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COLUMBIA SCIENCE REVIEW Volume 16 Issue II Spring 2020


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Cover illustrated by Lizka Vaintrob

Fair Use Notice Columbia Science Review is a student publication. The opinions represented are those of the writers. Columbia University is not responsible for the accuracy and contents of Columbia Science Review and is not liable for any claims based on the contents or views expressed herein. All editorial decisions regarding grammar, content, and layout are made by the Editorial Board. All queries and complaints should be directed to the Editor-In-Chief. This publication contains or may contain copyrighted material, the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of scientific significance. We believe this constitutes a “fair use” of any such copyrighted material, as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, this publication is distributed without profit for research and educational purposes. If you wish to use copyrighted material from this publication for purposes of your own that go beyond “fair use,” you must obtain permission from the copyright owner.


COLUMBIA SCIENCE REVIEW


EDITORIAL BOARD EDITOR-IN-CHIEF ALICE SARDARIAN CHIEF DESIGN OFFICER (CDO) AIDA RAZAVILAR INTERIM CDO JOANNE WANG EDITORS SERENA CHENG, ANNA CHRISTOU, BENJIE GREENFIELD, ENOCH JIANG, YOUNG JOON KIM, LINGHAO KONG, CHERYL PAN, RACHEL POWELL, EMILY SUN, ETHAN WU, VICTORIA YANG LAYOUT EDITORS MANSI GARNENI, SALLY HWANG

MANAGING EDITOR SARAH HO CHIEF ILLUSTRATOR EMILY WANG WRITERS LIZA CASELLA, BOYUAN CHEN, VICTORIA COMUNALE, JENNA EVERARD, ELIFSU GENCER, JACOB KANG, SIRENA KHANNA, OLADAPO LAPITE, ALLISON LIN, CLARE NIMURA, ELAINE ZHU ILLUSTRATORS AUDREY OH, CHERIE LIU, AEJA ROSETTE, SABRINA RUSTGI, STEFANI SHOREIBAH, REBECCA SIEGAL, EMILY WANG, LIZKA VAINTROB

EXECUTIVE BOARD PRESIDENT ABHISHEK SHAH PUBLIC RELATIONS JACQUELINE ERLER SECRETARY ARUSHI SAHAI MEDIA TEAM CHENOA BUNTSANDERSON, BRENDON CHOY, ERIC PARSONS, CATHERINE SERIANNI, MAGGIE ZHONG, NICHOLAS ZUMBA

VICE PRESIDENT JASON WANG TREASURER ADRIANA KULUSIC-HO SENIOR OCM ALLI GREENBERG MANASI SHARMA, KAT WU OCM'S AROOBA AHMED, CHINMAYI BALUSU, BOYUAN CHEN, ESME LI, HANNAH LIN, JOHN NGUYEN, ALANA PALOMINO, NICK VAUGHAN, JOJO WU

The Executive Board represents the Columbia Science Review as an ABC-recognized Category B student organization at Columbia University


SPRING 2020


LETTERS FROM THE EDITORS

COCKTAIL SCIENCE ARTICLES DON'T LET (HIGH) CHOLESTROL GET YOU DOWN CURING CANCER WITH ART

PANDEMIC ON EASY MODE WHAT MARSHMALLOWS CAN TELL US ABOUT SOCIOECONOMIC INEQUALITY

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table of contents


LETTERS FROM Dear Reader: As part of our commitment to STEM and scientific inquiry, we bring you this issue of the Columbia Science Review. With every publication, we aim to promote scientific engagement and literacy; therefore, we hope that some or all of the upcoming pages pique your interest. At the Columbia Science Review, we often ask, what does science mean to us? I extend that question to you as well. Is science an exploratory tool? Is it a catalyst for discovery and innovation? To our Editorial staff, science explains the implications of climate change on disease transmission and severity. Science provides the means with which to reevaluate psychological experiments. It is also interdisciplinary, fusing art with cancer cells. As we continue to grapple with the global impact of COVID-19, science becomes a guiding light, informing new policies, promoting health, and fueling optimism for relief and remedy in a coronavirus-free future. There’s no better time than now to lean on scientists and health professionals to provide a way forward amidst so much uncertainty. I hope you enjoy this issue. I am incredibly proud of the hard work and commitment demonstrated by our staff, who forged ahead despite the challenges presented by a disrupted academic semester and the multitude of limitations inherent to online communication. I wish you and yours health and a peace of mind. Stay safe wherever you may be! Sincerely,

Alice Sardarian Editor-in-Chief

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Dear Reader, Welcome to the Columbia Science Review’s Spring 2020 print issue! I am tremendously proud of all the work that our wonderful writers, editors, illustrators, and layout designers have invested into this issue. Due to the ongoing COVID-19 pandemic, our Editorial Board had to finalize this print issue remotely, across different geographic locations and time zones. I am so grateful that, even amidst the considerable challenges that the past few months have posed, members of the Editorial Board were willing to devote time, energy, and thought to this issue. This issue is filled with interesting and multifaceted articles, covering topics that range from psychology’s replication crisis to the implications that climate change has for emerging diseases. Given that much of this issue’s content was written before the pandemic reached the United States, we have instead decided to devote a Summer 2020 print issue entirely to exploring the epidemiology, public health implications, and science behind COVID-19. More than ever before, it is imperative that we base our votes, policy decisions, and actions on evidence that is vigorously supported by science. Other than once again thanking everyone on the Editorial Board for their passion and hard work, I would like to give a special thanks to our recently graduated seniors, Liza Casella, Benjie Greenfield, Sirena Khanna, Young Joon Kim, and Victoria Yang for the contributions that they have made to the Columbia Science Review. Warmly,

Sarah Ho Managing Editor

THE EDITORS 9


A CALL TO PROTECT A CRITICAL SENSE

Written by Alice Sardarian Illustrated by Lizka Vaintrob

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e are continuously exposed to elevated noise levels, which have the potential to bring about irreversible hearing loss and other ailments like tinnitus, which causes ringing in the ears, or hyperacusis, which causes intolerance to ordinary sounds due to elevated loudness perception [1]. The World Health Organization estimates that more than 1 billion people between the ages of 12 and 35 will suffer from hearing loss, however, 50% of global hearing loss cases can be prevented through protective measures and increased access to screening [2]. By disregarding auditory health, we are inadvertently accelerating the aging process.

