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Negatives with No, None, Not, Nor, and No-one (C1 Level)
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“There’s No Such Thing as Sound Science” by By Christie Aschwanden was a lead science writer for FiveThirtyEight. FiveThirtyEight, Science, Dec. 6, 2017 Science is being turned against itself. For decades, its twin ideals of transparency and rigor have been weaponized by those who disagree with results produced by the scientific method. Under the Trump administration, that fight has ramped up again. In a move ostensibly meant to reduce conflicts of interest, Environmental Protection Agency Administrator Scott Pruitt has removed a number of scientists from advisory panels and replaced some of them with representatives from industries that the agency regulates. Like many in the Trump administration, Pruitt has also cast doubt on the reliability of climate science. For instance, in an interview with CNBC, Pruitt said that “measuring with precision human activity on the climate is something very challenging to do.” Similarly, Trump’s pick to head NASA, an agency that oversees a large portion the nation’s climate research, has insisted that research into human influence on climate lacks certainty, and he falsely claimed that “global temperatures stopped rising 10 years ago.” Kathleen Hartnett White, Trump’s nominee to head the White House Council on Environmental Quality, said in a Senate hearing last month that she thinks we “need to have more precise explanations of the human role and the natural role” in climate change. The same entreaties crop up again and again: We need to root out conflicts. We need more precise evidence. What makes these arguments so powerful is that they sound quite similar to the points raised by proponents of a very different call for change that’s coming from within science. This other movement strives to produce more robust, reproducible findings. Despite having dissimilar goals, the two forces espouse principles that look surprisingly alike: Science needs to be transparent. Results and methods should be openly shared so that outside researchers can independently reproduce and validate them. The methods used to collect and analyze data should be rigorous and clear, and conclusions must be supported by evidence. These are the arguments underlying an “open science” reform movement that was created, in part, as a response to a “reproducibility crisis” that has struck some fields of science.1 But they’re also used as talking points by politicians who are working to make it more difficult for the EPA and other federal agencies to use science in their regulatory decision-making, under the guise of basing policy on “sound science.” Science’s virtues are being wielded against it. What distinguishes the two calls for transparency is intent: Whereas the “open science” movement aims to make science more reliable, reproducible and robust, proponents of “sound science” have historically worked to amplify uncertainty, create doubt and undermine scientific discoveries that threaten their interests. “Our criticisms are founded in a confidence in science,” said Steven Goodman, co-director of the Meta-Research Innovation Center at Stanford and a proponent of open science. “That’s a fundamental difference — we’re critiquing science to make it better. Others are critiquing it to devalue the approach itself.” Calls to base public policy on “sound science” seem unassailable if you don’t know the term’s history. The phrase was adopted by the tobacco industry in the 1990s to counteract mounting evidence linking secondhand smoke to cancer. A 1992 Environmental Protection Agency report identified secondhand smoke as a human carcinogen, and Philip Morris responded by launching an initiative to promote what it called “sound science.” In an internal memo, Philip Morris vice president of corporate affairs Ellen Merlo wrote that the program was designed to “discredit the EPA report,” “prevent states and cities, as well as businesses from passing smoking bans” and “proactively” pass legislation to help their cause. The sound science tactic exploits a fundamental feature of the scientific process: Science does not produce absolute certainty. Contrary to how it’s sometimes represented to the public, science is not a magic wand that turns everything it touches to truth. Instead, it’s a process of uncertainty reduction, much like a game of 20 Questions. Any given study can rarely answer more than one question at a time, and each study usually raises a bunch of new questions in the process of answering old ones. “Science is a process rather than an answer,” said psychologist Alison Ledgerwood of the University of California, Davis. Every answer is provisional and subject to change in the face of new evidence. It’s not entirely correct to say that “this study proves this fact,” Ledgerwood said. “We should be talking instead about how science increases or decreases our confidence in something.” The tobacco industry’s brilliant tactic was to turn this baked-in uncertainty against the scientific enterprise itself. While insisting that they merely wanted to ensure that public policy was based on sound science, tobacco companies defined the term in a way that ensured that no science could ever be sound enough. The only sound science was certain science, which is an impossible standard to achieve. “Doubt is our product,” wrote one employee of the Brown & Williamson tobacco company in a 1969 internal memo. The note went on to say that doubt “is the best means of competing with the ‘body of fact’” and “establishing a controversy.” These strategies for undermining inconvenient science were so effective that they’ve served as a sort of playbook for industry interests ever since, said Stanford University science historian Robert Proctor. The sound science push is no longer just Philip Morris sowing doubt about the links between cigarettes and cancer. It’s also a 1998 action plan by the American Petroleum Institute, Chevron and Exxon Mobil to “install uncertainty” about the link between greenhouse gas emissions and climate change. It’s industry-funded groups’ late-1990s effort to question the science the EPA was using to set fine-particle-pollution air-quality standards that the industry didn’t want. And then there was the more recent effort by Dow Chemical to insist on more scientific certainty before banning a pesticide that the EPA’s scientists had deemed risky to children. Now comes a move by the Trump administration’s EPA to repeal a 2015 rule on wetlands protection by disregarding particular studies. (To name just a few examples.) Doubt merchants aren’t pushing for knowledge, they’re practicing what Proctor has dubbed “agnogenesis” — the intentional manufacture of ignorance. This ignorance isn’t simply the absence of knowing something; it’s a lack of comprehension deliberately created by agents who don’t want you to know, Proctor said.2 In the hands of doubt-makers, transparency becomes a rhetorical move. “It’s really difficult as a scientist or policy maker to make a stand against transparency and openness, because well, who would be against it?” said Karen Levy, researcher on information science at Cornell University. But at the same time, “you can couch everything in the language of transparency and it becomes a powerful weapon.” For instance, when the EPA was preparing to set new limits on particulate pollution in the 1990s, industry groups pushed back against the research and demanded access to primary data (including records that researchers had promised participants would remain confidential) and a reanalysis of the evidence. Their calls succeeded and a new analysis was performed. The reanalysis essentially confirmed the original conclusions, but the process of conducting it delayed the implementation of regulations and cost researchers time and money. Delay is a time-tested strategy. “Gridlock is the greatest friend a global warming skeptic has,” said Marc Morano, a prominent critic of global warming research and the executive director of ClimateDepot.com, in the documentary “Merchants of Doubt” (based on the book by the same name). Morano’s site is a project of the Committee for a Constructive Tomorrow, which has received funding from the oil and gas industry. “We’re the negative force. We’re just trying to stop stuff.” Some of these ploys are getting a fresh boost from Congress. The Data Quality Act (also known as the Information Quality Act) was reportedly written by an industry