⢠Treason laws were made much harsher ⢠It ended the influence of the powerful Catholic Earls in the North ⢠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). ⢠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 ⢠In the 1870s-80s, there were 3 Catholic plots to assassinate Elizabeth & replace her with Mary. ⢠The plots were supported by France, Spain, the Pope and some Catholic nobles. ⢠They reinforced the form Mary & from Catholics at home and abroad. Also the threat from Spain. The Ridolfi Plot (1571) ⢠Ridolfi was an Italian banker living in England and a spy for the Pope. ⢠He organised a plot to murder Eliz, marry Mary QS to the Duke of Norfolk & make her Queen. ⢠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). ⢠The plot failed because Sir William Cecil intercepted coded letters & Norfolk was executed. ⢠Mary was kept under closer watch. ⢠Ridolfi was abroad when the plot was discovered and never returned to England. 1574: Catholic Priests and Priest Holes ⢠From 1574 Catholic priests were smuggled into England to keep the religion alive. ⢠They stayed with rich Catholic families, so Catholic families were kept under surveillance. ⢠Catholic homes were raided â to find âpriest holesâ where Catholic priests were hiding. ⢠Catholic priests who were found could be hung, drawn and quartered (although not all were) ⢠In 1581, Parliament also passed 2 new tougher laws against Catholics: ⢠Recusants would be fined ÂŁ20 (which would bankrupt most families) ⢠Trying to convert people to Catholicism was now treason (punishable by death) The Throckmorton Plot (1583) ⢠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). ⢠An Englishman, Throckmorton carried messages between Mary & Catholic plotters abroad. ⢠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: ⢠The plots showed that Maryâs presence in England posed a serious threat ⢠It also showed that France & Spain were a serious threat (& could invade) ⢠Throckmortonâs papers showed a list of Catholic supporters in England, so the threat from English Catholics was also real ⢠1,000s of Catholics were imprisoned or kept under surveillance/house arrest ⢠In 1585 another Act was passed to make helping Catholic priests punishable by death. ⢠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. ⢠This was a plot to murder Elizabeth and put Mary on the throne ⢠France would invade England with 60,000 men and Spain would also send an army ⢠Babington was passing coded letters between Mary & her supporters in England & Europe. ⢠But all of her letters were being intercepted and read by Walsingham. ⢠Walsingham used his spies to follow every stage of the plot & had the letters decoded ⢠One of Maryâs letters approved plans to murder the Queen and free Mary from prison ⢠They also contained the names of 6 Catholics who planned to kill Elizabeth ⢠They were arrested, hung, drawn and quartered for treason. ⢠Mary had been implicated in plots before, but Elizabeth was always reluctant to execute her ⢠But the proof found by Walsingham finally persuaded her to put Mary on trial ⢠In October 1586, Mary was found guilty & was sentenced to death ⢠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 ⢠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 ⢠Another reason was that by 1587, it was clear that Philip was planning to invade England ⢠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: ⢠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. ⢠He also had agents and spies in Spain, France, Germany and Italy ⢠He hired mathematicians to crack written codes and people to open/seal letters secretly ⢠He also pressured captured Catholic priests to spy on others for him in return for a pardon. ⢠He used double agents to infiltrate Catholic networks - to help him discover traitors ⢠But he only used torture against Catholic priests caught in England in the most serious cases ⢠But 130 priests and 60 of their supporters were still executed during Elizabethâs reign. Why did Relations with Spain get worse (1569-1588) ⢠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) ⢠But by the 1570s, Elizabeth wanted to have an empire of her own. ⢠She also needed to make more money to defend her country and throne (by improving trade) ⢠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 ⢠Under Elizabeth, English merchants wanted to make big profits in the New World (Americas). ⢠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 ⢠In 1572 Eliz hired Drake to sail to the New World & steal ÂŁ40,000 of Spanish silver ⢠In 1577 she sent Drake back again with a secret mission to rob Spainâs colonies/ships ⢠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 ⢠He boosted Englandâs finances at a time of growing concern over Spainâs threat ⢠He became famous as the first Englishman to circumnavigate the globe. ⢠Eliz knighted Drake as a reward, which infuriated Philip (as he saw Drake as a pirate) ⢠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) ⢠By the 1580s, tension between England & Spain had reached boiling point ⢠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 ⢠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) ⢠By 1576, the Spanish Govt in the Netherlands was bankrupt (the war was expensive) ⢠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): ⢠Spanish troops leave the Netherlands ⢠Spain allows the Dutch to rule themselves ⢠The persecution of Dutch Protestants stops What did Elizabeth do? ⢠Elizabeth sent ÂŁ100,000 to help the Dutch rebels ⢠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. ⢠Elizabeth then hired a mercenary army of 6000 English & Scottish volunteers to help the Dutch. ⢠But her plan backfired because the mercenaries destroyed Dutch Catholic churches, which caused the Catholics to make peace with Spain. ⢠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. ⢠In 1580 Spain got even stronger after Philip won control of Portugal & its empire. ⢠So Elizabeth gave the Duke of Alencon ÂŁ70,000 to help him fight the Spanish ⢠In 1582, Alencon took his army the Netherlands but failed to defeat Spain. ⢠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) ⢠1584 the Duke of Alencon died (so he could no longer fight the Spanish in the Netherlands) ⢠1 month later, William of Orange, the leader of the Dutch Protestant rebels was assassinated. ⢠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 ⢠Elizabeth now felt she had no choice but to send her official army to the Netherlands ⢠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 ⢠In 1587 Elizabeth ordered Drake to attack Spainâs most important port Cadiz ⢠He destroyed 30 ships in 3 days â known as the âSingeing of the King of Spainâs Beardâ ⢠He also stole lots of wood, meaning the Armada did not have quality barrels for food/water ⢠Drakeâs disruption delayed the Armada by a year (& meant that its food rotted in 1588). ⢠This bought England more time to prepare for war. The Spanish Armada (1588) The Plan ⢠By 1588, the Spanish Armada was ready to invade England ⢠It had 130 ships with 8000 sailors & 18,000 soldiers ⢠The Duke of Medina Sidonia would lead the Armada, but he had little experience at sea and didnât want the job ⢠The Armada would collect Parmaâs army from France & sail to England under the protection of the Armadaâs warships ⢠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 ⢠Years before the battle, England had started building smaller, faster ships (galleons) that could fire canon balls quicker & further than Spanish ships ⢠Spanish ships were huge and slow to change direction. 2) Bad Planning & Communication (Spanish) ⢠Philipâs plan to join with the Duke of Parmaâs army in France was risky. ⢠Parma had lots of small ships which took 48 hours to load, man and set sail. ⢠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. ⢠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 ⢠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. ⢠They chased the Armada down the Channel, with heavy cannon fire, which forced the Spanish to arrive in France before Parmaâs army was ready ⢠As the Armada was waiting, the English sent fireships into the Spanish fleet. ⢠This caused the Armada to panic, cut their anchors & sail away to the north ⢠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 ⢠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 ⢠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? ⢠Victory over the Spanish Armada gave Elizabeth a great propaganda victory ⢠A new portrait was made, and a medal was made to commemorate her victory, it said âGod blew and they were scatteredâ. ⢠Elizabeth claimed that God was on the side of Protestantism ⢠This led to a feeling of English pride and encouraged the Dutch rebels to renew their fight against the Spanish ⢠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 ⢠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 ⢠The Armada marked the start of a long decline in Spainâs power and fortunes. ⢠English ships were sent on voyages of discovery and set up valuable new trade routes ⢠By the end of Elizabethâs reign, the navy was also trying to set up a new colony in Virginia ⢠The English victory boosted Elizabethâs popularity & strengthened the Protestant cause