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Sound level, measured in decibels (dB), and length of exposure to sound are both contributing factors to hearing loss. The CDC states that prolonged exposure to sound over 70dB can be harmful; a normal conversation has a sound level of around 60dB [3]. Unfortunately, these sound levels are prevalent in our environment, and include city traffic, vacuum cleaners, firecrackers, concerts, and other, seemingly innocuous, sources. A study conducted in the NYC transit system found that over 5.5 million riders each day are exposed to average noise levels of 86dB, with some subway platforms reaching a maximum of 112dB [4,

5]. There has also been an increased, widespread use of headphones, especially amongst younger listeners, at loud volumes of up to 110dB [6]. Headphones with insufficient noisecanceling properties may also prompt listeners to increase the sound volume in response to louder environments. Hearing loss may occur in under five minutes when headphones are on maximum volume [3]. The most challenging aspect of combating hearing loss is that the auditory perpetrators often go unnoticed. We do not experience pain or discomfort until confronted with volumes at or above 120dB [3]. To preserve your hearing, consider adhering to the following recommendations from the National Health Service: limit exposure to loud noises such as firearms or musical events by using earplugs or noise-canceling headphones, limit headphone volume to 60% and a one hour listening time, and get your hearing screened annually [7]. With these measures, it may be possible to prevent aging our ears, which degrade 50 percent faster as a result of harmful exposure [8]. It is critical to educate the general population to avoid the growing public health crisis that is hearing loss.

cocktail


EXPLORING OUR OCEANS WITH AI

Written by Rachel Powell Illustrated by Sabrina Rustgi In 2018, Google engineers created a model for detecting humpback whale sounds [1]. Today, this algorithm is also used to recognize orca sounds in Canada’s Salish Sea [2]. Using this machine learning model, Canadian authorities can locate orcas in real time and monitor their behavior and health.

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lthough oceans cover 71 percent of the Earth’s surface, most available data about oceanic conditions is outdated and inaccurate. Researchers have begun using artificial intelligence (AI) and machine learning applications to study the largest bodies of water in the world and monitor populations of endangered marine species. Existing information about water conditions and marine species is not very specific or accurate, and it is rapidly becoming obsolete as climate change impacts temperatures, sea levels, and migration patterns [1]. Monitoring endangered species has

science

become even more crucial, but in order to do so, researchers must first be able to determine species’ population sizes and locations. AI is currently utilized for oceanic research and in efforts to protect endangered whales. Today, there are only about 70 Southern Resident Orcas and 400 North Atlantic right whales [1]. AI allows researchers to monitor these whales more accurately by collecting data from satellites, sonar, radar, and other sources. With AI, this data can be used to train models that approximate the locations of Southern Resident Orcas, North Atlantic right whales, and other endangered whale populations.

The more information that can be gathered about endangered whale populations, the more effectively researchers and government authorities can protect them from extinction; this data can influence government decisions about shipping lanes and fishing regulations, as well as raise awareness about the presence of injured and sick whales in a particular area [1]. AI and machine learning applications also measure water quality, locate shipping vessels, and detect harmful sound pressure levels underwater [3]. With more accurate and detailed information about oceanic conditions, sea vessels can take paths that interfere less with marine life, researchers can closely monitor water pollution and acoustics, and endangered species can be better protected in the face of climate change and other threats [3]. While AI expands researchers’ knowledge about the oceans, it is truly transforming the ways in which humans interact with marine life.

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ONES AND ZEROES Written by Linghao Kong

A quick introduction to transistors and their predecessor

Illustrated by Cherie Liu

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omputer processors have been integrated into almost all facets of modern life, from simply calling someone to advanced modeling simulations. Because these computer chips, present in laptops, mobile phones, and servers, simply work, many take for granted the intricate techniques that go into developing and improving their performance every year. One of the central components of the computer processor is the transistor, a miniscule piece of technology with numerous applications. The predecessor of the transistor is the vacuum tube, a glass container with internal electrodes in vacuum pressure. By heating one of the electrodes and applying a voltage to the other, a directional current can be generated, and a third electrode can be used to modulate the flow of this current. Essentially, the third electrode can turn the current in a vacuum tube on or off, creating the ones and zeros of the computational world. While vacuum tubes were revolutionary and still have niche applications today, they are large, require a lot of power, and wear out over time [1]. As such, transistors, which address all of these issues, have replaced vacuum tubes since their invention in 1947. A transistor essentially performs the same functions as the vacuum tube - amplifying incoming currents and acting as switches to be turned on or

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off. Transistors are based on altering the properties of the semiconductor silicon, rather than on heat. Silicon, treated in different ways, can act as either an electron acceptor or electron donor. When these two types of silicon are configured in a certain way, a small voltage can be applied to the transistor system to allow the flow of a current. Conversely, if no additional voltage is present, the current will be blocked due to the properties of the electron acceptor and donor silicon blocks. Thus, like vacuum tubes, currents can be turned on or off and therefore can store information in binary [2].

Because transistors can be made on the scale of nanometers, billions of transistors can be included on a single computer chip [3, 4]. Such density and other advances in transistors have allowed for even smartphones to be more powerful than roomsized vacuum tube-based computers of years past. However, as transistors decrease in size, the quantum properties of electrons themselves become constraining, decreasing further improvements. Despite this, the future still looks promising, as transistors based on other materials may help overcome such limitations [5].


THE BENEFICIAL SIDE OF VIRUSES Written by Anna Christou Illustrated by Emily Wang

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uring this pandemic, when we are constantly surrounded by information about how deadly and destructive a virus can be, it is easy to neglect the crucial role that viruses play in our bodies, ecosystems, and medicine. In reality, viruses have a variety of therapeutic functions— including potentially in vaccines against the novel coronavirus, SARSCoV-2. Viruses are composed of a nucleic acid, often a protein coat, and sometimes a lipid membrane. The replication of viruses depends on a host cell: after viruses attach to and enter the host cell, their genome is released and replicated, and proteins are made to assemble and release new viral particles. The virus takes over the cell both by changing gene expression so that host genes are not expressed and by altering the metabolism of the host cell [1].

used to destroy tumors; viruses that selectively replicate in tumor cells are especially useful for this therapy [1]. In addition, gene therapy can be used to treat diseases caused by a single mutated gene through the delivery of a normal copy of the gene through a viral vector. Pertinently, gene therapy can also be employed as a vaccine: a component of the virus in question, such as a glycoprotein on the membrane, can be delivered via a benign viral vector to stimulate an immune response. To successfully use this technique, genes in the viral vector that cause virulence are removed, and the target gene— from the virus being vaccinated against—is inserted. The many viruses that can be used as vectors each have advantages and disadvantages. For

example, the adenovirus vector has a fast onset of gene expression, efficient infection, and low risk of mutagenesis. However, as there are many serotypes that infect humans, many humans have immunity, which decreases the uptake of the vector. Moreover, if the target gene is inserted into the wrong location of the genome, it can turn on incorrect genes, cause harmful mutations, or lead to overexpression of the target protein [3]. Despite these problems, therapeutic viruses hold much promise and are being tested for the ability to deliver the spike glycoprotein of SARSCoV-2 in a vaccine [1]. Although viruses can be very deadly, as we have seen with COVID-19, understanding their beneficial side is crucial for broadening our view of science.

