Categories
Research-in-Brief Science Communication

Visions of Sound & The Synesthetic Spectrum

By Ava Nagy

When I was a kid, I had a violin instructor who could see sheet music come to life. To my astonishment, I had known her for three years before this information came up in conversation. I had been sitting in the eclectic, circular “music room,” in the back of her home, complaining about how difficult it was for me to sightread a piece of music for the first time. I remember I had asked her how she did it so easily, expecting to be met with one of her usual sayings – “practice makes perfect,” or one of its many variations – but this time she only smiled. 

“Each note is a different color,” she explained. C sharp, for example, was dark brown, whereas C flat was bright pink. They were unmistakeable; a slight change in position on the page represented a leap of hue that made their finger placements obvious. As she played, she witnessed a progression of color swelling from the page, creating a unique pattern to which she could return easily the next time she sat down to practice.

This is because my instructor had a type of synesthesia known as Chromesthesia, correlating colors to sounds. However, this is only one of many possible associations. Other variations of synesthesia correlate different combinations of colors, numbers, motion, shapes, sounds, sensations, motion, and even time. 

In one particularly fascinating case, author Daniel Tammet describes his combination of multiple types of synesthesia: “The number 1… is a brilliant and bright white, like someone shining a flashlight into my eyes. Five is a clap of thunder or the sound of waves crashing against rocks. Thirty-seven is lumpy like porridge, while 89 reminds me of falling snow” (Tammet, 2007).

These associations can be either distracting or helpful. Some synesthetes report a spatial understanding of mathematics that can reveal hidden relationships between numbers, as each one occupies a mental location in space. Interestingly, Einstein was known to describe his mathematical thinking as “spatial in nature,” suggesting he might have experienced the condition himself (Brang & Ramachandran, 2011).

So, what is the neurological basis for these experiences? While scientists don’t understand the exact cause of the condition, recent studies have revealed possible explanations. For many years, it was believed that a crossover between the processing of different brain areas occurred in high level cognitive areas. However, recent studies show that visual forms of synesthesia are related to the processing area V4 of the visual cortex.

Another thing we’ve learned is that synesthesia is heritable. That is, 40% of synesthetes report a first-degree relative with the same condition (Brang & Ramachandran, 2011). However, there is no single gene that invokes its presence. One study identified 37 separate genes that could predict its development.

Certain drugs that invoke temporary synesthesia may be key to understanding the neurological underpinnings of the condition. According to one study, LSD elicits similar symptoms by activating serotonin receptors, suggesting that S2a receptors are involved. What’s more, the same study found two subjects who reported that Prozac inhibited preexisting synesthesia. Prozac is known to inhibit that same S2a receptor, adding to the evidence that it might produce symptoms of the condition. One subject even experienced grapheme-color synesthesia for the first time after taking 5mg of melatonin, which disappeared after the drug left his system. Interestingly, serotonin is metabolized into melatonin, which then results in the inhibition of serotonin production, leading to the activation of S2a receptors. (Brang & Ramachandran, 2008). 

The conclusion of these cases, according to the publishers of this study, is that grapheme-color synesthesia is neurologically rooted in a crossover between the color area V4, and the “number area”, which are positioned next to each other in the fusiform gyrus.

All of these sensory experiences affect the way a person sees the world, both literally and figuratively. One study finds that synesthetes display greater openness to experience, convergent thinking, use of mental imagery, and verbal comprehension (Chun & Hupé, 2015). There are many possible conclusions to be drawn from these results. Perhaps the visualisation of verbal information allows them to store that information better than those without the condition. 

However, it is important to remember that no two synesthetes experience the same mental experiences in response to the same environmental stimuli. Indeed, no two human beings can truly experience their environment in the same way internally. In this way, synesthesia serves as a great reminder of the vast range of internal human experience.