Make a multiple choice quiz for my year 8 science students based on the science in this transcript from a video: 3°C 0:04 It can be the difference between snow and sleet 0:08 Wearing a jacket or not 0:11 In your day-to-day life, it may not seem significant 0:15 But 3°C of global warming would be catastrophic 0:20 Heatwaves, droughts, extreme precipitation, even fire 0:25 3°C of warming is really disastrous 0:28 The scary thing is, the world is well on its way there 0:32 Since the industrial revolution, the Earth has warmed between 1.1°C and 1.3°C 0:40 This is a problem that babies you pass in the street will have to live with 0:46 Children born today... 0:47 ...are up to seven times more likely to face extreme weather than their grandparents 0:52 If global temperatures do rise by 3°C... 0:55 ...what would their world look like? Climate change is already having devastating effects 1:03 Rising sea levels 1:05 Desertification 1:07 Hollywood has always enjoyed imagining the end of the world 1:11 While blockbusters like this are clearly fiction... 1:14 ...this film will show the scenario we all face... 1:17 ...unless more drastic measures are taken to stop burning fossil fuels 1:30 In some parts of the world the effects of inaction are already clear 1:35 The slums of Bangladeshâs capital are filling up with climate migrants 1:41 Minara comes from Bhola District, an area in southern Bangladesh 1:46 There, like many other parts of the country... 1:49 ...rivers swollen by heavier rain and melting Himalayan glaciers... 1:53 ...are washing away peopleâs homes 1:56 Many, like her, have lost everything 2:00 Our home in Bhola had endless amounts of land 2:03 There was lots of space for farming, we had a spacious house 2:08 There were different types of fruits, vegetation and trees growing at home 2:12 We used to eat the fruit from our own trees 2:18 I canât eat them now because they don't exist anymore 2:21 Since the river flooded for the third time, I had to flee to Dhaka 2:26 Life was much better back home 2:29 It was unbearable to live through, truly intolerable 2:33 We didnât have the time to save anything at all 2:38 1.1°C to 1.3°C of global warming has already transformed Minaraâs life 2:45 Itâs one of the reasons why so many migrants like her... 2:47 ...are moving to the city each year... 2:50 ...nearly 400,000 according to the last estimate 2:53 And climate models show there could be much worse to come How climate modelling works 3:02 Climate scientist Joeri Rogelj... 3:04 ...has spent the last ten years modelling future climate scenarios... 3:08 ...for the United Nations 3:10 The models we use to carry out this exercise... 3:13 ...really represent the state of the art... 3:15 ...of our current knowledge of climate change and where we are heading 3:19 Joeriâs projections use data collected by hundreds of scientists around the world 3:26 Here this is the 3°C level... 3:28 ...and so there is at least a one-in-four chance that under current policies... 3:32 ...we would hit 3°C by the end of the century 3:36 This is just one of the scenarios Joeri looks at 3:40 Another one imagines that all policy promises are kept 3:44 The most optimistic assumes that all promises have been kept... 3:47 ...and net-zero targets are met 3:50 Where our best estimate ends up around 2°C at the end of the century... 3:54 ...there is still a one-in-20 chance that we end up with 3°C instead 3:59 One would not be entering a plane if there is a one-in-20 chance... 4:03 ...that the plane will crash Nowhere is safe from global warming 4:07 A rise of 3°C would affect everyone 4:10 Even wealthy cities in rich countries wouldnât be immune to the consequences 4:15 European capitals like Paris and Berlin... 4:18 ...would bake under more extreme heatwaves 4:22 Frequent storm-surges in New York could turn parts of the city desolate 4:27 In many ways, cities magnify, intensify climate events 4:33 Cities are hotter than the places around them... 4:36 ...they tend to be more vulnerable to flooding 4:39 And you can get a really bad event in a city in a way that you canât in the countryside 4:46 And because of their denser populations... 4:49 ...disasters in a city affect far more people 4:52 Some cities might be badly prepared for the changes coming 4:56 But they have the means to adapt 4:59 Cities tend to be wealthier than surrounding places 5:03 They have a lot of amenities 5:05 A city that has taken seriously the risks of a 3°C world... 5:08 âŚwouldnât necessarily be a worse place to be in a 3°C world 5:12 But a city that hasnât prepared for these sort of eventualities... 5:16 ...that might be a really nasty place The impact of prolonged droughts 5:20 So far, many developed cities have got off lightly... 5:24 ...but some rural parts of the world are suffering disproportionately 5:29 Smallholdersâsmall-scale farmersâare particularly vulnerable to climate change 5:35 And there are over 600 million around the world 5:38 Smallholders with farms under two hectares... 5:40 ...produce around a third of the global food supply 5:46 Central Americaâs âDry Corridorâ... 5:48 ...supports a mix of smallholdings and medium-sized farms 5:53 Sandwiched between the Pacific Ocean and the Caribbean Sea... 5:56 ...the area is prone to droughts 6:08 Israel RamĂrez Rivera is a smallholder in Guatemala 6:12 Here, climate change is making the dry seasons longer, and more severe 6:18 This is the biggest ear of maize that this plot could deliver 6:23 He depends on his crops of corn and beans 6:26 But theyâre getting harder to grow 6:30 The surrounding mountains... 6:32 ...used to provide us with native food... 6:38 ...and now that isnât an option anymore... 6:41 ...due to climate change and its effects 6:46 Nearly two-thirds of the smallholders in the Dry Corridor now live in poverty 6:52 The impact of all of this for us... 6:59 ...malnutrition among children 7:03 Weâve lost a few 7:07 For my crops especially, the midsummer heat is harder than before 7:16 The plant dries up and canât provide us... 7:19 ...with the necessary food provision 7:24 Severe droughts in Central America... 7:26 ...are now four times more likely than they were last century 7:30 Many families from here have gone to the States 7:37 The economic despair and debts... 7:44 ...have pushed many people from this community to do this journey 7:53 Migration from Guatemala to the United States has quadrupled since 1990 7:59 Not all of this has been due to climate change 8:02 But longer droughts would force even more to move 8:05 In a 3°C world, annual rainfall in this region... 8:09 ...could drop by up to 14% 8:12 At 3°C, over a quarter of the worldâs population... 8:16 ...could endure extreme droughts for at least a month of the year 8:19 Northern Africa could see droughts that last for years at a time Rising sea levels, storm surges and flooding 8:24 But for some, too much water will be the problem 8:29 10% of the worldâs population lives on a coastline... 8:32 ...thatâs less than 10 metres above sea level 8:35 For these coastal inhabitants, a 3°C world would spell disaster 8:40 By 2100, global sea levels could have climbed by half a metre from 2005 levels 8:46 Low-lying cities like Lagos would be especially vulnerable... 8:49 ...with up to up to a third of the population displaced 8:54 And in Fiji, rising waters are already upending lives 9:04 You can see the graveyard there, itâs all under water now... 9:08 ...due to this rising sea level and climate change 9:15 The village of Togoru in Fiji is being swallowed by the sea 9:19 Barney Dunn, the village headman, has seen over half the village disappear 9:24 Relativesâ houses have been abandoned, and family graves are now under water 9:29 We have been asked by the government to relocate... 