Although this can cause disease, many viruses are beneficial and are important components of ecosystems [2]. In addition, the capacity of viruses to hijack the host cell and introduce their genetic material can be harnessed for therapeutic purposes, such as phage therapy, gene therapy, delivering antigens for vaccines, and oncotherapy [1,3]. Phage therapy uses lytic bacteriophages to kill a bacterial host and is used to treat bacterial infections. Also, because viruses can take over and destroy the host cell, viral oncotherapy can be 13


ONES AND ZEROES [1] Alba, M. (2018, January 18). Vacuum Tubes: The World Before Transistors. Retrieved from https://new.engineering.com/story/vacuumtubes-the-world-before-transistors. [2] Woodford, C. (2019, June 29). Transistors. Retrieved from https://www.explainthatstuff. com/howtransistorswork.html. [3] Chandler, N. (2001, January 1). How Transistors Work. Retrieved from https://electronics. howstuffworks.com/transistor4.htm. [4] Zyga, L. (2008, February 4). Intel Microchip Packs Two Billion Transistors. Retrieved from https://phys.org/news/2008-02-intel-microchipbillion-transistors.html. [5] Thompson, A. (2016, October 12). Scientists Have Made Transistors Smaller Than We Thought Possible. Retrieved from https://www. popularmechanics.com/technology/a23353/1nmtransistor-gate/. EXPLORING OUR OCEANS WITH AI [1] Schlossberg, T. (2020). A.I. Is Helping Scientists Understand an Ocean’s Worth of Data. Retrieved from https://www.nytimes. com/2020/04/08/science/ai-ocean-whales-study. html [2] Cattiau, J. (2020). AI’s killer (whale) app. Retrieved from https://www.blog.google/technology/ai/protecting-orcas/ [3] Ponce de Leon, S. (2020). Can AI Save Our Oceans? Let's Start With The Data. Retrieved

A CALL TO PROTECT A CRITICAL SENSE [1] Baguley, D. (2003). Hyperacusis. JRSM, 96(12), 582-585. https://doi.org/10.1258/jrsm.96.12.582. [2] Deafness and hearing loss. (n.d.). Retrieved from https://www.who.int/health-topics/hearingloss#tab=tab_1. [3] What Noises Cause Hearing Loss? (2019). Retrieved from https://www.cdc.gov/nceh/hearing_loss/ what_noises_cause_hearing_loss.html. [4] Gershon, R., Neitzel, R., Barrera, M., & Akram, M. (2006). Pilot Survey of Subway and Bus Stop Noise Levels. Journal Of Urban Health, 83(5), 802812. https://doi.org/10.1007/s11524-006-9080-3. [5] Subway and bus ridership for 2019. (2019). Retrieved from https://new.mta.info/agency/new-yorkcity-transit/subway-bus-ridership-2019. [6] Cohen, J. (May 21, 2020). How to Protect Kids’ Ears From Constant Headphone Use. Retrieved from https://www.nytimes.com/2020/05/21/parenting/ children-headphones-hearing-loss.html. [7] 5 ways to prevent hearing loss. (2018). Retrieved from https://www.nhs.uk/live-well/healthy-body/ top-10-tips-to-help-protect-your-hearing/. [8] How to Rock Out With Ear Buds or Headphones Without Damaging Your Hearing. (2018). Retrieved from https://health.clevelandclinic.org/ how-to-rock-out-with-ear-buds-or-headphoneswithout-damaging-your-hearing/.

THE BENEFICIAL SIDE OF VIRUSES [1] Flint, S. J., Racaniello, V. R., Rall, G. F., & Skalka, A. M. (2015). Principles of Virology. John Wiley & Sons. [2] Viruses: You’ve heard the bad; here’s the good. (April 30, 2015). Retrieved from https://www.sciencedaily.com/releases/2015/04/150430170750. htm. [3] Gene Therapy Viral Vectors Explained. (n.d.). Retrieved from http://www.genetherapynet.com/ viral-vectors.html.

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cocktail science REFERENCES


Don’t Let (High) Cholesterol Get You Down Written by Allison Lin Illustrated by Sabrina Rustigi

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igh cholesterol is a global concern that has troubled us for generations. In 2008, 39% of adults had elevated levels of cholesterol [1]. According to the World Health Organization, as of 2008, this statistic has not seen a significant decrease since 1980 [1]. Although the percentage of individuals with high cholesterol has not yet noticeably decreased worldwide, there is a silver lining. Heightened awareness and increased research means not only a better understanding of the underlying mechanisms of cholesterol, but also the development of better treatment options for high cholesterol. Moreover, the origins of high cholesterol provide interesting insight into Mother Nature’s logic. Cholesterol is a component of the human body that maintains cell membranes and helps produce key hormones such as estrogen and testosterone [2]. Structures called lipoproteins, which are part-lipid, part-protein molecules, help transport this cholesterol to different places in the body [2]. In order to understand the epidemiology behind high cholesterol, we should begin by distinguishing the two common types of cholesterol-transport devices. You’ve probably heard of the “good” and “bad” types of cholesterol, but contemporary science gives us a more detailed distinction: low-density lipoprotein (LDL), also known as the “bad” type, and high density lipoprotein (HDL), also known as the “good” type. While HDL is about 20% lipid and 50% protein, LDL is approximately 50% lipid and 20% protein. The “high-density” and “low-density” are aptly named, given that protein is denser than fat. HDL moves excess cholesterol away from one’s major arteries and transports it to the liver, where it can easily be expelled from the 15


body [3]. LDL, on the other hand, can deliver cholesterol throughout arteries, possibly causing it to collect in blood vessel walls [3]. Ultimately, the two molecules differ in structure, which results in a difference in function. High levels of LDL, as previously discussed, cause cholesterol to build up in the arteries, making them less flexible for blood flow and ultimately resulting in atherosclerosis [2]. Blood flows more viscously through blood vessels and in turn, increases the strain on the heart to maintain circulation. If this plaque build-up happens in coronary arteries, which lead to the heart, it can cause angina, or chest pain. This is your body’s warning sign that if things do not change soon, a heart attack could be next, caused by the plaque breaking off and completely blocking blood flow to the heart [3]. The same can happen to the brain. Plaque that chips off and obstructs critical carotid arteries, the main arteries that carry blood to the brain, leads to neural degeneration and stroke [3]. Besides the grave repercussions of high cholesterol on the heart and the brain, plaque build-up in general means less blood circulation throughout the body, which can lead to peripheral arterial disease (PAD), in which one’s arteries are damaged beyond repair. It can also lead to Type 2 diabetes and hypertension, or high blood pressure [4]. In addition, high levels of cholesterol can cause the formation of hard, painful

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stones inside your gallbladder called known to be responsible for skin gallstones, along with numbness in aging due to its longer wavelength the legs due to hardened arteries [2]. and lower energy, UVB radiation is known for its contribution to burnDespite these dangers of high cho- ing skin because of its shorter and lesterol, this organic molecule plays more penetrative wavelength. Dura critical role in many homeostatic ing the winter, when our skin is exprocesses in the body. For example, posed to very little UVB sunlight, with the right amount of light expo- we can usually rely on our vitamin D sure, cholesterol has the fascinating reserves that have accumulated from ability to become vitamin D, which the summer months [7]. is essential for maintaining strong bones and absorbing minerals such Long ago, high as calcium from the foods we eat cholesterol levels, [6]. In turn, low levels of cholesterol could translate to insufficient levserving as a reserve els of vitamin D. Without vitamin for vitamin D, could D, muscles would cease to contract and expand, and nerves would lose have evolved with a the ability to transfer messages bebeneficiary intent tween the brain and other parts of the body [6]. Further, a lack of vita— to heal, not to min D can cause bone diseases, such harm. as osteoporosis (porous bone) and rickets (weakening bone structures in children). More specifically, the skin cells that absorb UVB radiation are called How well does the conversion from melanocytes. Skin color is depencholesterol to vitamin D happen? dent on the amount and type of That all depends on the skin, the melanin, a special pigment created largest organ in the body [5]. While and used by our bodies. Created by perhaps an unlikely candidate, skin melanocytes, two forms of melanin is crucial to the conversion of cho- are known to exist: red/yellow phelesterol to Vitamin D. The cells that omelanin and black/brown eumelamake up our skin absorb ultraviolet nin [8]. While every person has the B sunlight (UVB) that our bod- same number of melanocytes, differies need to convert cholesterol into ent skin colors come from how acvitamin D [6]. Ultraviolet radia- tive those melanocytes are and what tion from the sun reaches the Earth type of melanin they make [8]. As through two main forms—ultra- soon as your eyes sense sunlight, the violet A (UVA) and ultraviolet B optic nerve (a bundle of fibers con(UVB) radiation. While UVA is necting your eyes to your brain) sig-