lobbyist and quietly passed as part of an appropriations bill in 2000. The rule mandates that federal agencies ensure the “quality, objectivity, utility, and integrity of information” that they disseminate, though it does little to define what these terms mean. The law also provides a mechanism for citizens and groups to challenge information that they deem inaccurate, including science that they disagree with. “It was passed in this very quiet way with no explicit debate about it — that should tell you a lot about the real goals,” Levy said. But what’s most telling about the Data Quality Act is how it’s been used, Levy said. A 2004 Washington Post analysis found that in the 20 months following its implementation, the act was repeatedly used by industry groups to push back against proposed regulations and bog down the decision-making process. Instead of deploying transparency as a fundamental principle that applies to all science, these interests have used transparency as a weapon to attack very particular findings that they would like to eradicate. Now Congress is considering another way to legislate how science is used. The Honest Act, a bill sponsored by Rep. Lamar Smith of Texas,3 is another example of what Levy calls a “Trojan horse” law that uses the language of transparency as a cover to achieve other political goals. Smith’s legislation would severely limit the kind of evidence the EPA could use for decision-making. Only studies whose raw data and computer codes were publicly available would be allowed for consideration. That might sound perfectly reasonable, and in many cases it is, Goodman said. But sometimes there are good reasons why researchers can’t conform to these rules, like when the data contains confidential or sensitive medical information.4 Critics, which include more than a dozen scientific organizations, argue that, in practice, the rules would prevent many studies from being considered in EPA reviews.5 It might seem like an easy task to sort good science from bad, but in reality it’s not so simple. “There’s a misplaced idea that we can definitively distinguish the good from the not-good science, but it’s all a matter of degree,” said Brian Nosek, executive director of the Center for Open Science. “There is no perfect study.” Requiring regulators to wait until they have (nonexistent) perfect evidence is essentially “a way of saying, ‘We don’t want to use evidence for our decision-making,’” Nosek said. Most scientific controversies aren’t about science at all, and once the sides are drawn, more data is unlikely to bring opponents into agreement. Michael Carolan, who researches the sociology of technology and scientific knowledge at Colorado State University, wrote in a 2008 paper about why objective knowledge is not enough to resolve environmental controversies. “While these controversies may appear on the surface to rest on disputed questions of fact, beneath often reside differing positions of value; values that can give shape to differing understandings of what ‘the facts’ are.” What’s needed in these cases isn’t more or better science, but mechanisms to bring those hidden values to the forefront of the discussion so that they can be debated transparently. “As long as we continue down this unabashedly naive road about what science is, and what it is capable of doing, we will continue to fail to reach any sort of meaningful consensus on these matters,” Carolan writes. The dispute over tobacco was never about the science of cigarettes’ link to cancer. It was about whether companies have the right to sell dangerous products and, if so, what obligations they have to the consumers who purchased them. Similarly, the debate over climate change isn’t about whether our planet is heating, but about how much responsibility each country and person bears for stopping it. While researching her book “Merchants of Doubt,” science historian Naomi Oreskes found that some of the same people who were defending the tobacco industry as scientific experts were also receiving industry money to deny the role of human activity in global warming. What these issues had in common, she realized, was that they all involved the need for government action. “None of this is about the science. All of this is a political debate about the role of government,” she said in the documentary. These controversies are really about values, not scientific facts, and acknowledging that would allow us to have more truthful and productive debates. What would that look like in practice? Instead of cherry-picking evidence to support a particular view (and insisting that the science points to a desired action), the various sides could lay out the values they are using to assess the evidence. For instance, in Europe, many decisions are guided by the precautionary principle — a system that values caution in the face of uncertainty and says that when the risks are unclear, it should be up to industries to show that their products and processes are not harmful, rather than requiring the government to prove that they are harmful before they can be regulated. By contrast, U.S. agencies tend to wait for strong evidence of harm before issuing regulations. Both approaches have critics, but the difference between them comes down to priorities: Is it better to exercise caution at the risk of burdening companies and perhaps the economy, or is it more important to avoid potential economic downsides even if it means that sometimes a harmful product or industrial process goes unregulated? In other words, under what circumstances do we agree to act on a risk? How certain do we need to be that the risk is real, and how many people would need to be at risk, and how costly is it to reduce that risk? Those are moral questions, not scientific ones, and openly discussing and identifying these kinds of judgment calls would lead to a more honest debate. Science matters, and we need to do it as rigorously as possible. But science can’t tell us how risky is too risky to allow products like cigarettes or potentially harmful pesticides to be sold — those are value judgements that only humans can make.
Think before you act online Sometimes what we post on our favourite social networks have consequences we didn't expect. One weekend, 20-year-old James Miller posted on his Facebook page that his job was soooo boring. When he got to work on Monday his boss told him to clear his desk and get out. He gave him a letter, too. It said: 'After reading your comments on Facebook about our company, we understand you are not happy with your work. We think it is better for you to look for something that you will find more interesting." A few years ago, a girl's birthday party turned into a nightmare. Fifteen-year-old Cathy posted an invitation to her birthday party online. She posted her address, too. When her parents got back from the cinema that evening, they couldn't believe their eyes. There were 500 people at the party, and some of them were smashing windows, breaking potted plants and making a total mess of the house. Most teens think they know everything about social media, and that things like this could never happen to them. A study shows that last year alone, more than three million young people worldwide got into trouble because of their online activities. Here are some important tips. None of them can guarantee 100% Internet security, but all of them will help you to be safer online. RULE 1: Share with care! Not everyone will like what you write on Facebook or Twitter. Think before you post something. You can never completely control who sees your profile, your texts, your pictures, or your videos. Before clicking 'post', everyone should ask themselves two questions: 'How will I feel if my family or teachers see this?' and 'How might this post be bad for me in three, five or ten years from now?" RULE 2: Be polite when you write! Imagine someone is unfriendly in real life. You don't like it, right? Well, the same is true of online communication. Politeness matters, and anyone can be polite. No one likes it when you 'shout' in your messages. DON'T USE ALL CAPITALS!!!!!!!! If you feel angry or frustrated while you're writing a message, wait a bit. Read it again later and then send it. RULE 3: Protect and respect! Don't share your passwords with anyone. Don't post your home or email address online. Beware of 'cyberbullying' - don't forward rumours about other people, and don't say negative things about them. If you get messages like that or see them online, talk to an adult you know.