9:32 ...but no one wants to relocate... 9:34 ...because we have our great-great-grandparents down there in the sea 9:39 This is the place weâve been brought up in 9:41 ...itâs not easy to leave 9:44 Past attempts to build a seawall havenât worked 9:48 But Barney sees building a new one as the villageâs only hope 9:52 If they do that, maybe we can save whatever is left 9:56 But if we donât have the seawall, then it will be keep eroding and time will come... 10:01 ...maybe in ten,15 years, Togoru will be all eroded 10:05 Rising seas also mean storms cause more floods 10:11 And many more countries could suffer 10:14 The Philippines and Myanmar are just two countries... 10:17 ...that will also see an increase in storm surges in a 3°C world 10:21 To escape, many will move⌠10:24 âŚoften, to urban areas Extreme heat and wet-bulb temperatures 10:27 Half the worldâs population already lives in cities... 10:31 ...almost a third in slums 10:36 For them, a 3°C world could be deadly 10:40 Minara has moved to Dhaka to escape the impact of climate change 10:44 But life could get even worse for her 10:47 Iâm struggling a lot nowadays 10:49 The heat during the day is unbearable 10:52 Even late at night it doesnât cool down 10:57 The heat is getting more intense every day 10:59 I mean, itâs going to get much worse 11:03 I can barely survive it now, how will I live through it in the future? 11:08 Dhaka is getting hotter 11:11 In the last 20 years the average daytime temperature... 11:13 ...has crept up by nearly half a degree 11:17 Days that approach 40°C are now being reported 11:20 And high so-called wet-bulb temperatures are on the rise 11:26 A wet-bulb temperature is a measure of heat and humidity 11:30 Humans cool themselves by sweating⌠11:32 But in these conditions, when relative humidity is near 100%... 11:36 ...sweat doesnât evaporate well 11:38 So people canât cool down⌠11:41 ...even if given unlimited shade and water 11:45 At a high wet-bulb temperature, the body canât lose heat... 11:49 ...and so it gets hotter and hotter... 11:51 ...and the body is designed to work at a given temperature 11:53 And if it gets too hot inside, you will die 11:58 The human limit for wet-bulb temperatures is 35°C... 12:02 ...around skin temperature 12:04 Dhaka will have a much higher chance... 12:05 ...of reaching dangerous wet-bulb temperatures... 12:07 ...if global warming reaches 3°C 12:12 You canât really adapt to that 12:14 You have to get out. If the temperature is so high that you canât work... 12:20 ...canât do hard manual labour outside for significant parts of the year... 12:25 ...then many places will become functionally no longer part of the economy 12:33 Jacobabad in Pakistan, and Ras al Khaimah, in the United Arab Emirates... 12:37 ...have already recorded deadly wet-bulb temperatures 12:40 More of the tropics and the Persian Gulf... 12:43 ...as well as parts of Mexico and the south-eastern United States... 12:47 ...could all get to this threshold by the end of the century 12:50 Climate modelling might show us the weather Increased migration and conflict 12:52 But it doesnât show us its other effects on society 12:56 Established migration patterns could change 12:59 Climate disasters may exacerbate reasons people cross borders 13:03 Within countries, more people will move to cities 13:07 In a 3°C world, tens of millions of people a year... 13:10 ...could be displaced by disasters made worse by climate change 13:15 When people are displaced by climate... 13:18 âŚthey may well go to cities... 13:19 ...because cities are the places that attract people from the countryside already 13:25 A lot of people who can get to the developed world... 13:28 ...not least because the developed world tends to be less hot, will give that a go 13:35 As migration around the world increases... 13:38 ...there could be more competition for fewer resources 13:42 Waterâalready a highly contested resourceâwill be a focal point 13:47 Turkeyâs new Ilisu dam has reduced the flow of water into Iraq 13:53 China lays claim to rivers vital to India and Pakistan 13:57 The prospect of a water-conflict makes people very uneasy 14:03 How national tensions would exacerbate those sorts of reactions... 14:08 ...in a 3°C world... 14:09 ...is the sort of thing that no one should really want to find out 14:14 I think youâd have to be incredibly sanguine... 14:16 ...not to think that the sort of climate extremes that we talk about... 14:19 ...in a 3°C world wouldnât lead some places... 14:22 ...to the brink of societal collapse 14:25 Those lucky enough to escape unrest... Adaptation and mitigation are crucial 14:28 ...would still have to adapt to a radically different world 14:32 People can adapt to climate change in all sorts of ways, one of the most obvious ones... 14:37 ...is air conditioning 14:39 But other ways to adapt at a local or regional level... 14:42 ...I mean, one of the most obvious is diversifying agriculture 14:47 There are physical things you can do, like seawalls 14:52 The fact that people can adapt and that adaptation will reduce suffering... 14:57 ...doesnât mean that it will eliminate suffering 15:00 Suffering is built into this whole process of heating up the planet 15:06 Adaptation will only get the world so far 15:09 The best way to deal with a 3°C world... 15:12 ...is not to go to a 3°C world 15:14 And thatâs why increasing efforts on mitigation are important 15:17 Itâs why working towards negative emissions... 15:20 ...that could bring down the temperature after it peaks are important 15:25 Once you get to a 3°C world, you are in real bad global trouble 15:33 The scale of change needed... 15:35 ...and the slow progress of governments so far... 15:38 ...means 3°C of warming is uncomfortably likely unless more is done 15:44 Despite existing pledges, greenhouse-gas emissions... 15:48 ...are still set to rise by 16% from 2010 levels by 2030 15:54 The need to act has never been clearer 15:57 Thereâs still time to reduce emissions, so that a 3°C world remains fiction... 16:02 ...rather than becoming fact
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 DesirĂŠe 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. Š 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-Îą 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- Îą 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-Îą 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-Îą, 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-Îą 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-Îą, 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, WidĂŠn 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, SchĂśnbeck 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. BĂśttner A, Jr K, MĂźller 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, IĂąiguez 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
Hi, I'm John Green, this is Crash Course U.S. History, and today, we're going to talk about slavery, which is not funny. 0:06 Yeah, so we put a lei on the eagle to try and cheer you up, but let's face it, this is going to be depressing. 0:10 With slavery, every time you think, like, "Aw, it couldn't have been that bad," it turns out to have been much worse. 0:14 Mr. Green, Mr. Green! But what about â 0:15 Yeah, Me from the Past, I'm going to stop you right there, because you're going to embarrass yourself. Slavery was hugely important to America. 0:20 I mean, it led to a civil war and it also lasted what, at least in U.S. history, counts as a long-ass time, from 1619 to 1865. 0:29 And yes, I know there's a 1200-year-old church in your neighborhood in Denmark, but we're not talking about Denmark! 0:35 But slavery is most important because we still struggle with its legacy. 0:38 So, yes, today's episode will probably not be funny, but it will be important. 0:42 [Theme Music] North & South economic ties 0:51 So the slave-based economy in the South is sometimes characterized as having been separate from the Market Revolution, but that's not really the case. 0:57 Without southern cotton, the North wouldn't have been able to industrialize, at least not as quickly, because cotton textiles were one of the first industrially products. 1:04 And the most important commodity in world trade by the nineteenth century, and 3/4 of the world's cotton came from the American South. 