nals to the pituitary gland to activate the dormant melanocytes [8]. So, the less sunlight your eyes sense, the less melanocyte-awakening hormone is produced, and the less melanin is produced. Ultimately, the amount of melanin that a melanocyte produces is tied to how well cholesterol is converted into vitamin D: the less melanin produced, the less UVB radiation is absorbed and the less cholesterol is converted into vitamin D [10]. Melanin is not only involved with cholesterol conversion, but also serves as protection against sunburn [8]. Therefore, darker skin’s adaptive advantages made it a trait to be selected for by evolution [9]. Once evolution found out that lighter-skinned individuals were more prone to sunburn and other diseases, it selected for darkerskinned individuals, those protected against the harmful rays of the sun [9]. They would procreate and produce offspring that were, evolutionarily speaking, better adapted for the species. With their protective skin, early human ancestors thrived in the warm temperatures and climate of northern Africa, soaking in sunlight to efficiently convert cholesterol into vitamin D and establishing a healthy lifestyle due to agriculture and hunting [9].

These migration patterns are evident through fossilized remains of human bones and artifacts, which were found in mud layers that could be linked to certain time periods [9]. Civilizations formed as individuals settled in their new homes and northward migrants began to see physical changes, such as lighter skin due to less sun exposure. Indeed, when early human ancestors migrated northward from Africa, they were met with cooler climates and less sun exposure, and thus, less access to vitamin D. These humans still retained the high cholesterol levels that had been entirely converted to vitamin D with the help of Africa’s robust sunlight. However, with limited sun exposure and lighter skin (and thus, less melanin with which to absorb UVB), less of that once-helpful cholesterol was immediately converted into vitamin D. This left the remaining cholesterol to be maintained in the body. In the end, high cholesterol—the disorder as we now know it—was born [10].

Today, high cholesterol has a negative reputation, but many years ago, it was the unseen and unaccredited helper in the fight against serious bone diseases [10]. The people who had high levels of cholesterol were much less likely to develop a vaFrom Africa, the human species riety of illnesses, thus improving gradually pursued intercontinental their chances of surviving to repromigration, up the Middle East to duce and pass their genes onto the parts of Asia, while other branch- next generation [10]. This is prees of the species went to Europe. cisely natural selection at work: the

traits that help individuals survive increase the fitness (reproductive quality) inherited by the next generation. Long ago, high cholesterol levels, serving as a reserve for vitamin D, could have evolved with a beneficiary intent —to heal, not to harm. Devastation in the present, but salvation in the past. What can you say? Evolution’s not perfect. //REFERENCES// [1] Raised Cholesterol. (2010). WHO. Retrieved from https://www.who.int/gho/ncd/ risk_factors/cholesterol_text/en/ [2] Watson, S. (August 29, 2018). The Effects of High Cholesterol On The Body. Retrieved from https://www.healthline.com/health/cholesterol/effects-on-body#2 [3] Kamps, A. (December 9, 2018). How do LDL and HDL Differ Structurally and Functionally? Retrieved from https://healthyeating. sfgate.com/ldl-hdl-differ-structurally-functionally-2003.html [4] Diseases Caused by High Cholesterol. (December, 12, 2016). Retrieved from https:// my.clevelandclinic.org/health/articles/11918cholesterol-high-cholesterol-diseases [5] Leen, S. ( January 17, 2017). Skin Information and Facts. Retrieved from https://www. nationalgeographic.com/science/health-andhuman-body/human-body/skin/ [6] Vitamin D- Consumer. (March 24, 2020). Retrieved from https://ods.od.nih.gov/factsheets/VitaminD-Consumer/ [7] Chien, A. ( June 2019). UV Radiation. Retrieved from https://www.skincancer.org/riskfactors/uv-radiation/ [8] NCI Dictionary of Cancer Terms. National Cancer Institute. Retrieved from https://www. cancer.gov/publications/dictionaries/cancerterms/def/melanoma [9] Lewis, D. (December, 2017). Where Did We Come From. Cosmos. Retrieved from https://cosmosmagazine.com/palaeontology/ where-did-we-come-from-a-primer-on-earlyhuman-evolution [10] Moalem, S., (2007). Survival of the Sickest: The Surprising Connections Between Disease and Longevity. NY: William Morrow and Company.

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Curing Curing Cancer Cancer wi wi Written by Clare Nimura Illustrated by Emily Wang

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f you hear the word “science,” what comes to mind? Maybe laboratory experiments, data, NASA, Einstein. What about “art”? Self-expression, color, sculpture, Van Gogh. Starting in elementary school, art and science are treated as distinct fields—one creative, the other empirical. However, those involved in either discipline know that this distinction is arbitrary. For instance, there is chemistry involved in oil painting and in developing film, and engineering the newest iPhone model requires immense creativity. Not only does each field require the other, but the work of a scientist or an artist is enhanced by knowledge of the other discipline. No one understands the importance of this symbiotic relationship between science and art better than the researchers at the Danino Lab at Columbia University. Professor Tal Danino is the Principal Investigator of a synthetic biology lab in the Department of Biomedical Engineering. The lab primarily focuses on engineering bacteria to act as vessels for localized delivery of cancer therapeutics. Bacteria have a unique ability to sense their environment and will only proliferate under specific conditions of temperature, acidity, oxygen level, and other factors. In the human body, this means that certain bacteria will colonize only the necrotic core of tumors where the environment is low in oxygen and deprived of nutrients from the bloodstream. This charac18

Left: Art made with cancer cells and dye (using the technique described in paragraph 5) Right: Close-ups of individual cancer cells that make up the image. Images created with cancer cells and dye. Reprinted from [3].