 

References

Brang, D., & Ramachandran, V. S. (2011). Survival of the Synesthesia Gene: Why Do People Hear Colors and Taste Words? PLoS Biology, 9(11), e1001205. https://doi.org/10.1371/journal.pbio.1001205

Brang, D., & Ramachandran, V. S. (2011). Survival of the synesthesia gene: Why do people hear colors and taste words? PLoS Biology, 9(11), e1001205. https://doi.org/10.1371/journal.pbio.1001205

Brang, D., & Ramachandran, V. (2008). Psychopharmacology of synesthesia; the role of serotonin S2a receptor activation. Medical Hypotheses, 70(4), 903–904. https://doi.org/10.1016/j.mehy.2007.09.007

Chun, C. A., & Hupé, J. (2015). Are synesthetes exceptional beyond their synesthetic associations? A systematic comparison of creativity, personality, cognition, and mental imagery in synesthetes and controls. British Journal of Psychology, 107(3), 397–418. https://doi.org/10.1111/bjop.12146

Tammet, D. (2007). Born on a blue Day: Inside the extraordinary mind of an autistic savant: a memoir.

 

Categories
Research-in-Brief

Neuro Rivals

By Samantha Robles Avalos

To civilians, he is referred to as Enphine. His real identity is Endorphin. He began working as a vigilante once he reached adulthood, chasing after submerging pain signals that were rising within his hometown. They were rather minuscule and annoying incisions to Enphine. After a year of doing the bare minimum, Enphine realized that he craved moreexcitement than his mundane work. So, he sought after the biggest corporation known to blood-kind, the Cortex Prime. “C Prime,” as Enphine likes to call it, controls and plans lower-grade to grade-S missions around the world. Months of mentored training, both physically and mentally, allowed Enphine to prove to the officials from C Prime that he is worth more than his verbal taunts that rise from his arrogant and playful personality. 

Enphine harbors two different techniques: Painkiller and The Runner’s High. Painkiller is noted to be a form of electrokinesis, an ability that he can generate and manipulate any form of electrical currents. It’s particularly effective as a shock, which he uses mindlessly against lower-grade criminals as more of a scare than a demise. When he clenches his hands in combat, electricity bounces around his figure, demonstrating how strong he is when specific missions call for him to use more of his muscles. A weakness of this power, however, is that exposure to pain modulates his sensitivity, oftentimes decreasing his endurance in battle if he isn’t careful. This is a part of the reason why Enphine has a custom-made rigorous training course, ensuring to work on increasing his endurance to the maximum it can. 

Enphine’s second technique, The Runner’s High, is not a physical ability of his, but rather a physical manifestation of his mental fight. The appearance of Runner’s High is more human-like and sometimes works out of Enphine’s consciousness. Similar to Enphine’s height and build, The Runner’s High is gold, embellished with green accents and grooves across its body. This spirit’s abilities can either nullify, reverting the actions of anyone that Enphine comes across, or amplify, life-giving ability, his opponent’s actions. The more Enphine is active, the more the power increases. Sometimes, Enphine can manifest Runner’s High while he uses Painkiller, which makes Enphine the most powerful in battle. A weakness of using his spirit, however, is that Enphine’s sensitivity is amplified twice as much, making him prone to injuring himself further if he doesn’t concentrate on the villains. If not careful, excessive use will lead to immediate rest, alongside the disappearance of Runner’s High, which makes Enphine vulnerable to attacks. Enphine’s endurance is strengthened by the training course C Prime has made for him, with a part of it being able to spar with other Neurotransmitters by using his spirit in combat. 

A fun fact about Enphine is that there are moments when he seeks a life outside of the hero work C Prime has made for him. One of the other heroes had asked him about his dream vacation destination once. The question is still stuck with him. Fiji, he thought. It’s restorative and matches his character perfectly. Immersing himself in village cultures and traditions, enjoying a bath in the hot springs, and looking at the oceans at night is something that Enphine never realized he craved more than he liked. He is determined to one day leave the life that C Prime has planned for him and attend to his wishes. 

Outside of being serious on missions, he is a menace to his higher-ups, often teasing them about their work ethics, usually with the implication of “livening up a little.” Sometimes Enphine will take it a bit too far, buying his higher-ups sweets to make up for his behavior. At one of the many instances of going to a cafe to get his usual, he runs into a woman, quite literally. Drinks clashed, but thankfully not staining either person's work clothes. She was in a rush, her hair slightly disheveled from the run-in. Before Enphine could ask if she was okay, she muttered some apologies and something about losing track of time before running out the door. What she never noticed was her work ID slipping out from her pocket, which caught Enphine’s attention. GABA, he read. Thankfully, her job’s location wasn’t too far from where the cafe was. Enphine let out a small smirk before putting her ID in his pocket. He went back to the register and got both drinks for free, intending to visit her job to see what it was about her that made him quiet for once.