1:11 And speaking of cotton, why has no one mentioned to me that my collar has been half popped this entire episode, like I'm trying to recreate the Flying Nun's hat. 1:18 And although there were increasingly fewer slaves in the North as northern states outlawed slavery, cotton shipments overseas made northern merchants rich. 1:26 Northern bankers financed the purchase of land for plantations. 1:29 Northern insurance companies insured slaves who were, after all, considered property, and very valuable property. 1:35 And in addition to turning cotton into cloth for sale overseas, northern manufacturers sold cloth back to the South, where it was used to clothe the very slaves who had cultivated it. 1:45 But certainly the most prominent effects of the slave-based economy were seen in the South. Slave-based agriculture in the South 1:49 The profitability of slaved-based agriculture, especially King Cotton, meant that the South would remain largely agricultural and rural. 1:56 Slave states were home to a few cities, like St. Louis and Baltimore, but with the exception of New Orleans, 2:00 almost all southern urbanization took place in the upper South, further away from the large cotton plantations. 2:06 And slave-based agriculture was so profitable that it siphoned money away from other economic endeavors. 2:11 Like, there was very little industry in the South. 2:13 It produced only 10% of the nation's manufactured goods. 2:16 And, as most of the capital was being plowed into the purchase of slaves, there was very little room for technological innovation, like, for instance, railroads. 2:23 This lack of industry and railroads would eventually make the South suck at the Civil War, thankfully. 2:27 In short, slavery dominated the South, shaping it both economically and culturally, and slavery wasn't a minor aspect of American society. Popular attitudes concerning slavery 2:35 By 1860, there were four million slaves in the U.S., and in the South, they made up one third of the total population. 2:42 Although in the popular imagination, most plantations were these sprawling affairs with hundreds of slaves, 2:47 in reality, the majority of slaveholders owned five or fewer slaves. 2:51 And, of course, most white people in the South owned no slaves at all, though, if they could afford to, they would sometimes rent slaves to help with their work. 2:57 These were the so-called yeoman farmers who lived self-sufficiently, raised their own food, and purchased very little in the Market Economy. 3:04 They worked the poorest land and, as a result, were mostly pretty poor themselves. 3:08 But even they largely supported slavery, partly, perhaps, for aspirational reasons, and partly because the racism inherent to the system gave even the poorest whites legal and social status. 3:18 And southern intellectuals worked hard to encourage these ideas of white solidarity and to make the case for slavery. 3:23 Many of the founders, a bunch of whom you'll remember, held slaves, saw slavery as a necessary evil. 3:29 Jefferson once wrote, quote, "As it is, we have the wolf by the ear, and we can neither hold him, nor safely let him go. 3:37 Justice is on one scale, and self-preservation in the other." 3:41 The belief that justice and self-preservation couldn't sit on the same side of the scale was really opposed to the American idea, 3:47 and, in the end, it would make the Civil War inevitable. 3:50 But as slavery became more entrenched in these ideas of liberty and political equality were embraced by more people, 3:55 some southerners began to make the case that slavery wasn't just a necessary evil. 3:59 They argued, for instance, that slaves benefited from slavery. 4:03 Because, you know, because their masters fed them and clothed them and took care of them in their old age. 4:07 You still hear this argument today, astonishingly. 4:09 In fact, you'll probably see asshats in the comments saying that in the comments. 4:12 I will remind you, it's not cursing if you are referring to an actual ass. 4:15 This paternalism allowed masters to see themselves as benevolent and to contrast their family-oriented slavery with the cold, mercenary Capitalism of the free-labor North. 4:26 So yeah, in the face of rising criticism of slavery, some southerners began to argue that the institution was actually good for the social order. 4:33 One of the best-known proponents of this view was John C. Calhoun, who, in 1837, said this in a speech on the Senate floor: 4:40 "I hold that, in the present state of civilization, 4:43 where two races of different origin and distinguished by color and other physical differences as well as intellectual, are brought together, 4:51 the relation now existing in the slave-holding states between the two is, instead of an evil, a good. A positive good." 4:59 Now, of course, John C. Calhoun was a fringe politician, and nobody took his views particularly seriously. 5:04 Stan: Well, he was Secretary of State from 1844 to 1845. 5:07 John: Well, I mean, who really cares about the Secretary of State, Stan? 5:10 Danica: Eh, he was also Secretary of War from 1817 to 1825. 5:13 John: All right, but we don't even have a Secretary of War anymore, so... 5:16 Meredith: And he was Vice President from 1825 to 1832. 5:19 John: Oh my god, were we insane?! 5:21 We were, of course, but we justified the insanity with Biblical passages and with the examples of the Greeks and Romans, 5:28 and with outright racism, arguing that black people were inherently inferior to whites. 5:33 And that not to keep them in slavery would upset the natural order of things. 5:37 A worldview popularized millennia ago by my nemesis, Aristotle. God, I hate Aristotle. 5:42 You know what defenders of Aristotle always say? 5:44 "He was the first person to identify dolphins." 5:47 Well, ok, dolphin identifier. 5:50 Yes, that is what he should be remembered for, but he's a terrible philosopher! Lives & experiences of enslaved people 5:53 Here's the truth about slavery: 5:55 It was coerced labor that relied upon intimidation and brutality and dehumanization. 6:00 And this wasn't just a cultural system, it was a legal one. 6:03 I mean, Louisiana law proclaimed that a slave "owes his master... a respect without bounds, and an absolute obedience." 6:09 The signal feature of slaves' lives was work. 6:12 I mean, conditions and tasks varied, but all slaves labored, usually from sunup to sundown, and almost always without any pay. 6:20 Most slaves worked in agriculture on plantations, and conditions were different, depending on which crops are grown. 6:25 Like, slaves on the rice plantations of South Carolina had terrible working conditions, 6:29 but they labored under the task system, which meant that once they had completed their allotted daily work, they would have time to do other things. 6:36 But lest you imagine this is like how we have work and leisure time, bear in mind that they were owned and treated as property. 6:42 On cotton plantations, most slaves worked in gangs, usually under the control of an overseer, or another slave who was called a "driver." 6:49 This was back-breaking work done in the southern sun and humidity, and so it's not surprising that whippings â or the threat of them â were often necessary to get slaves to work. 6:58 It's easy enough to talk about the brutality of slave discipline, but it can be difficult to internalize it. 7:03 Like, you look at these pictures, but because you've seen them over and over again, they don't have the power they once might have. 7:09 The pictures can tell a story about cruelty, but they don't necessarily communicate how arbitrary it all was. 7:14 As, for example, in this story, told by a woman who was a slave as a young girl: 7:18 "[The] overseer... went to my father one morning and said, "Bob, I'm gonna whip you this morning." 7:22 Daddy said, "I ain't done nothing," and he said, "I know it, I'm going to whip you to keep you from doing nothing," 7:28 and he hit him with that cowhide â you know it would cut the blood out of you with every lick if they hit you hard." 7:33 That brutality â the whippings, the brandings, the rape â was real, and it was intentional, because, in order for slavery to function, slaves had to be dehumanized. 7:43 This enabled slaveholders to rationalize what they were doing, and it was hoped to reduce slaves to the animal property that is implied by the term "chattel slavery." 