teristic of bacteria makes them an efficient mechanism for drug delivery because they will affect the tumors but leave the healthy cells of the body untouched, eliminating the adverse systemic effects of some other cancer treatment methods. Chemotherapy, for example, is a type of drug that targets all rapidly-dividing cells in the body. This helps to slow the growth of malignant cancer cells, but also affects healthy cells that naturally divide rapidly, such as the cells of hair follicles and the lining of the stomach, which can lead to side effects like hair loss and nausea. The Danino Lab seeks to minimize these deeply unpleasant side effects by

developing a cancer treatment that knocks out the cancer cells, but leaves the healthy cells untouched [2]. Unlike most cancer research labs, however, the Danino Lab has one bench that is covered not just with petri dishes and bottles of reagents, but also with colorful dyes, large canvases, and a scanner. This portion of the lab is entirely dedicated to art. Soonhee Moon, the Visual Researcher, uses these materials to make beautiful images from the same bacteria and cancer cells that are used to model and test the lab’s novel cancer treatment. The lab bench is piled with petri


dishes of bacterial colonies stained to look like explosions of watercolor and intricate plates of cancer cells arranged into mandalas, floral patterns, and even portraits. During his time as a graduate student, Danino learned that his discoveries working with bacteria in the lab were much more convincing when they were presented in a manner that was pleasing to the eye. The fantastical combina-

ith ith Art Art tion of art and science that is created in his lab today first began at MIT, where Danino, then a postdoctoral researcher, and artist Vik Muniz began a collaborative project that merged their specialties [1]. Muniz was enchanted by the idea of making art from tiny living things. Their first project was a print series, but rather than using ink, their medium of choice was cancer cells. The art itself was alive. To make one of these prints, a rubber stamp of the image is cast and used to make a sticky image on a petri dish that the cancer cells can adhere to. Finally, the bacterial or cancer cells can be applied to the dish; they bind to the sticky material and arrange themselves to create the desired image. The cells can be imaged with a microscope and color can be added. Danino and Muniz created many different patterns with this technique: traffic jams, crowds of people, circuit boards, even a portrait of Henrietta Lacks, whose own cancer cells gave rise to the first immortalized cell line, which is a vital tool in modern research [1].

usually abstract, mysterious, and daunting. Another medium for artwork in the Danino Lab is the same bacteria that the lab has engineered to fight cancer. Different types of bacteria form different characteristic patterns as they grow; while some form a “bullseye” with concentric circles emanating outwards, others form more feathery shapes or resemble the leaves of plants.With the addition of dye, these patterns become a whimsical array of shapes and colors [3]. Presenting bacteria and cancer cells as art not only demystifies these microscopic invaders, but also creates a tool for outreach and for spreading scientific literacy about how cancer and cancer treatments work.

planations of the science behind the art [3]. The Danino Lab has created living proof that art and science are not only related but intertwined. What began as a creative graduate school collaboration has grown into a worldwide movement promoting accessible means of scientific literacy and outreach. Looking at cancer cells and bacterial cancer treatments through the lens of art is a reminder of the power of nature both to destroy and to create. Taking a more holistic approach to scientific research can reveal other, less obvious forms of healing. Erasing the artificial line between art and science benefits both endeavors.

Danino’s artwork and the artwork from his lab have been exhibited from New York, to Tokyo, to Tel Aviv, and many other locations throughout the world. The art has expanded beyond images of cell prints on petri dishes. These designs have been incorporated into clothing, black and white prints, illuminated displays, and even dishware. The collections appear on display in a variety of venues, from events at New York City public schools to world-famous galleries, and are accompanied by videos and ex-

//REFERENCES// [1] Synthetic Biological Systems Laboratory. (2020). Retrieved from http://daninolab.nyc/ colonies. [2] Danino, T. (2015). Programming Bacteria To Detect Cancer (And Maybe Treat It). Retrieved from https://www.ted.com/talks/ tal_danino_programming_bacteria_to_detect_ cancer_and_maybe_treat_it?language=en. [3] Tal Danino Art. (2020). Retrieved from http://www.taldaninoart.com/.

Through a microscope, one can see the details of each individual cancer cell— the abstract outline and the dark shadow of the nucleus at the center. Only from a more distant perspective do the groupings of cells come together into a full image. At some point as you zoom out, there is a transition from science to art, from cells to portraits. Not only does this medium provide elegant proof that there is no real distinction between art and science, it transforms something that is frightening to many people into something that is beautiful [1]. Art made from cancer cells provides a way to visualize a disease that is 19


Global Temperature Anomaly (°F)

PANDEMIC ON E

How climate change and human m have escalated the dangers of pa transmission

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estroying civilization in its entirety simply starts with a pathogen, a susceptible population, and time. My familiarity with the systematic infection of humanity lies in the game “Plague, Inc.”, a simulation game in which a player controls and modifies various pathogen types with the goal of killing all humans. The round starts by choosing a difficulty level: “Casual” creates a society that doesn’t practice hygiene, “Normal” creates a moderately careful society, while “Brutal” and “Mega Brutal” create a compulsive society obsessed with public health and pharmaceutical research. From there, the gameplay starts. Pop DNA bubbles, quickly evolve transmission traits. Pop DNA bubbles, follow up with cold resistance and heat resistance. Pop DNA bubbles, finish off the game with lethal symptoms. As a seasoned Plague, Inc. player, I’ve discovered that the heart of the game lies in infecting every nook and cranny on the globe (yes, looking at you, Greenland) by first giving pathogens the ability to survive every climate and quickly spread. 20

Yet, despite possessing the fundamental ability to dictate a plague’s failure, the world unknowingly works in the opposite direction—but not by popping DNA bubbles or investing points into infectious diseases. Instead, in contributing to climate change, we’ve cleared the path for pathogens to survive, thrive, and eventually kill large human populations. Even worse, in this ultra-realistic version of Plague, Inc., we’ve chosen “Casual” instead of “Mega Brutal” in the sense that our actions reflect extensive scientific illiteracy despite the extensive research conducted on climate change. Humanity’s disregard for our environment simultaneously benefits pathogens and makes society more vulnerable to disease through the effects of climate change, which grants traditionally sensitive microbe strains greater ability to reproduce and infect. Climate change, for the most part, has followed a consistent trend in a worldwide increase in temperature and atmospheric carbon dioxide levels, the latter of which


EASY MODE

Written by Jacob Kang Illustrated by Audrey Oh

migration athogenic

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tinents. The pressing issue surrounded the genetic nature of the appearances, as each outbreak on each continent involved distinct variants of a common relative of C. auris [2]. In tackling the question of how each substrain of C. auris was miraculously able to acclimate to the conditions of each continent, Johns Hopkins infectious diseases and public health professor Arturo Casadavell points to a novel explanation—rapid temperature increases around the world.

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traps UV radiation and creates the “greenhouse effect.” According to a 2019 NASA-sponsored study conducted by UC Berkeley geophysicists, most climate models created since the 1970s that predict temperaturechange severity and the amount of energy absorbed by Earth’s surface have remained accurate when cross-referenced with modern day climate change rates, which predict a massive increase in surface air temperatures of 3 degrees Celsius for most regions on Earth [1]. While society is mostly aware of more visible consequences such as rising ocean levels and increasingly extreme weather patterns, these effects also work behind the scenes, perfecting conditions that allow for unprecedented mobility and survivability in specific pathogen types that typically require specific niches to survive. In the early to mid 2010s, multiple never-before-seen strains of Candida auris, a fungus species often contracted by hospital patients, made unexpected and simultaneous appearances on three different con-

The emergence of C. auris as climate-driven is not only unprecedented but also transcends factors that typically facilitate a pathogen’s survivability, including drug resistance and mutation. While drug resistance, wherein a microbe population’s exposure to over-administered treatments eventually results in a population with resistant characteristics, has manifested in a significant number of pathogen species and is in the World Health Organization’s “Ten Threats to Global Health in 2019,” it cannot explain how quickly Candida independently appeared in Asia, Africa, and South America: an unmatched, defining characteristic of C. auris [3]. Likewise, the rate at which mutation occurs cannot match how quickly C. auris would have to be able to genetically differentiate in order to simultaneously infect different environments.