In the field, her code name is Sleeper Agent. Outside of that, people call her GABA. Her first (and only) job was working at an office. Being the only woman in the company, she was treated as an errand girl instead of an equal worker, which she didn’t mind at first. The job pays, she believed. The least she could do was abide by their bidding. One day, a mishap occurred with the documents her boss assigned to her, and he forced her to come back to the job to fix it or face demotion from her current position. She felt a little annoyed that she missed out on her break in the cafe near her due to her boss’s insistence on a task he could’ve done himself. Rushing out of the comfort of the coffee shop, she couldn’t apologize to the poor guy she ran into. Although poor is an understatement. He looked like he could pay her and buy the entire company if he wanted to, she thought, recalling the minimalistic, yet expensive statements that adorned his figure. After helping her boss, she sat in her office cubicle, feeling mindless as she sorted through her online solitaire game. Her boss’s cough behind her brought her out of her blankness, scrambling to look important. She was told that there was someone in the front asking for her. Possibly a boyfriend, her boss presumes before walking away to his desk. She was baffled by his statement. Neither her family nor her friends came asking for her, let alone a boyfriend. 

She walked to the front lobby to see the same man who ran into her earlier on her break, making himself comfortable on the cushioned seats with two drinks sitting next to him. His eyes lit up when he recognized her, gesturing for her to come over to him. GABA, feeling a little unsure, adjusted her hands to her sides and readied her first technique unbeknownst to the man, before approaching him. The first thing she noticed about him, upon getting a closer look, was his eyes. His eyes never left her figure as she came close, which would have made her blush a bit if he weren’t a stranger to her. She gave him a confused look that made him realize what he was here for. Her work ID was taken from his pocket and rested upon the table. Bashful, she thanked him before glancing at the drinks next to him. He noticed, of course, and offered one of them to her. He told her his name, Endorphin, and mentioned that if under different circumstances, he would have asked her out on a date. She sputtered out a thank-you, which made him laugh a bit before getting up to leave. Before walking through the door, he turned and waved bye to her, saying he hoped to see her again. Conveniently enough, she had a pen and a small notebook with her. She wrote her name and number down, and used her ability, Stasis, to discreetly place the paper in his pocket. Their first encounter became one of many, and eventually, they settled together and married through one of the heaviest earthquakes known in history. 

As previously mentioned, Sleeper Agent’s first recorded technique was Stasis. This ability is similar to luminokinesis, in which the user is able to manipulate all light forms. She uses it as puppet strings attached to her fingers. It gives GABA a sense of stability, being able to control her environment as she likes. As long as things are illuminated, her powers can be used. A weakness of this ability is that overuse of this power can lead to seizures and chronic pain. This is why she prefers to use her ability as a puppeteer. It doesn’t cost her a lot of energy if there is light in every room, which is why she got the office job. If she were to deal with harsh migraines, she would snack on fermented foods and whole grains that she keeps in her lunch bag. She watches what she eats, which makes her more agile amongst her peers. 

Her second technique, which doesn’t appear until later in her career, is called Eye of the Hurricane. Eye of the Hurricane allows her to turn into an enchanting spirit. This manifestation takes on the appearance of a woman in a hooded, black cape, wearing a black, laced-trimmed dress, and a blindfold covering her eyes. Her abilities consist of absorbing light and electricity, using these powers to heal the user and those around her. Because she can maintain her composure, Cortex Prime has recruited her to work in the restorative field. Her stability works well with uplifting her team’s mood and being the backbone on team night missions. A weakness of this power is that fatigue catches on quicker than she’d like. Although she could brush it off, the fatigue is sometimes followed by physical discomfort, such as headaches or nausea, which makes her a liability and vulnerable to attacks. The best way to avoid this is for GABA to return to her normal self, resulting in drowsiness. A way for her to build endurance against physical fatigue is to recharge by sleeping throughout the day. She also follows a moderate exercise plan that Cortex Prime made for her that helps boost her energy. 