Contact with the Americas In 1001, Viking sailors led by Leif Erikson reached the eastern tip of North America. Archaeologists have found evidence of the Viking settlement of Vinland in present-day Newfoundland, Canada. The Vikings did not stay in Vinland long and no one is sure why they left. However, Viking stories describe fierce battles with Skraelings, the Viking name for the Inuit. Evidence suggests that Asians continued to cross the Bering Sea into North America after the last ice age ended. Some scholars believe that ancient seafarers from Polynesia may have traveled to the Americas using their knowledge of the stars and winds. Modern Polynesians have sailed canoes thousands of miles in this way. Still others think that fishing boats from China and Japan blew off course and landed on the western coast of North or South America. Perhaps such voyages occurred. If so, they were long forgotten. Before 1492, the peoples of Asia and Europe had no knowledge of the Americas and their remarkable civilizations. The Voyages of Columbus Portuguese sailors had pioneered new routes around Africa toward Asia in the late 1400s. Spain, too, wanted a share of the riches. King Ferdinand and Queen Isabella hoped to keep their rival, Portugal, from controlling trade with India, China, and Japan. They agreed to finance a voyage of exploration by Christopher Columbus. Columbus, an Italian sea captain, planned to reach the East Indies by sailing west across the Atlantic. Finding a sea route straight to Asia would give the Spanish direct access to the silks, spices, and precious metals of Asia. The spice trade was a major cause for European exploration and a reason the Spanish rulers supported Columbus’s voyage. They also wanted wealth from any source. “Get gold,” King Ferdinand said to Columbus. “Humanely if possible, but at all hazards—get gold.” Crossing the Atlantic In August 1492, Columbus set out with three ships and about 90 sailors. As captain, he commanded the largest vessel, the Santa María. The other ships were the Niña and the Pinta. After a brief stop at the Canary Islands, the little fleet continued west into unknown seas. Fair winds sped them along, but a month passed without the sight of land. Some sailors began to grumble. They had never been away from land for so long and feared being lost at sea. Still, Columbus sailed on. On October 7, sailors saw flocks of birds flying southwest. Columbus changed course to follow the birds. A few days later, crew members spotted tree branches and flowers floating in the water. At 2 a.m. on October 12, the lookout on the Pinta spotted white cliffs shining in the moonlight. “Tierra! Tierra!” he shouted. “Land! Land!” At dawn, Columbus rowed ashore and planted the banner of Spain. He was convinced that he had reached the East Indies in Asia. He called the people he found there “Indians.” In fact, he had reached islands off the coasts of North America and South America in the Caribbean Sea. These islands later became known as the West Indies. For three months, Columbus explored the West Indies. To his delight, he found signs of gold on the islands. Eager to report his success, he returned to Spain. Columbus Claims Lands for Spain In Spain, Columbus presented Queen Isabella and King Ferdinand with gifts of pink pearls and brilliantly colored parrots. Columbus brought with him many things that Europeans had never seen before: tobacco, pineapples, and hammocks used for sleeping. Columbus also described the “Indians” he had met, the Taino (ty noh). The Taino, he promised, could easily be converted to Christianity and could also be used as slaves. The Spanish monarchs were impressed. They gave Columbus the title Admiral of the Ocean Sea. They also agreed to finance future voyages. The promise of great wealth, and the chance to spread Christianity, gave them a reason to explore further. Columbus made three more voyages across the Atlantic. In 1493, he founded the first Spanish colony in the Americas, Santo Domingo, on an island he called Hispaniola (present-day Haiti and the Dominican Republic). A colony is an area settled and ruled by the government of a distant land. Columbus also explored present-day Cuba and Jamaica. He sailed along the coasts of Central America and northern South America. He claimed all of these lands for Queen Isabella of Spain. Columbus proved to be a better explorer than governor. During his third expedition, settlers on Hispaniola complained of his harsh rule. Queen Isabella appointed an investigator, who sent Columbus back to Spain in chains. In the end, the queen pardoned Columbus, but he never regained the honors he had won earlier. He died in 1506, still convinced that he had reached Asia. The Impact of Columbus’s Voyages Columbus has long been honored as the bold sea captain who “discovered America.” Today, we recognize that American Indians had discovered and settled these lands long before 1492. We also recognize that Columbus and the Europeans who followed him treated the ancient inhabitants of the Americas brutally. Still, Columbus’s voyages did change history. They marked the beginning of lasting contact among the peoples of Europe, Africa, and the Americas. For a great many American Indians, contact had tragic results. Columbus and those who followed were convinced that European culture was superior to that of the Indians. The Spanish claimed Taino lands and forced the Taino to work in gold mines, on ranches, or in Spanish households. Many Taino died from harsh conditions or European diseases. The Taino population was wiped out. Still, the voyages of Columbus signaled a turning point for the Americas. A turning point is a moment in history that marks a decisive change. Curious Europeans saw the new lands as a place where they could settle, trade, and grow rich. Spanish Exploration Continues After the voyages of Columbus, the Spanish explored and settled other Caribbean islands that Columbus had found. They sought gold, land for crops, people to enslave, and converts to Christianity for the Spanish crown. By 1511, they had conquered Puerto Rico, Jamaica, and Cuba. They also explored the eastern coasts of North America and South America in search of a western route to Asia. In 1513, Vasco Núñez de Balboa (bal boh uh) crossed the Isthmus of Panama. American Indians had told him that a large body of water lay to the west. With a party of Spanish soldiers and Indians, Balboa reached the Pacific Ocean and claimed the ocean for Spain. The Spanish had no idea how wide the Pacific was until a sea captain named Ferdinand Magellan (muh jel un) sailed across it. The expedition—made up of five ships and about 250 crew members—left Spain in 1519. Fifteen months later, it cut through the stormy southern tip of South America by way of what is now known as the Strait of Magellan and entered the Pacific Ocean. Crossing the vast Pacific, the sailors ran out of food: Primary Source “We remained 3 months and 20 days without taking in provisions or other refreshments and ate only old biscuit reduced to powder, full of grubs and stinking from the dirt which rats had made on it. We drank water that was yellow and stinking.” —Antonio Pigafetta, The Diary of Antonio Pigafetta Magellan himself was killed in a battle with the local people of the Philippine Islands off the coast of Asia. In 1522, only one ship and 18 sailors returned to Spain. They were the first people to circumnavigate, or sail completely around, the world. In doing so, they had found an all-water