In contributing to climate change, we've cleared the path for pathogens to survive, thrive, and eventually kill large human populations. However, a new angle arises when considering human’s innate defense against fungi and how it links with climate change. As described by Casadavell, natural human resistance to fungal infections is proposed to result from 21


the human’s high resting body temperature, conditions that fungi are unable to survive in, let alone reproduce in. This natural security measure becomes compromised when the difference in temperature between the human body and the surrounding environment becomes smaller. It was this shrinkage that allowed C. auris to transition from infecting human surfaces (such as the inner ear canal) to occupying internal anatomical regions [4].

recovered possessed resistances to several widely used treatments, indicating that these isolates had the potential to become pathogenic. Birds, with their ability to travel and maintain suitable conditions for Candida, act as a genetic microcosm that a wide variety of subspecies of resistant Candida inhabit and utilize to travel. Given that fungal resistance to multiple treatments is already worsening, it can be expected that resistant species will become even more prevalent—as described earlier, inConcern over Candida increases when understanding creasing temperatures mean that fungal populations its transmission capabilities, which are speculated to confined to wetland ecosystems over time gain thermoarise from Candida’s original environment: wetlands. resistance, allowing for the fungus to successfully occuIn a study concerning C. albicans, a genetic relative of py warm-blooded avian vectors and transfer to humans. C. auris, researchers discovered that wetland conditions (low oxygen levels, richness in nutrients) parallel human While drastic increases in gastrointestinal conditions that C. albicans reside in [5]. The transition from wetlands to humans may potential- temperature are most commonly ly link C. auris’ recent appearance to a similar transition associated with extreme weather from wetland to marsh. As climate change becomes more patterns and rising sea levels, severe, wetlands are likely to become even more aligned with intestinal conditions as atmospheric oxygen levels the effects of these phenomfall and wetland nutrient levels increase due to favored ena are slated to increase human plant growth from higher carbon dioxide levels [6]. susceptibility to disease. Wetlands, while serving as a perfect environmental niche for Candida, also provide opportunities for the pathogen to transmit elsewhere by housing biological vectors that interact more freely with humans living near bodies of water. Considering Candida’s origination as a water-borne fungus and appearance in areas containing wetland ecosystems, Candida’s transition from exclusively wetlands to human populations combined with its ability to infect birds is hypothesized to be a contributing factor to the multi-continental spread of the pathogen in the past decade. In fact, the connection between birds and Candida is well-documented; a study conducted on synanthropic (wild species that occupy niches near humans) birds in Kuala Lumpur found that they tested positive for 14 different strains of Candida [7]. Considering the high contraction rate in birds, their general migratory behavior, and their close proximity to high-density populations, the spread of Candida in three separate countries becomes a reality and is likely to grow into a larger problem as increasingly erratic climate patterns affect both Candida adaptability and bird migration patterns.

If Candida's improved capability to thrive in hotter environments can be compared to upgrading a pathogen’s heat resistance in Plague. Inc, then the expansion of a disease vector’s occupied niche can also be compared to upgrading a transmission perk that allows for the player’s pathogen to spread to a wider variety of locations. For mosquitoes, whose disease transmission kills over 700,000 people annually, a warming Earth grants an increased capability in breeding and migration, or an opportunity for diseases typically confined to tropical regions to reach previously unattainable colder regions [8]. Tracking mosquito population distribution in relation to projected climate models and vulnerable populations reveals that in our current environmental state, at least 6.01 billion individuals already live in areas capable of hosting Aedes aegypti, the vector mosquito species for dengue, Zika virus, and yellow fever virus [9]. By 2050 and 2080, however, half a billion and one billion more individuals respectively will become at risk for transmission by A. aegypti with major increases in Europe, the United States, Canada, east Africa, and east Asia. Despite theoretical models leaving out variables Concerns over the zoonotic (animal to human transmis- like economic improvements and weather patterns, the sion) nature of Candida become amplified considering possibility of a dramatic uptick in mosquito vector zones that researchers found that nearly 70% of fungal isolates becomes even worse when factoring in the genetic im22


plications that climate change holds for mosquito populations. The sheer number of mosquitoes that inevitably travel towards higher latitudes will amplify fundamental evolutionary pressures (such as reproductive capabilities and food accessibility). This intensified competition will augment the rate at which mosquito populations’ genes shift via natural selection, making them ever more resistant to human interventions. This combination of high genetic variance and large numbers is expected to make mosquitoes a formidable enemy to global health.

enhances, humanity can witness a glimpse of future types of pathogens that can be expected to manifest.