7:51 So the idea was that slaveholders wouldn't think of their slaves as human, and slaves wouldn't think of themselves as human. 7:57 But it didn't work. Let's go to the Thought Bubble. 7:59 Slaves' resistance to their dehumanization took many forms, but the primary way was by forming families. Family, love, & religion of enslaved people 8:05 Family was a refuge for slaves and a source of dignity that masters recognized and sought to stifle. 8:10 A paternalistic slave owner named Bennet H. Barrow wrote in his rules for the Highland Plantation: 8:15 "No rule that I have stated is of more importance than that relating to Negroes marrying outside of the plantation... It creates a feeling of independence." 8:23 Most slaves did marry, usually for life, and, when possible, slaves grew up in two-parent households. 8:28 Single-parent households were common, though, as a result of one parent being sold. 8:32 In the upper South, where the economy was shifting from tobacco to different, less labor-intensive cash crops, the sale of slaves was common. 8:40 Perhaps one-third of slave marriages in states like Virginia were broken up by sale. 8:45 Religion was also an important part of life in slavery. 8:47 While masters wanted their slaves to learn the parts of the Bible that talked about being happy in bondage, 8:52 slave worship tended to focus on the stories of Exodus, where Moses brought the slaves out of bondage, 8:57 or Biblical heroes, who overcame great odds, like Daniel and David. 9:01 And, although most slaves were forbidden to learn to read and write, many did anyway. And some became preachers. 9:07 Slave preachers were often very charismatic leaders, and they roused the suspicion of slave owners, and not without reason. 9:13 Two of the most important slave uprisings in the South were led by preachers. 9:16 Thanks, Thought Bubble. 9:17 Oh, it's time for the Mystery Document? Mystery Document 9:19 We're doing two set pieces in a row? All right. [buzzing noise] [music] 9:24 The rules here are simple. 9:26 I wanted to re-shoot that, but Stan said no. 9:29 I guess the author of the Mystery Document. 9:30 If I am wrong, I get shocked with the shock pen. 9:33 "Since I have been in the Queen's dominions I have been well contented, yes well contented for sure, man is as God intended he should be. 9:40 That is, all are born free and equal. 9:43 This is a wholesome law, not like the southern laws which puts man made in the image of God on level with brutes. 9:49 O, what will become of the people, and where will they stand in the day of judgment. 9:53 Would that the 5th verse of the 3rd chapter of Malachi were written as with a bar of iron, 9:59 and the point of a diamond upon every oppressor's heart that they might repent of this evil, and let the oppressed go free..." 10:06 All right, it's definitely a preacher, because only preachers have read Malachi. 10:10 Probably African American, probably not someone from the South. 10:13 I'm going to guess that it is Richard Allen, the founder of the African Methodist Episcopal Church? 10:18 [buzzing noise] DAAAH, DANG IT! 10:19 It's Joseph Taper, and Stan just pointed out to me that I should have known it was Joseph Taper because it starts out, 10:24 "Since I have been in the Queen's dominions..." 10:27 He was in Canada. He escaped slavery to Canada. The Queen's dominions! 10:31 All right, Canadians, I blame you for this, although, thank you for abolishing slavery decades before we did. 10:36 [electric sounds] AHHH! How people resisted & escaped slavery 10:37 So, the Mystery Document shows one of the primary ways that slaves resisted their oppression: by running away. 10:42 Although some slaves like Joseph Taper escaped for good by running away to northern free states, 10:47 or even to Canada, where they wouldn't have to worry about fugitive slave laws, even more slaves ran away temporarily, hiding out in the woods or the swamps, and eventually returning. 10:55 No one knows exactly how many slaves escaped to freedom, but the best estimate is that a thousand or so a year made the journey northward. 11:01 Most fugitive slaves were young men, but the most famous runaway has been hanging out behind me all day long: Harriet Tubman. 11:07 Harriet Tubman escaped to Philadelphia at the age of 29, and over the course of her life, she made about 20 trips back to Maryland to help friends and relatives make the journey north on the Underground Railroad. 11:17 But a more dramatic form of resistance to slavery was actual, armed rebellion, which was attempted. 11:22 Now, individuals sometimes took matters into their own hands and beat or even killed their white overseers or masters. 11:27 Like Bob, the guy who received the arbitrary beating, responded to it by killing his overseer with a hoe. 11:33 But that said, large-scale slave uprisings were relatively rare. 11:36 The four most famous ones all took place in a 35-year period at the beginning of the 19th century. Slave rebellions 11:41 Gabriel's Rebellion in 1800 â which we've talked about before â was discovered before he was able to carry out his plot. 11:45 Then, in 1811, a group of slaves upriver from New Orleans seized cane, knives, and guns, and marched on the city before militia stopped them. 11:52 And in 1822, Denmark Vesey, a former slave who had purchased his freedom, may have organized a plot to destroy Charleston, South Carolina. 11:59 I say "may have" because the evidence against him is disputed and comes from a trial that was not fair. 12:05 But regardless, the end result of that trial was that he was executed, as were 34 slaves. Nat Turner's Rebellion 12:09 But the most successful slave rebellion, at least in the sense that they actually killed some people, was Nat Turner's in August 1831. 12:15 Turner was a preacher, and with a group of about 80 slaves, he marched from farm to farm in South Hampton County, Virginia, 12:21 killing the inhabitants, most of whom were women and children, because the men were attending a religious revival meeting in North Carolina. 12:27 Turner and 17 other rebels were captured and executed, but not before they struck terror into the hearts of whites all across the American South. 12:34 Virginia's response was to make slavery worse, passing even harsher laws that forbade slaves from preaching, and prohibited teaching them to read. 12:42 Other slave states followed Virginia's lead and, by the 1830s, slavery had grown, if anything, more harsh. 12:47 So, this shows that large-scaled armed resistance was â Django Unchained aside â not just suicidal, but also a threat to loved ones and, really, to all slaves. How enslaved people resisted their oppression & why it matters 12:55 But, it is hugely important to emphasize that slaves did resist their oppression. 12:59 Sometimes this meant taking up arms, but usually it meant more subtle forms of resistance, 13:03 like intentional work slowdowns or sabotaging equipment, or pretending not to understand instructions. 13:08 And, most importantly, in the face of systematic legal and cultural degradation, they re-affirmed their humanity through family and through faith. 13:16 Why is this so important? 13:17 Because too often in America, we still talk about slaves as if they failed to rise up, 13:21 when, in fact, rising up would not have made life better for them or for their families. 13:26 The truth is, sometimes carving out an identity as a human being in a social order that is constantly seeking to dehumanize you, is the most powerful form of resistance. 13:34 Refusing to become the chattel that their masters believed them to be is what made slavery untenable and the Civil War inevitable, so make no mistake, slaves fought back. 13:45 And in the end, they won. I'll see you next week. Credits 13:48 Crash Course is produced and directed by Stan Muller. 13:50 The script supervisor is Meredith Danko. 13:52 Our associate producer is Danica Johnson. 13:54 The show is written by my high school history teacher Raoul Meyer and myself. 13:57 And our graphics team is Thought Cafe. 13:58 Every week, there's a new caption to the Libertage, but today's episode was so sad that we couldn't fit a Libertage in... 14:04 UNTIL NOW! [Libertage Rock Music] 14:08 Suggest Libertage caption in comments, where you can also ask questions about today's video that will be answered by our team of historians. 14:13 Thanks for watching Crash Course, and as we say in my home town, don't forget to be abolitionist.