western route to Asia. Europeans became aware of the true size of the Earth. How Did the Columbian Exchange Affect the Rest of the World? The encounter between the peoples of the Eastern and Western Hemispheres sparked a global exchange of goods and ideas. Because it started with the voyages of Columbus, this transfer is known as the Columbian Exchange. The Columbian Exchange refers to a biological and cultural exchange of animals, plants, human populations, diseases, food, government, technology, the arts, and languages. The exchange went in both directions. Europeans learned much from American Indians. At the same time, Europeans contributed in many ways to the culture of the Americas. This exchange also brought about many modifications, or changes, to the physical environment of the Americas, with both positive and negative results. Changing Environments Europeans introduced domestic animals such as chickens from Europe and Africa. European pigs, cattle, and horses often escaped into the wild and multiplied rapidly. Forests and grasslands were converted to pastures. As horses spread through what would become the United States, Indians learned to ride them and used them to carry heavy loads. Plants from Europe and Africa changed the way American Indians lived. The first bananas came from the Canary Islands. By 1520, one Spaniard reported that banana trees had spread “so greatly that it is marvelous to see the great abundance of them.” Oranges, lemons, and figs were also new to the Americas. In North America, explorers also brought such plants as bluegrass, the daisy, and the dandelion. These plants spread quickly in American soil and modified American grasslands. Tragically, Europeans also brought new diseases, such as smallpox and influenza. American Indians had no resistance to these diseases. Historians estimate that within 75 years, diseases from Europe had killed almost 90 percent of the people in the Caribbean Islands and in Mexico. American Indian Influences on Europe, Africa and Asia American Indians introduced Europeans to valuable food crops such as corn, potatoes, sweet potatoes, beans, tomatoes, manioc, squash, peanuts, pineapples, and blueberries. Today, almost half the world’s food crops come from plants that were first grown in the Americas. Europeans carried the new foods with them as they sailed around the world. Everywhere, people’s diets changed and populations increased. In South Asia, people used American hot peppers and chilies to spice stews. Chinese peasants began growing corn and sweet potatoes. Italians made sauces from tomatoes. People in West Africa grew manioc and corn. European settlers often adopted American Indian skills. In the North, Indians showed Europeans how to use snowshoes and trap beavers and other fur-bearing animals. European explorers learned how to paddle Indian canoes. Some leaders studied American Indian political structures. In the 1700s, Benjamin Franklin admired the Iroquois League and urged American colonists to unite in a similar way. Positive and Negative Consequences Through the Columbian Exchange, Europeans and American Indians modified their environments and gained new resources and skills. At the same time, warfare and disease killed many on both sides. Europeans viewed expansion positively. They gained great wealth, explored trade routes, and spread Christianity. Yet their farming, mining, and diseases took a toll on the physical environment and left many American Indians dead. Despite these negatives, the Columbian Exchange shaped the modern world, including what would become the United States.
Two step equations with no negative numbers
Understanding Quantum Theory of Electrons in Atoms The goal of this section is to understand the electron orbitals (location of electrons in atoms), their different energies, and other properties. The use of quantum theory provides the best understanding to these topics. This knowledge is a precursor to chemical bonding. As was described previously, electrons in atoms can exist only on discrete energy levels but not between them. It is said that the energy of an electron in an atom is quantized, that is, it can be equal only to certain specific values and can jump from one energy level to another but not transition smoothly or stay between these levels. The energy levels are labeled with an n value, where n = 1, 2, 3, …. Generally speaking, the energy of an electron in an atom is greater for greater values of n. This number, n, is referred to as the principal quantum number. The principal quantum number defines the location of the energy level. It is essentially the same concept as the n in the Bohr atom description. Another name for the principal quantum number is the shell number. The shells of an atom can be thought of concentric circles radiating out from the nucleus. The electrons that belong to a specific shell are most likely to be found within the corresponding circular area. The further we proceed from the nucleus, the higher the shell number, and so the higher the energy level (Figure 9.4.1). The positively charged protons in the nucleus stabilize the electronic orbitals by electrostatic attraction between the positive charges of the protons and the negative charges of the electrons. So the further away the electron is from the nucleus, the greater the energy it has. This quantum mechanical model for where electrons reside in an atom can be used to look at electronic transitions, the events when an electron moves from one energy level to another. If the transition is to a higher energy level, energy is absorbed, and the energy change has a positive value. To obtain the amount of energy necessary for the transition to a higher energy level, a photon is absorbed by the atom. A transition to a lower energy level involves a release of energy, and the energy change is negative. This process is accompanied by emission of a photon by the atom. The following equation summarizes these relationships and is based on the hydrogen atom: The values nf and ni are the final and initial energy states of the electron. The principal quantum number is one of three quantum numbers used to characterize an orbital. An atomic orbital, which is distinct from an orbit, is a general region in an atom within which an electron is most probable to reside. The quantum mechanical model specifies the probability of finding an electron in the three-dimensional space around the nucleus and is based on solutions of the Schrödinger equation. In addition, the principal quantum number defines the energy of an electron in a hydrogen or hydrogen-like atom or an ion (an atom or an ion with only one electron) and the general region in which discrete energy levels of electrons in a multi-electron atoms and ions are located. Another quantum number is l, the angular momentum quantum number. It is an integer that defines the shape of the orbital, and takes on the values, l = 0, 1, 2, …, n – 1. This means that an orbital with n = 1 can have only one value of l, l = 0, whereas n = 2 permits l = 0 and l = 1, and so on. The principal quantum number defines the general size and energy of the orbital. The l value specifies the shape of the orbital. Orbitals with the same value of l form a subshell. In addition, the greater the angular momentum quantum number, the greater is the angular momentum of an electron at this orbital. Orbitals with l = 0 are called s orbitals (or the s subshells). The value l = 1 corresponds to the p orbitals. For a given