As our “casual-mode” oriented society braces itself for a greater onslaught of Candida-like strains, it becomes increasingly clear that climate change serves as the ultimate disease catalyst: one that combines all desirable traits in Plague, Inc. and creates an unstoppable pathogen. With devastating events such as COVID-19 rapidly growing into an international pandemic and ever-increasing occurrences of forWith every aspect of a pathogen’s success seemingly midable pathogenic strains, it has become clear that gaining massive benefit from a changing environment, society will need to play in “Mega-Brutal” mode as the question of how climate change will affect humans’ long as climate change is not sufficiently dealt with. long-term ability to defend against disease naturally arises, but modern society has limited insight into //REFERENCES// this question. While drastic increases in temperature are most commonly associated with extreme weather [1] Buis, A. “Study Confirms Climate Models Are Getting Future Warmpatterns and rising sea levels, the effects of these phe- ing Projections Right – Climate Change: Vital Signs of the Planet.” NASA, NASA, Jan. 2020, climate.nasa.gov/news/2943/study-confirmsnomena are slated to increase human susceptibility to climate-models-are-getting-future-warming-projections-right/. disease, especially as individuals living in vulnerable [2] Casadevall, A., Kontoyiannis, D. P., & Robert, V. (2019). On the emerregions such as those near large bodies of water may gence of Candida auris: climate change, azoles, swamps and birds. American Society for Microbiology. doi: 10.1101/657635 be forced to migrate. In order to analyze the extent of [3] “Ten Health Issues WHO Will Tackle This Year.” World Health human migration, USC computer science researcher Organization, World Health Organization, 18 Jan. 2019, www.who.int/ Bistra Dilkina and his team used an extensive machine news-room/feature-stories/ten-threats-to-global-health-in-2019. [4] “General Information about Candida Auris.” Centers for Disease learning model to anticipate the severity of sea level Control and Prevention, Centers for Disease Control and Prevention, 13 rise and flooding using a coastal dataset [10]. Coupled Nov. 2019, www.cdc.gov/fungal/candida-auris/candida-auris-qanda.html. with another neural network with inputted migration [5] Stone, W., et al. “External Ecological Niche for Candida Albicans within Reducing, Oxygen-Limited Zones of Wetlands.” Applied and Endata from specific counties, the researchers were able vironmental Microbiology, American Society for Microbiology, Apr. 2012, to predict large migration influxes ranging from tens www.ncbi.nlm.nih.gov/pmc/articles/PMC3302598/. to hundreds of thousands of people in regions such as [6] Leahy, S. “Thirsty Future Ahead as Climate Change Explodes Plant Growth.” Climate Change Will Make Plants-and Us-Thirstier, National Houston, Dallas, and Las Vegas—rapidly increasing Geographic, 4 Nov. 2019, www.nationalgeographic.com/science/2019/10/ risk of disease contraction [11]. Climate change’s in- plants-consume-more-water-climate-change-thirsty-future/. fluence over such a large population demographic em- [7] Lord, A.T., Mohandas, K., Somanath, S. et al. Multidrug resistant yeasts in synanthropic wild birds. Ann Clin Microbiol Antimicrob 9, 11 phasizes the extent of which public health—a persistent (2010). https://doi.org/10.1186/1476-0711-9-11 human challenge—is compromised. All the aforemen- [8] Gates, B. “The Deadliest Animal in the World.” Gatesnotes.com, tioned benefits to pathogens, such as increased range GatesNotes, 25 Apr. 2014, www.gatesnotes.com/Health/Most-LethalAnimal-Mosquito-Week. and survivability, become amplified when advantages [9] Ryan, S. J., Carlson, C. J., Mordecai, E. A., & Johnson, L. R. (2019). that humans traditionally hold over pathogens become Global expansion and redistribution of Aedes-borne virus transmission factored out as a result of migration. For example, with risk with climate change. PLOS Neglected Tropical Diseases, 13(3). doi: 10.1371/journal.pntd.0007213 dense migration clustering negating humans’ mobility [10] Robinson, C., Dilkina, B., & Moreno-Cruz, J. (2020). Modeling miand distancing capabilities, pathogens with improved gration patterns in the USA under sea level rise. Plos One, 15(1). doi: transmission options and genetic resistance can freely 10.1371/journal.pone.0227436 [11] Hu, H., Nigmatulina, K., & Eckhoff, P. (2013). The scaling of contact spread and disrupt public health tactics, which revolve rates with population density for the infectious disease models. Mathearound isolation and population control. These effects matical Biosciences, 244(2), 125-134. are especially observable with the current COVID-19 [12] Mackenzie, J.S., & Smith, D.W. “COVID-19: a Novel Zoonotic Disease Caused by a Coronavirus from China: What We Know and What pandemic, given its zoonotic properties, its reliance on We Don't.” Microbiology Australia, CSIRO Publishing, 17 Mar. 2020, group density for transmission, and the difficulties that www.ncbi.nlm.nih.gov/pmc/articles/PMC7086482/. scientists have faced in treating it [12, 13]. With the [13] Harvard Health Publishing. “Treatments for COVID-19.” Harvard Health, Harvard Medical School, 24 Apr. 2020, www.health.harvard.edu/ coronavirus covering all the bases that climate change diseases-and-conditions/treatments-for-covid-19. 23


What Marshmallows Can Tell Us About Socioeconomic Inequality

Written by Liza Casella Illustrated by Lizka Vaintrob

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I

n 1972, researchers at Stanford conducted a nowfamous experiment, now known as “The Marshmallow Test” [1]. The marshmallow test was designed to investigate self-control and voluntary delay of gratification in children, measuring how long they were willing to wait for a reward after it was offered. The basic experimental setup is as follows: 50 children aged three to five were divided into five groups. In the first three groups, each child was put in a room with a pretzel and a marshmallow in a cake tin. A researcher, whom each child had previously spent time getting to know, said, “Let's see what's under here? I'll bet it's a surprise! Oh boy, look at that! A marshmallow and a pretzel! Which would you like to eat?” The researcher then told the child that they were going to leave the room for an unspecified amount of time (15 minutes) and would later return, but would return immediately if the child rang a bell that was provided. In the first group, the children were given toys to play with while they waited. In the second, they were instructed to think about fun things while they waited. In the third, they were not told anything after the initial instructions. Any child who ate either of the snacks while the researcher was out of the room was excluded from the dataset. Six of the children who were given toys and four of the children thinking about fun things waited the full 15 minutes. The fourth and fifth groups were control groups to determine if delayed gratification changed depending on how long the children waited before calling the researcher back in. They were not offered any snacks, but were either given toys to play with or instructed to think about fun things. None of these children waited the full 15 minutes before ringing the bell, nor did any of the children from the third group.

the table. They were instructed to either think fun thoughts, sad thoughts, or about the reward. The children thinking fun or sad thoughts waited significantly longer than the children thinking about the reward. Several similar studies focusing on delayed gratification were performed at this time, with a variety of experimental setups and different rewards (such as a wrapped package or desirable toys), all of which are often grouped under the moniker “marshmallow test” in popular culture. While the original purpose of all these experiments was to investigate cognitive mechanisms affecting the delay of gratification in children, the experiments are more famous for the many follow-up studies, the results of which altogether suggest that a child’s performance in the experiment could predict many aspects of their success later in life, including their performance in school, SAT scores, and even their BMIs [2]. The first follow-up study was published in 1983 [3]. It compared the children’s ability to delay gratification to a myriad of behavioral and psychological traits, which were measured by descriptions from their elementary school teachers. Researchers found a child’s ability to delay gratification to be significantly correlated with traits such as “unusual thought processes,” “dramatizes mishaps, and “arouses liking in adults.” They even extended their survey to examine characteristics such as, “House is decorated in an ornate style.” The follow-up study’s results strongly emphasized sex differences among behavioral correlates, stating in the abstract of their article that: “Boys who delayed gratification tended to be independently and consistently described as deliberative, attentive and able to concentrate, reasonable, reserved, cooperative, and generally manifesting an ability to modulate motivational and emotional impulse. Boys who did not delay gratification, by contrast, were irritable, restless and fidgety, aggressive, and generally not selfcontrolled. Girls who delayed gratification were independently and consistently described as intelligent, resourceful, and competent. Girls who did not delay tended to go to pieces under stress, to be victimized by other children, and to be easily offended, sulky, and whiny.”

The researchers performed a second experiment with a new cohort of children, in which the children were all offered a snack as a reward for waiting and were instructed to either think about fun things, sad things, or about the reward itself. The children thinking fun thoughts waited longer than the children thinking sad thoughts, who waited about the same amount of time as the children thinking about the reward. The researchers also performed a third version of the ex- This obviously gendered language emphasizes the periment with yet another cohort, in which the snacks gender bias in the study. The authors went as far as to were placed under the cake tin, which was put under conclude that children who scored worse on delayed

25


gratification tests were more likely to come from environments in which “the mother was relatively neurotic.” Note that neuroticism was removed from the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1980, four years before this study was published. Further follow-up studies found that children who performed better on the marshmallow test or a similar study scored higher on the SAT (by a significant but small amount) and had lower BMIs [1, 4].