Make mcq quiz with 4 option in which one is correct -'10 Basis of Material Science ⢠.....;;;";;;"~~;;,,;;,,,,;.;.,,;;,,,;,,;.;,.,------------ 6. Temporary materials: Some materials are meant to be placed in the oral cavity for a short period of time for different reasons. ⢠Temporary crowns: While a permanent crown is prepared in the dental laboratory, the patient must wait for few days before it can be fabricated and cemented into place. Does patient experience any problems during this time period? If the tooth is vital (the pulp is alive), the patient is likely to experience pain and sensitivity while eating and drinking, also it looks unesthetic. What can be done to solve this problem? A temporary crown is placed before the patient leaves the clinic. It is constructed and luted in the same appointment in which the crown preparation is done. Temporary crowns are not very strong or esthetic but they serve adequately till the permanent crown is ready to be cemented. ⢠Temporary restorations: Sometimes it is difficult to decide immediately the best line of treatment for a particular tooth. The exact condition of the pulp may not be obvious to the dentist from the patient's symptoms. A dentist removes all or part of the decay and then places a temporary restoration to have time to observe the behaviour of the pulp or to give the pilip time to heal before deciding the further treatment required. Classification based on Location of Fabrication 4,9 Materials can be classified based on the location of fabrication into: ⢠Direct restorative materials. ⢠Indirect restorative materials Direct restorative materials: They include those materials which are used to restore cavity preparations directly in the oral cavity (Box 1.5). Box 1.5: Examples of direct restorative materials Amalgam, composites, glass ionomer and other materials, which set by chemical reactions in the mouth. Indirect restorative materials: It includes those restorations which must be fabricated outside the mouth, indirectly on a cast/ model/ die, because their processing condition would harm oral tissues. Materials used in the construction of such prosthesis are called indirect restorative materials (Box 1.6). Box 1.6: Examples of indirect restorative materials Gold inlays, crowns of metal, ceramic and polymers, which are processed at elevated temperatures. Some indirect composite restorations can be processed under specific wavelength of light, e.g. Ceramage. Classification based on Longevity of Use 1. Permanent restorations: These restorations are not planned to be replaced for a particular time period. Though they are referred to as permanent, actually they are not, e.g. fillings, crowns, bridges and dentures do not last forever (Fig. 1.5). 2. Temporary restorations: These restorations are planned to be replaced in a short period of time, such as few days to weeks. For ~ Permanent C/) c c -.2 0 c- :;::; Cll co Interim ~ Q; 0 .8ll::1iJ C/) o~ Cll a:: c:=:J Temporary Time period Fig. 1.5: Diagram depicting the time period of use of a restoration. (Arrow in permanent restoration depicts that such restorations are not planned to be replaced for a long period of time.) Introducton to Dental Materials Dental materials Box 1.7: Characteristics of metals 1. High thermal and electrical conductivity 2. Ductility (pure metals are very soft and they can be bent without breaking) 3. Opacity (they do not transmit light) 4. Luster (they have a surface that strongly reflects light and appears bright and shiny) 5. They tend to dissolve to some extent in water or other aqueous solutions, producing cations. 6. All metals are white (actually gray) except for gold, which is yellow, and copper, which is reddish. 7. All metals are solid at room temperature except mercury, which is liquid at room temperature and is used with silver alloys as amalgam. 8. All metals have high melting temperatures because of high strength of the metallic bond that holds the atoms together. 3. Polymers 4. Composites Composites are mixtures of two or more of the first three classes in which the different components remain distinct from one another in the final structure. A common example is composite resin. Fig. 1.7a: Three-dimensional structure of iron (metal) Metals Metals are the oldest of the three classes of materials that have been used as dental materials. Metals are characterized by metallic bonds (Box 1.7) which will be discussed in the next chapter. Metals solidify with their atoms in a regular or crystalline arrangement (see Chapter 2), often in the form of a cube (Fig. 1.7a). example, temporary fillings done in a tooth during root canal treatment, which have to be replaced within 2-4 days during subsequent visits. They are used to protect the tooth and provide function till the final restoration is done. 3. Interim restoration: At times, dental treatment requires "long-term" definite temporary restorations or "interim" restorations. For examle, a 7-year-old child, met with trauma and fractured one of his central incisors. A large composite build- up may serve his immediate requirement until the root formation is completed and a permanent crown is placed. 5 Classification based on the Chemical Nature of the Material These are the atoms that make up a material and the way they are bonded together determine the properties of that materiaLS Weak bonds make for weak materials and vice versa (Table 1.4). Materials can be classified into different categories based on their primary atomic bonds (Fig. 1.6): 1. Metals 2. Ceramics Fig. 1.6: Classification of dental materials based on chemical nature 12 Basis of Material Science Box 1.9: Benefits of ceramics in dentistry 1. Many ceramic oxides are used as pigmenting agents. These oxides produce good range of colors. Due to this characteristic, we are able to match almost any tooth color with good esthetic results. 2. They are inert, i.e. not chemically reactive. This quality provides ceramics with good bio- compatibility. 3. Ceramic materials are translucent, like natural teeth. This translucency gives the ceramic crown a more natural appearance than any other dental material. Fig. 1.7b: Internal arrangement of tetrahedral structure of ceramic (silica) four large oxygen atoms surround smaller silicon atom Ceramics A ceramic is a compound formed by the union of a metallic and a non-metallic element (Box 1.8). Most of these materials are oxides, formed by the union of oxygen with metals such as silicon, aluminum, calcium and magnesium (Fig.1.7b). Ceramics may be simple or complex. Examples of simple ceramics are alumina and silica. Examples of complex ceramics are feldspar (potassium aluminum silicate) and kaolin (hydrated aluminum silicate). Ceramics may be crystalline or non- crystalline (i.e. amorphous). Porcelain is a specific type of ceramic used extensively in dentistry (Box 1.9). Box 1.8: Characteristics of ceramics 1. High melting points. 2. Brittleness, which means they cannot be bent or deformed (no sliding) to any extent without actually cracking and breaking. 3. They are poor conductor of heat and electricity. 4. They are chemically inert. 