n, p orbitals constitute a p subshell (e.g., 3p if n = 3). The orbitals with l = 2 are called the d orbitals, followed by the f-, g-, and h-orbitals for l = 3, 4, 5, and there are higher values we will not consider. There are certain distances from the nucleus at which the probability density of finding an electron located at a particular orbital is zero. In other words, the value of the wavefunction ψ is zero at this distance for this orbital. Such a value of radius r is called a radial node. The number of radial nodes in an orbital is n – l – 1. Consider the examples in Figure 9.4.2. The orbitals depicted are of the s type, thus l = 0 for all of them. It can be seen from the graphs of the probability densities that there are 1 – 0 – 1 = 0 places where the density is zero (nodes) for 1s (n = 1), 2 – 0 – 1 = 1 node for 2s, and 3 – 0 – 1 = 2 nodes for the 3s orbitals. The s subshell electron density distribution is spherical and the p subshell has a dumbbell shape. The d and f orbitals are more complex. These shapes represent the three-dimensional regions within which the electron is likely to be found. Principal quantum number (n) & Orbital angular momentum (l): The Orbital Subshell: https://youtu.be/ms7WR149fAY If an electron has an angular momentum (l ≠ 0), then this vector can point in different directions. In addition, the z component of the angular momentum can have more than one value. This means that if a magnetic field is applied in the z direction, orbitals with different values of the z component of the angular momentum will have different energies resulting from interacting with the field. The magnetic quantum number, called ml, specifies the z component of the angular momentum for a particular orbital. For example, for an s orbital, l = 0, and the only value of ml is zero. For p orbitals, l = 1, and ml can be equal to –1, 0, or +1. Generally speaking, ml can be equal to –l, –(l – 1), …, –1, 0, +1, …, (l – 1), l. The total number of possible orbitals with the same value of l (a subshell) is 2l + 1. Thus, there is one s-orbital for ml = 0, there are three p-orbitals for ml = 1, five d-orbitals for ml = 2, seven f-orbitals for ml = 3, and so forth. The principal quantum number defines the general value of the electronic energy. The angular momentum quantum number determines the shape of the orbital. And the magnetic quantum number specifies orientation of the orbital in space, as can be seen in Figure 9.4.3. Figure 9.4.4 illustrates the energy levels for various orbitals. The number before the orbital name (such as 2s, 3p, and so forth) stands for the principal quantum number, n. The letter in the orbital name defines the subshell with a specific angular momentum quantum number l = 0 for s orbitals, 1 for p orbitals, 2 for d orbitals. Finally, there are more than one possible orbitals for l ≥ 1, each corresponding to a specific value of ml. In the case of a hydrogen atom or a one-electron ion (such as He+, Li2+, and so on), energies of all the orbitals with the same n are the same. This is called a degeneracy, and the energy levels for the same principal quantum number, n, are called degenerate energy levels. However, in atoms with more than one electron, this degeneracy is eliminated by the electron–electron interactions, and orbitals that belong to different subshells have different energies. Orbitals within the same subshell (for example ns, np, nd, nf, such as 2p, 3s) are still degenerate and have the same energy. While the three quantum numbers discussed in the previous paragraphs work well for describing electron orbitals, some experiments showed that they were not sufficient to explain all observed results. It was demonstrated in the 1920s that when hydrogen-line spectra are examined at extremely high resolution, some lines are actually not single peaks but, rather, pairs of closely spaced lines. This is the so-called fine structure of the spectrum, and it implies that there are additional small differences in energies of electrons even when they are located in the same orbital. These observations led Samuel Goudsmit and George Uhlenbeck to propose that electrons have a fourth quantum number. They called this the spin quantum number, or ms. The other three quantum numbers, n, l, and ml, are properties of specific atomic orbitals that also define in what part of the space an electron is most likely to be located. Orbitals are a result of solving the Schrödinger equation for electrons in atoms. The electron spin is a different kind of property. It is a completely quantum phenomenon with no analogues in the classical realm. In addition, it cannot be derived from solving the Schrödinger equation and is not related to the normal spatial coordinates (such as the Cartesian x, y, and z). Electron spin describes an intrinsic electron “rotation” or “spinning.” Each electron acts as a tiny magnet or a tiny rotating object with an angular momentum, even though this rotation cannot be observed in terms of the spatial coordinates. The magnitude of the overall electron spin can only have one value, and an electron can only “spin” in one of two quantized states. One is termed the α state, with the z component of the spin being in the positive direction of the z axis. This corresponds to the spin quantum number ms=12. The other is called the β state, with the z component of the spin being negative and ms=−12. Any electron, regardless of the atomic orbital it is located in, can only have one of those two values of the spin quantum number. The energies of electrons having ms=−12 and ms=12 are different if an external magnetic field is applied. Figure 9.4.5 illustrates this phenomenon. An electron acts like a tiny magnet. Its moment is directed up (in the positive direction of the z axis) for the 12 spin quantum number and down (in the negative z direction) for the spin quantum number of −12. A magnet has a lower energy if its magnetic moment is aligned with the external magnetic field (the left electron) and a higher energy for the magnetic moment being opposite to the applied field. This is why an electron with ms=12 has a slightly lower energy in an external field in the positive z direction, and an electron with ms=−12 has a slightly higher energy in the same field. This is true even for an electron occupying the same orbital in an atom. A spectral line corresponding to a transition for electrons from the same orbital but with different spin quantum numbers has two possible values of energy; thus, the line in the spectrum will show a fine structure splitting. The Pauli Exclusion Principle An electron in an atom is completely described by four quantum numbers: n, l, ml, and ms. The first three quantum numbers define the orbital and the fourth quantum number describes the intrinsic electron property called spin. An Austrian physicist Wolfgang Pauli formulated a general principle that gives the last piece of information that we need to understand the general behavior of electrons in atoms. The Pauli exclusion principle can be formulated as follows: No two electrons in the same atom can have exactly the same set of all the four quantum numbers. What this means is that electrons can share the same orbital (the same set of the quantum numbers n, l, and ml), but only if their spin quantum numbers ms have different values. Since the spin quantum number can only have two values (±12), no more than two electrons can occupy the same orbital (and if two electrons are located in the same orbital, they must have opposite spins). Therefore, any atomic orbital can be populated by only zero, one, or two electrons. The properties and meaning of the quantum numbers of electrons in atoms are briefly