The children who had worked with reliable researchers waited, on average, 12 minutes and 2 seconds before eating the marshmallow. In contrast, the children who had worked with unreliable researchers waited, on average, 3 minutes and 2 seconds.

While this study does not prove that self-control is irrelevant to a child’s performance on the marshmallow test, it strongly suggests that their decision is heavily influenced by the reliability of their environThe ability to forgo an immediate reward in favor of a ment. When in an unreliable environment, the child better reward in the future (or accept an immediate loss makes the rational decision to eat the first marshto avoid a greater loss in the future) is an important skill mallow, as they can reasonably expect that the unrethat we develop as we get older. An inability to delay grat- liable researcher will not bring them another one. ification is associated with addictive behaviors such as substance abuse and gambling [5]. It has also been shown Another problem with the original marshmallow test to have a negative effect on academic performance [6]. and the many similar tests like it is that the majority were conducted at Stanford University, and the chilTests like the marshmallow test have long been consid- dren participating in each test attended a preschool ered accurate ways to predict achievement and success located on Stanford’s campus [1]. This introduces a in later life. But can a test of whether a preschooler can huge amount of bias into the results. Children from sit for 15 minutes when promised a marshmallow re- the same area and who attend the same school are ally predict how successful they are years later? Despite far more likely to be in the same socioeconomic class the legacy and fame of these experiments in the field, than children from a more diverse sample. Thus, alnew research suggests that many of the outcomes as- though these data were generalized to the general sociated with a child’s performance in the marshmal- population, this generalization is ultimately inaccurate. low test are actually due to environmental factors that the original researchers failed to control for or consider. A study done in 2018 by Watts et al. took it a step further, and factored a myriad of socioeconomic facA follow-up study from 2013 by Kidd et al. conducted a tors into the data analysis from a delayed-gratificasimilar experiment to measure how well children could tion test [8]. The researchers recreated a larger and delay gratification, but had some of the children work more socioeconomically diverse cohort of children. with a researcher the children believed to be unreliable Similar to the previous tests, each child was given [7]. Before the experiment, each child was given an art project and told they could either use old, unappealing art supplies right now or wait two and a half minutes They found that for the researcher to bring new, better supplies. The unwhose families belonged to reliable researchers did indeed bring better art supplies after the two and a half minutes, while the unreliable researchers returned and told the child that they had made a mistake and they did not have any new art supplies.

children

The children were given a marshmallow test immediately after: the researcher put a marshmallow on the table and said the child could eat the marshmallow immediately, or, if they could wait for the researcher to go get another marshmallow, they would be allowed to eat both. The test ended after the child ate the marshmallow or after 15 minutes had elapsed. 26

higher socioeconomic groups waited significantly longer than children whose families belonged to

lower socioeconomic groups.


a treat by a researcher and told that if they waited for the researcher to return to eat it, they would be given a second treat and allowed to eat both. The maximum wait time in this study was seven minutes.

Psychology has been facing a replication crisis for several years now. Many of the early experiments that helped to define the field have been disproven, were inaccurately reported, or would be considered incredibly unethical today. The marshmallow test is just one of them. The Like in previous studies, researchers followed up with dozens of follow-up and related studies assumed that the children’s academic performance and behavioral the conclusions of the experiment were accurate, when traits at several time points after the initial test. Unlike in actuality it failed to take into account environmental in previous studies, they factored socioeconomic sta- influences, gender biases, and whether or not a group of tus into their analysis. They found that children whose participants was sufficiently representative or diverse. families belonged to higher socioeconomic groups waited significantly longer than children whose fami- Reproducibility is essential in any scientific experilies belonged to lower socioeconomic groups. More ment. Results that cannot be replicated cannot be specifically, researchers found that the mother’s educa- assumed accurate without further testing. As is the tion level, children’s home environment, and family’s case with many studies (not only in psychology but economic status were correlated to how long the chil- across several disciplines including medicine, socioldren were able to delay gratification. Importantly, the ogy, and economics), the marshmallow experiment authors of the study found no significant correlates be- laid the groundwork for a huge number of studies, tween preschool-age delay of gratification and behav- the validity of which must now be called into quesior or academic performance at age 15 for either group. tion. While we may never know the full extent to which flawed and unreproducible experiments have afPsychology has been facing a fected further research in their fields, growing awareness of the phenomenon and extensive replication replication crisis for several experiments will serve not only to correct previous results, but also to lead to new findings and discovery. years now. Many of the early

experiments that helped to define the field have been disproven, were inaccurately reported, or would be considered incredibly unethical today.

For years, the marshmallow test was used as evidence that one’s ability to delay gratification in preschool was an incredibly reliable predictor of their later success. Watts’ and Kidd’s study results provide an alternative explanation: that it is, at least partially, the socioeconomic conditions in which one grew up that impacts their academic performance and behavioral outcomes. A child’s performance in the marshmallow test is based on a rational decision that reflects the environment in which they grew up. The marshmallow test makes biased, gendered, and inaccurate assumptions about children based on their performance, without considering that the participants are making what they believe is the smartest decision.

//REFERENCES// [1]Mischel, W., Ebbesen, E. B., & Raskoff Zeiss, A. (1972). Cognitive and attentional mechanisms in delay of gratification. Journal of Personality and Social Psychology, 21(2), 204–218. https://doi.org/10.1037/ h0032198 [2]Mischel, W., Shoda, Y., & Rodriguez, M. L. (1989). Delay of Gratification in Children. Science, 244(4907), 933–938. JSTOR. [3]Funder, D. C., Block, J. H., & Block, J. (1983). Delay of gratification: Some longitudinal personality correlates. Journal of Personality and Social Psychology, 44(6), 1198–1213. https://doi.org/10.1037/00223514.44.6.1198 [4]Schlam, T. R., Wilson, N. L., Shoda, Y., Mischel, W., & Ayduk, O. (2013). Preschoolers’ Delay of Gratification Predicts their Body Mass 30 Years Later. The Journal of Pediatrics, 162(1), 90–93. https://doi. org/10.1016/j.jpeds.2012.06.049 [5]Amlung, M., Vedelago, L., Acker, J., Balodis, I., & MacKillop, J. (2017). Steep delay discounting and addictive behavior: A meta-analysis of continuous associations. Addiction, 112(1), 51–62. https://doi. org/10.1111/add.13535 [6]Cheng, V., & Catling, J. (2015). The Role of Resilience, Delayed Gratification and Stress in Predicting Academic Performance. Psychology Teaching Review, 21(1), 13–24. [7]Kidd, C., Palmeri, H., & Aslin, R. N. (2013). Rational snacking: Young children’s decision-making on the marshmallow task is moderated by beliefs about environmental reliability. Cognition, 126(1), 109–114. https://doi.org/10.1016/j.cognition.2012.08.004 [8]Watts, T. W., Duncan, G. J., & Quan, H. (2018). Revisiting the Marshmallow Test: A Conceptual Replication Investigating Links B etween Early Delay of Gratification and Later Outcomes. Psychological Science, 29(7), 1159–1177. https://doi.org/10.1177/0956797618761661 27


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Volume 16, Issue 2: Spring 2020  

Volume 16, Issue 2: Spring 2020  

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