5. They have excellent esthetic result in terms of matching natural teeth. Fig. 1.8: Stucture of synthetic polymer Polymers They are the latest addition (early to mid- 1900s) to dental materials. Most of the polymers are nowadays synthesized by humans. Polymers are giant, long-chain organic molecules (Fig. 1.8). Polymers are characterized by covalent bonds within each molecule, giving them tremendous strength in a single direction. Try to break a nylon rope by pulling it! They are poor conductors of heat and electri- city. Most polymers have a structure containing thousands of carbon atoms linked together like beads on a string. Others, such as silicone polymers are formed with silicon-oxygen bonds. Introducton to Dental Materials Table 1.4: Characteristics of different materials 13 Characteristics Bond Properties Crystal structure Metals Metallic bonding High strength and hardness, high electrical and thermal conductivity BCC, FCC, or HCP unit cells Ceramics Ionic or covalent bonding, or both High hardness and stiffness, electrically insulating, refractory, and chemically inert Crystalline or amorphous Polymers Covalent bonding Low sensitivity, high electrical resistivity, and low thermal conductivity, strength and stiffness vary widely Amorphous and crystalline Composites Composites are combinations of any of the basic ceramic, metallic and polymeric materials (Box 1.10). Each material that makes up composites is called a phase. Their properties tend to be somewhere between those of their basic constituents and are used to enhance their performance, longevity and handling chracterstics. Box 1.10: Types of composites in dentistry 1. Ceramic - metallic composite: Tungsten carbide bur. 2. Metal - polymer composite: Die materials in dental laboratory. 3. Ceramic - polymer composite: Enamel, dentin, bone and restorative composites. A composite is a kind of "combination" of materials, which compliment each other. The properties lacking in one material are compensated by those of the other material. For example, restorative composite has two phases, namely resin and fillers. Teeth and bones are examples of natural composites. Enamel is a composite of hydroxyapatite (which is a ceramic material) and protein (which is a polymer). EVALUATION OF DENTAL MATERIALS Most manufacturers of dental materials maintain a quality assurance programme (As per international standard like ADA specifications) and materials are thoroughly tested before being released into the market for dental practitioner (Fig. 1.9). Laboratory Evaluations Most ADA/ ANSI specifications involve laboratory tests. The tests performed as per these specifications are useful but they all are performed in vitro, (carried out in the laboratory away from the clinical conditions) which have a lot of limitations in clinical practice.lO Clinical Notes 1. For example, most of the direct restorative materials are tested for their compressive strength but ultimately the material is subjected to a combination of compressive, tensile and shear stresses, which may decide the final success or failure of the material under masticatory load. 2. Similarly upper dentures mostly fracture along the midline because of bending. Hence a bending or transverse strength ~B-a-s-is-o-f-M-a-t-e-ria-I-S~c-ie-n-c-e-------------- ---------. test is far more meaningful for denture base materials than a compression test. Clinical Trials The majority of new materials are subjected to extensive clinical trials normally in co-operation with a dental college or hospital departments prior to their release. CONCLUSION As the number of available materials is going up, it is important that the dentist remains more aware about new products so that their judgement about the selection of material remains successful. Materials which have not been thoroughly evaluated should be avoided, specially with clinical dentistry falling under Consumer Protection Act (CPA). I Research and development I iI Manufacturer/analysis Ideal requirements for clinical use: Thermal, optical, mechanical, chemical, biological Available materials and their properties are evaluated Launch of new I product Choice and selection of material by the dentist Critical assessment based on clinical performance I I H feedback to I
Of the 7 billion people on Earth roughly 0:02 6 billion own a cell phone which is 0:05 pretty shocking given that only 4 and2 0:07 billion have access to a working toilet 0:09 so how are these popular gadgets 0:11 changing your body and brain If you're 0:13 looking down at your phone right now 0:15 your spine angle is equivalent to that 0:17 of an 8-year-old child sitting on your 0:19 neck which is fairly significant 0:21 considering people spend an average of 0:23 4.7 hours a day looking at their phone 0:26 this combined with the length of time 0:28 spent in front of computers has led to 0:30 an increase in the prevalence of myopia 0:32 or nearsightedness in North America in 0:34 the 1970s about one quar of the 0:36 population had myopia where today nearly 0:39 half do and in some parts of Asia 80 to 0:41 90% of the population is now nearsighted 0:44 and it can be hard to put your phone 0:46 down take for example the game Candy 0:48 Crush as you play the game you achieve 0:50 small goals causing your brain to be 0:52 rewarded with little bursts of dopamine 0:54 and eventually you're rewarded in the 0:56 game with new content this novelty also 0:58 gives little bursts of dopamine and 1:00 together create what is known as a 1:01 compulsion Loop which just happens to be 1:04 the same Loop responsible for the 1:05 behaviors associated with nicotine or 1:07 cocaine our brains are hardwired to make 1:10 us novelty seeking and this is why apps 1:12 on our phones are designed to constantly 1:14 provide us with new content making them 1:16 hard to put down as a result 93% of 1:19 young people aged 18 to 29 report using 1:21 their smartphone as a tool to avoid 1:23 boredom as opposed to other activities 1:26 like reading a book or engaging with 1:27 people around them this has created a 1:29 new term nomophobia the fear or anxiety 1:32 of being without your phone we also see 1:35 a change in brain patterns Alpha rhythms 1:37 are commonly associated with wakeful 1:39 relaxation like when your mind wanders 1:41 off whereas gamma waves are associated 1:44 with conscious attentiveness and 1:46 experiments have shown that when a cell 1:47 phone is transmitting say during a phone 1:49 call the power of these Alpha Waves is 1:52 significantly boosted meaning phone 1:54 Transmissions can literally change the 1:56 way your brain functions your smartphone 1:58 can also disrupt your sleep the screen 2:00 emits a blue light which has been shown 2:02 to alter our circadian rhythms 2:03 diminishing the time spent in deep Sleep 2:06 which is linked to the development of 2:07 diabetes cancer and obesity Studies have 2:10 shown that people who read on their 2:11 smartphone at night have a harder time 2:13 falling asleep and produce less 2:15 melatonin a hormone responsible for the 2:17 regulation of sleep wake Cycles Harvard 2:20 medical school advises the last 2 to 3 2:22 hours before bed be technology free so 2:24 pick up a book before bed instead of 2:26 course smartphones also completely 2:28 change our ability to access information 2:30 most notably in poor and minority 2:32 populations 7% of Americans are entirely 2:35 dependent on smartphones for their 2:37 access to the internet a 2014 study 2:40 found that the majority of smartphone 2:41 owners use their phone for online 2:43 banking to look up medical information 2:45 and searching for jobs so while phones 2:47 are in no way exclusively bad and have 2:50 been part of a positive change in the 2:51 world there's no denying that they are 2:53 changing us but many successful people 2:56 have now decided to take smartphone 2:58 vacations in order to increase 3:00 productivity in our new ASAP thought 3:01 video we break down the top six reasons 3:04 you should take a smartphone vacation 3:06 and how it could benefit your life right 3:08 now and subscribe for more weekly 3:09 science videos