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 Desirée Nieuwenhuis | Natàlia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-α alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- α and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-α 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-α, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-α and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. The majority of the studies examining boys with obesity indicate an early onset of puberty, while not all reported an earlier onset of puberty. In detail, high leptin, TNF-α, and IL-6 levels combined with low adiponectin levels stimulate the activation of the HPG axis in girls and boys with obesity, and 5, 45, 50, 51 REFERENCES 1. Kumar S, Kelly AS. Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. May- o Clin Proc. 2017;92(2):251-265. 2. Reinehr T, Roth CL. Is there a causal relationship between obesity and puberty? The Lancet Child & adolescent health. 2019;3(1):44-54. 3. WorldHealthOrganization. Facts and figures on childhood obesity. 2017. 4. Guglielmi V, Sbraccia P. Obesity phenotypes: depot-differences in adipose tissue and their clinical implications. Eat Weight Disord. 2018; 23(1):3-14. 5. Gomez-Hernandez A, Beneit N, Diaz-Castroverde S. Escribano O. 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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 ‘onset of puberty and adiposity/obesity’, ‘onset of puberty’, ‘children with obesity’, ‘adipose tissue’, ‘childhood obesity’, ‘adiposity’, ‘obesity’, ‘adipokine(s)’, ‘HPG axis’, ‘adipokines ovary/ova- ries’, or ‘adipokines testes’, 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. 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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
What is Electric Force? Electric force is just one of many types of forces in the world of physics. Forces are how and why things move, and can be explained by Newton's Laws of Motion. On the smallest scale, electric force is the resulting interaction between two charged particles. These charges can be either positive or negative. Larger objects can be charged by having an abundance of either of these particles, and therefore can create an electric force on a larger scale. Electric force is the reason why hair will sometimes stand up on its own and is also why we have electricity, allowing us to live in the modern world with lights and technology. Even out in nature electric force is present, as electric force causes lightning to strike. Electric force is fundamental to our everyday way of living. Reviewing Newton's Laws of Motion Newton's Laws of motion are the basic principles or ground rules that are applied all across physics. They describe how objects move and can be used to describe the interaction of charges. They are the following: An object in motion will stay in motion unless an external force is applied The force exerted on an object is equal to the mass times the acceleration of the object. ( ) Every force has an equal and opposite force Newton's laws explain how and why charged particles move. Since there is a force involved (e.g. electric force), particles will move around, which is explained by the first law. The second law describes how acceleration of charges can be calculated once the electric force is known. The third law explains how attractive and repulsive forces between charged objects are equal and opposite. Electric Force Examples and Types of Charge As previously mentioned, there are only two types of charges; positive and negative. Two like charges will repel (or move away from) each other, and two opposite charges will attract (or move towards) each other. In other words, two positive or two negative charges will repel, while a positive and a negative charge will attract. Opposite charges will attract while like charges will repel. Attraction versus Repelling Forces Notice how the forces acting upon each other are equal and opposite, as Newton's third law states. Both charges are exerting forces onto each other. Charges in Atoms An atom is made up of three types of particles; protons, neutrons, and electrons. Protons have a positive charge, neutrons have no charge, and electrons have a negative charge. There are no positive or negative charges smaller than protons and electrons. Objects on a larger scale result in an overall positive or negative charged due to an uneven distribution of protons to electrons. An atom consisting of more protons than electrons would be considered positive, and an atom with more electrons than protons would be considered negative. Protons are held close to the nucleus and are tightly bound to an atom, so it's difficult for protons to escape an atom. Electrons, on the other hand, are much further away from the nucleus of an atom. This makes it much easier for them to be removed from an atom. Electrons can leave or join atoms, making them positive or negative depending on the amount of protons. Similarly, for the bigger picture, overall materials and objects with more electrons than protons would be considered negative, and vice versa. Electric Force Examples Hair standing up: When hair is brushed, the hairbrush can strip electrons from hair strands, resulting in the hair being positively charged. This addition of electrons to the hairbrush in turn makes the hairbrush negatively charged. Since the hair is now positively charged, and like forces repel, hair strands will move away from each other, resulting in the hair standing up. Current electricity: All of our everyday technology is powered through current electricity, which is the consistent flow of electrons through conductive materials. This flow is caused by the electric force, as the electrons flow from a negative source to a positive source. Lightning: During a storm, it is common for an abundance of electrons to build up on the bottom of a cloud, making that part of the cloud negatively charged. Positive charges in the ground start to gather on the surface or even on tall objects such as trees as they are attracted towards the negatively charged undersides of clouds. Lightning strikes as a result of these charges becoming extremely built up. Lightning is caused by electric force Lightning Electric Force Equation: Coulomb's Law The magnitude of the electric force, or the amount of force in which objects repel or attract, depends on the distance between the two charged objects and the amount of charge each object carries. The electric force is stronger the closer together the two charges are, and weaker as the two charges move apart. Electric force is also stronger with more charge, and weaker with less charge. This effect on electric force is predictable, and is known as Coulomb's Law. It can be calculated using a mathematical equation, and the resulting magnitude of electric force is measured in Newtons. Coulomb's Law Electric force can be calculated using the following equation known as Coulomb's Law: In this equation, F is the electric force measured in newtons, K is a constant known as the electrostatic constant, and are charges one and two measured in coulombs, and is the radial distance in meters between the two charges. Since the distance is squared and on the denominator, the electric force drops off exponentially as charges move away