Animal Rights and Diet Success Criteria I can explain key terms which describe the type of diets people have I can explain the advantages and disadvantages of different types of diet Animal Rights and Diet Match up the terms with the meaning Term Meaning Omnivore - eats fish but no other type of meat Vegetarian - eats most types of meat and vegetables Pescetarian - doesnât eat any products that come from animals Vegan - doesnât eat meat but will eat dairy products like milk Place the different diets on a spectrum All meat No animal products at all Vegetarian Vegan Omnivore Pescetarian Omnivore Omnivore Most people in the UK are omnivores Match the countries with the amount of meat eaten per person per year Country Meat per person per year India 9.9 kg USA 4.4 kg Bangladesh 120 kg UK 111.5kg Nepal 84.2 kg Australia 4 kg Numeracy How much meat is consumed in the UK per year? (Amount of meat eaten X the UK population) 2. How much meat is consumed in Bangladesh per year? (Amount of meat eaten X the Bangladesh population) Country Meat per person per year USA 120 kg Australia 111.5kg UK 84.2 kg Nepal 9.9 kg India 4.4 kg Bangladesh 4 kg UK â 64 million Bangladesh â 165 million http://www.telegraph.co.uk/travel/maps-and-graphics/world-according-to-meat-consumption/ 7 Why do people eat meat? Discuss Tradition (their family has always done it) Culture (celebrations) Taste Convenience Nutrients such as B12, protein and iron Consumption of meat is rising across developing countries because higher incomes generally mean more meat eating. Pescetarian "Yeah, I'm a vegetarian." "But that looks like fish you're eating." "Oh yeah, I eat fish.â An estimated 5% - 6% of people in the UK are pescetarians. How many people is this? Approx. 3.6 million Calculation â 66,000,000 /100 x 5.5 = 3,630,000 9 Which group is cuter? Animals Fish 10 People often donât feel as much love for fish as they do for fluffy, cute mammals. The may think fish donât feel pain. They may be fussy. They think fish isnât meat. Not farmed as much as mammals; can be wild. To get nutrients they wouldnât get from just vegetables and grains. (Omega 3 is in plants but in higher concentrations in oily fish) Why are people pescetarians? https://www.vegsoc.org/sslpage.aspx?pid=753 http://articles.mercola.com/omega-3.aspx Fish â In a perfect world, fish can provide you all the omega-3s you need. Unfortunately, the vast majority of the fish supply is now heavily tainted with industrial toxins and pollutants, such as heavy metals which include mercury, lead, arsenic, and cadmium, PCBs, and radioactive poisons. These toxins make eating fish no longer recommended. 11 Vegetarianism Vegetarians will not eat any meat or product that comes from the slaughter of animals e.g. gelatine. About 3% of the UK population are vegetarian. How many people is this? 1.9 million 12 Why are people vegetarian? They donât like the idea that animals are killed so they can eat Health reasons Donât like meat Brought up vegetarian Environmental reasons Religious reasons (e.g. some Buddhist, Hindus) Watch the following clip twice. The second time, write down the fact which surprises you the most. https://www.youtube.com/watch?v=VW6wfpHFdaI The World Health Organization has classified processed meats â including ham, salami, sausages and hot dogs â as a Group 1 carcinogen (same as smoking/alcohol) which means that there is strong evidence that processed meats cause cancer. Red meat, such as beef, lamb and pork has been classified as a 'probable' cause of cancer. 13 Veganism Not just a diet Around 1% of the population of UK are vegans. A vegan is described by the Vegan Society as âa philosophy and way of living which seeks to excludeâas far as is possible and practicableâall forms of exploitation of, and cruelty to, animals for food, clothing or any other purpose; and by extension, promotes the development and use of animal-free alternatives for the benefit of humans, animals and the environment. In dietary terms it denotes the practice of dispensing with all products derived wholly or partly from animalsâ Why are people vegan? Why are people vegan? James Aspey: https://www.youtube.com/watch?v=a22XxXP3nU8 Warning: some of the content in this video clip may upset some viewers from 7:14 â 8:11 https://www.youtube.com/watch?v=BtqXeym7H8A Why are people vegan? âDonât want bad karmaâ Feel healthier Reduce chances of diseases. Example heart disease. Donât want to exploit animals Believe in animal rights Sustainability Environment Create a Table of Pros & Cons of Veganism Pros â Cons - Create a Table of Pros & Cons of Veganism Pros Cons No animals have died for you to eat Some people think it is healthier Help the environment Fewer antibiotics/chemicals that are given to some animals Makes you feel good No vitamin B12 so have to supplement Harder to find food at shops or restaurants May be harder to get enough iron May be more expensive to get substitute meats Judged by family and friends Could put farmers out of business Group Work Source 1 Summarise it in your jotter Explain what the source is/what it says What does it suggest? What is your opinion? Feedback to rest of class https://www.youtube.com/watch?v=SYyjel5VuHg Farmerâs Poem
The price of electricity has risen (1) ______ over the last year. A) specially | B) obviously | C) significantly | D) remarkably The heavy rain led to floods, (2) ______ a lot of trouble for local farmers. A) causing | B) making | C) resulting | D) affecting I have never seen (3) ______ a beautiful sunset in my entire life! A) as | B) like | C) so | D) such It is very (4) ______ that some people still don't believe in climate change. A) doubtful | B) suspicious | C) worrying | D) uncertain My brother is learning how to (5) ______ a small business. A) adjust | B) run | C) manage | D) direct Can you (6) ______ the person who took your bag? A) inform | B) identify | C) tell | D) know On a daily (7) ______, we should try to use less plastic. A) basis | B) motive | C) cause | D) method Regular exercise and a healthy diet are very (8) ______ for your heart. A) rewarding | B) valuable | C) beneficial | D) productive She was (9) ______ to win the race, so she practiced every single day. A) fixed | B) decided | C) committed | D) determined An (10) ______ student spends about three hours on homework every evening. A) everyday | B) average | C) normal | D) regular