from each other. This means that the Electric force is inversely proportional to distance. As charges move away from each other, the electric force between them gets smaller and smaller, until the force is negligible. The amount of charges are in the numerator of this equation, making the magnitude of the force larger with more charge. This means that the force is directly proportional to the amount of charge. When the charges are smaller, the amount of force will be smaller. When there is a lot of charge, the force will be much greater. When calculating the electric force using Coulomb's law, the resulting answer only gives the magnitude of the force and not the direction. In order to know the direction, you must know the types of charges. Once again, like forces repel, and unlike forces attract. It helps to draw a visual representation, or a free-body diagram, of the charges and forces acting upon them in order to understand the resulting force direction. Electric Field versus Electric Force An electric field is a direct result of an electric force. Its pure definition is electric force per unit charge, and can be thought of as a mapping of the force vectors. An electric field is present anytime there is an electric force. Therefore, when there are two or more charged particles, there is a surrounding electric field. The direction of the electric field is the direction a positive charge would flow if it were placed within the field. The electric field moves out from a positive charge and goes into a negative charge. Particles with unlike charges move towards each other, and their corresponding electric field lines move out from the positive charge and into the negative charge. The strength of the force at any given point can be seen through the spacing of the electric field lines. The electric force is strongest where the electric field lines are closest together, and weaker as these lines move apart. Like Coulomb's law expresses, electric field lines show how the electric force is strongest with a minimum distance between the two charges. Unlike charges will result in a repelling force, and the resulting electric field is a visual representation of this effect. Electric fields of two positive charges have the electric field moving out away from both of them. As with two negative charges, the field lines move in towards each negative. Lesson Summary An electric force is created when there are two or more charged particles or objects. These charges can be either positive or negative. Like charges will attract (move towards each other) while unlike charges will repel (move away from each other). As Newton's third law suggests, the forces acting upon each other are both equal and opposite. Electrons and protons within an atom are the two smallest types of charges there are. Electrons carry a negative charge while protons carry a positive charge. Electrons can be easily removed or added to atoms, making the overall charge positive or negative. Objects with more electrons than protons are negatively charged. Electric force is strengthened with increased charge and a shorter distance between the charges. This effect is known as Coulomb's law and can be calculated with the Coulomb's law equation. The magnitude of the force is measured in Newtons, and the direction can be determined by knowing whether the charges are attracting or repelling each other. An electric field is present wherever there is an electric force. The direction of this electric field is the direction a positive charge would flow if it where to be dropped in the field, which is from the positive to the negative.
Health 11/12 Review for Final Exam Core Concepts - Mental and Emotional Health, Substance Abuse Prevention, Safety and Violence Prevention, Family Life and Human Sexuality, Disease Prevention and Control, Healthy Eating Health Education Skills - goal setting, decision making, accessing information/resources, analyzing influences, communication, self-management, advocacy DIMENSIONS of Wellness - social, spiritual, emotional/mental, environmental, financial, intellectual, multicultural, occupational, physical, sexual RISK factors - anything that increases the risk of disease, injury, or illness. PROTECTIVE factors - anything that decreases the risk of disease, injury, or illness. INTERNAL health factors - health factors that can be either hereditary and genetic or acquired elements -- include smoking and personal diet or eating habits. Example – a genetic predisposition to an illness. EXTERNAL health factors - health factors that are part of the direct outer environment, the geographical location, micro-organisms, socio-economic elements that could affect an individual's health. Example – being unable to afford mental health services. Unit 1- Managing Personal and Community Wellness Explain Maslow’s Hierarchy of Needs in your own words using the image provided. Explain how each Social Determinant of Health may impact a person’s health. Levels of Disease Prevention • PRIMARY The goal is to avoid conditions altogether. • SECONDARY The goal is early detection. • TERTIARY The goal is to minimize the damage (manage). Define the following terms. Fads/Trends Sleep hygiene Driver safety Unit 2- Investigating Social Ecological Factors on Well-Being Socio-Ecological Model – The SEM examines how health behaviors form based on characteristics of individuals, communities, nations and levels in between. Each level overlaps with other levels signifying how the best public health strategies are those that encompass and target a wide range of perspectives. Interpersonal (personal) health vs. intrapersonal (relationship) health Health INEQUITY - systemic, ingrained and unjust barriers that prevent segments of the population from having the opportunity of health leading to health disparity. IMPLICIT BIAS - a form of bias that occurs automatically and unintentionally, that nevertheless affects judgments, decisions, and behaviors. Research has shown implicit bias can contribute to unequal access to quality healthcare, negative patient-provider relationships and interactions; and create mistrust in the healthcare system and practitioners among patients. This can contribute to health disparities. Health DISPARITY - represents a difference in health between populations. It is often used to describe disease burden and other negative health outcomes socially disadvantaged groups may face. Health EQUITY - The opposite of health inequity. It describes a system that supports a high standard of health and healthcare for all people. Racism - Beliefs, attitudes, institutional arrangements, and acts that tend to denigrate individuals or groups because of phenotypic characteristics or ethnic group affiliation. DISCRIMINATION - An unjust differential treatment of a person or a group. PRIVILEGE- The unearned access to resources and social power that are only available to some because of their membership within certain social groups. OPPRESSION is the act of taking away choices from others and can be defined as a system that maintains advantage and disadvantage based on social identities and that acts on multiple levels from interpersonal to institutional and societal. (internalized, interpersonal, institutional, structural) Systematic Oppression - Intentional disadvantage of groups of people based on their identity while advantaging members of dominant group (race, gender, sexual orientation, language, size, ability, etc.). Intersectionality - The complex, cumulative way in which the effects of multiple forms of discrimination (such as racism, sexism, and classism) combine, overlap, or intersect especially in the experiences of marginalized individuals or groups Unit 3- Accessing Resources and Communicating to Support Mental and Emotional Health What is anger? What is anxiety? What is stress? STRESSORS are the things that cause stress. Stressors can be internal and external. A stressor may be a one-time or short-term occurrence, or it can happen repeatedly over a long time. INTERNAL Stressors - are made by your belief system and the way you evaluate yourself. Examples include pessimistic attitude, negative self-talk, deep need to be perfect, low self-esteem or body image, unhealthy standards for self. EXTERNAL Stressors - are stressful things that happen in your surroundings and/or in your environment. Examples include busy schedules, work problems, family issues, financial trouble, social problems, injury, unforeseen circumstances. Socio-economic issues are also a part of external stressors such as poverty, violence, and racism. Define the following mental health conditions. Depression Eating disorders NSSI Non-suicidal self-injury Grief/Loss Suicide prevention A.C.T. • ACKNOWLEDGE- Tell them in a caring way that you recognize that they are having a problem • CARE- You can show you care by actively listening - put away anything else you are doing, make eye contact, sit down, ask questions. • TELL-(call 988 for additional help and support) - Tell them it is important that they speak with a trusted adult. Help them figure out who this may be and offer to go with your friend. A social norm is an unwritten, informal rule meant to guide behavior among the of society. It distinguishes between acceptable and unacceptable, good and bad, and so on. Social norms can influence a person with emotional or mental health disorders, access to care and stigmatize their situation. STIGMA- a mark of disgrace associated with a particular circumstance, quality, or person. • Self-stigma - This describes the internalized stigma that people with mental health conditions feel about themselves. • Public stigma - This refers to the negative attitudes around mental health from people in society. • Institutional stigma - This is a type of systemic stigma that arises from corporations, governments, and other institutions. Unit 4- Evaluating Risks of Substance Use and Abuse Harm Reduction - a set of practical strategies and ideas aimed at reducing negative consequences associated with drug use. Explain how each level of the Social Ecological Model is impacted by addiction. Individual Relationship Community Society SEM Level Contributing/Risk Factors to substance use Preventative/Protective Factors for substance use Individual Interpersonal/Relationship Community Society Unit 5- Analyzing Influences to Examine Ways to Increase Safety and Reduce Violence HATE CRIME - a crime, usually violent, motivated by prejudice or intolerance toward an individual’s national origin, ethnicity, color, religion, gender, gender identity, sexual orientation, or disability. Explain how the media influences violence in society. The Pyramid of Hate Explain the escalation of hate using the Pyramid of Hate visual. List several hate crime motivators. Example: age HEALTHY Relationship Signs - comfortable pace, trust, honesty, independence, respect, equality, kindness, taking responsibility, healthy conflict, fun UNHEALTHY Relationship Signs - intensity, possessiveness, manipulation, isolation, sabotage, belittling, guilting, volatility, deflecting responsibility, betrayal Sexual Assault is a sexual behavior WITHOUT consent. Human trafficking - the recruitment, harboring, transportation, provision, or obtaining of a person for labor or services, using force, fraud, or coercion for the purpose of subjection to involuntary servitude, peonage, debt bondage, or slavery. Sex trafficking - commercial sex act induced by force, fraud, or coercion, or in which the person induced to perform such an act has not attained 18 years of age. Trafficking happens using… • Force - using violence to control someone. • Fraud - using lies to control someone. • Coercion - using threats to control someone. Unit 6- Family Life and Human Sexuality Agency - A belief about yourself and the extent to which you can act on that belief. • The ability to choose freely one’s own narrative. • To embrace the idea that I am the cause (or agent) of my own thoughts and actions. • Personal agency is a personal responsibility for who we are, what we experience, what we do about that experience, and how we shape our world to give us more of the experiences we want. SEXUAL Agency • The ability to choose your own interests and desires vs. what we see in the media or others’ perceptions • The ability to identify, communicate, and negotiate one’s sexual needs • The ability to initiate behaviors that allow for the satisfaction of those needs Sexually Explicit Material - photographs, videos, films, magazines, and books whose primary themes, topics, or depictions involve sexuality that may cause sexual arousal. Sexual scripts - thoughts, patterns, or behavior that a person has about themselves in a romantic or sexual context. It is how people picture themselves or want to project themselves in front of others. Reproductive Rights of Teens - In Maryland, teens have the right to an abortion, keep their child, obtain and use birth control, paternity tests, adoption, give up custody of their child within 10 days of birth (Safe Haven Law). • REPRODUCTIVE RIGHTS- legal rights and the freedom of the individual to control decisions regarding contraception, abortion, sterilization and childbirth. • SAFE HAVEN LAW- a distressed parent who is unable or unwilling to care for their infant can safely give up custody of their baby, no questions asked. CONSENT is an agreement between participants to engage in sexual activity. • It is clearly and freely communicated, verbal, and affirmative. Consent CANNOT be given if… • A person is underage, one or both partners is intoxicated or incapacitated by drugs or alcohol, one partner is asleep or unconscious, one partner feels pressured, threatened or intimidated, or one partner holds a position of power or authority over the other. Unit 7- Advocating for Enhanced Nutrition, Food Systems, and Health Outcomes Dietary Guidelines for Americans Guideline 1: Follow a Healthy Dietary Pattern at Every Life Stage Guideline 2: Customize and Enjoy Food and Beverage Choices to Reflect Personal Preferences, Cultural Traditions, and Budgetary Considerations Guideline 3: Focus on Meeting Food Group Needs with Nutrient-Dense Foods and Beverages, and Stay Within Calorie Limits Guideline 4: Limit Foods and Beverages Higher in Added Sugars, Saturated Fat, and Sodium, and Limit Alcoholic Beverages FOOD DESERT- a neighborhood where there is little or limited access to healthy and affordable food such as fruits, vegetables, whole grains, low-fat milk and other foods that make up the full range of a healthy diet. FOOD INSEQURITY lack of access to a sufficient amount of food because of limited funds. More than 49 million American households are considered food insecure and are vulnerable to poor health as a result. PROCCESED FOODS- any raw agricultural commodities that have been washed, cleaned, milled, cut, chopped, heated, pasteurized, blanched, cooked, canned, frozen, dried, dehydrated, mixed or packaged — anything done to them that alters their natural state.