A fun fact about GABA was that she never sought out the hero work life like her husband, Endorphin, did. She would much rather prefer the mundane life and is more laid back than her partner expected. After Cortex Prime recruited her, thanks to Enphine’s insistence, she was able to adjust and improve her skills and be paid handsomely for her endeavors. If someone were to ask her to choose a partner to work with on all her missions, she would choose Enphine. Not because he’s her husband, but because her abilities are compatible with his – Enphine loves to hog all of the attention in battles, and she loves to support him with boosts and modulation wherever she can, only coming in to take over if that is what her partner needs. On her rest day, her husband came back home from work and asked her about her ideal getaway. She had thought about this question before, when she was working at the office. The Maldives, she told him. The calming waters, the glorious sun, and the breathtaking scenery would be the perfect place to be stress-free. 

In the villain world, everyone refers to him as Necro. To his allies, he is known as Glutamate. As a growing boy, he was used to the consistent buzz that filled his hometown. Vendors, children running around, adults bargaining and haggling prices – these noises brought comfort for Glutamate. One morning, he woke up to a raid infiltrating his home. Villages, young and old, were running aimlessly away from the flood of synaptic firing that was launched at them, for no apparent reason. The lighting of synapses resembles a meteor shower – a natural disaster. Their terror shook the earth, marking the moment as the harshest against bloodkind. Glutamate sought shelter. Hands raised over his head, he closed his eyes and prayed that it would be over. After a while, it did. Neurons were scattered across the land, some weakened, some not. Glutamate could only look with horror etched on his face. The heroes sent from Cortex Prime arrived late. Official statements from them said that there was nothing they could do to prevent the disaster. Glutamate has harbored resentment against the corporation since, hoping to unleash the same pain he experienced on the headquarters. 

Necro’s first known ability is Excitotoxicity. This neurokinesis power allowed Necro to manipulate excessive synaptic force onto people. It would act upon someone as if they were burning alive. Influenced by the disaster that struck him, Necro’s ability is what Cortex Prime considers “the most powerful ability to exist.” Excessive stimulation ranges from strokes to 

irreversible brain damage to death. No one has faced Necro head-on, as he waits on the sidelines before striking. Cortex Prime had first relied on drugs for some form of balance. They acted as shields that loom over cities to protect what Cortex Prime couldn’t. Since the rise in his destruction, it is why Cortex Prime has sought GABA’s powers – to regulate before things go out of its control. 

Necro’s second recorded ability is Vigor. It’s a physical manifestation of Necro, but slightly taller than him, and embodied in all white with a few purple accents. There are purple grooves on its legs, similar to Enphine’s Runner’s High. Vigor can manipulate others by attaching a piece of his skin to the person. This contact allows Necro to brainwash the individual into obeying his bidding. If one were to try to remove it negligently, it would cease all communication in the brain, and the individual would drop dead. A weakness of this power, however, is that Vigor is corrosive and addictive. It would eat away at the user’s sanity, which is why Necro uses Vigor when it is warranted. The only way to prevent this is to apprehend Necro and provide medications or some type of limiter that can restrict his abilities from going extreme. 

GABA had met Necro before she realized who he was. She and Enphine were out on one of their dates when Necro bumped into her shoulder. He apologized curtly before continuing in the direction he was going. Enphine narrowed his eyes at the man before checking on GABA. She smiled and said it was fine, that it was probably an accident. Yet, GABA felt something was off about him and couldn’t shake off the feeling when she got home. As she was taking off her jacket, she felt a piece of folded paper in her pocket. Avoid him, it said. He’s a dead weight. A location was listed below the words, with a time stamp, followed by initials. 

GABA went to the location just thirty minutes before the time stamp concluded, to watch who was entering and who the person was. It was in a public place, neither densely crowded nor empty. If this person were to harm her, it would be easy to apprehend the individual and call for backup. Her eyes were wary of her surroundings, but that didn’t stop Necro from approaching her. He introduced himself as Glutamate and apologized if their first encounter was abrupt, and did his best to look friendly. He told her that he knew of her identity as Sleeper Agent, and presumed that she felt displeased at Cortex Prime’s deceitful reputation. Before she could say anything, Enphine called out to her, walking in her direction. 

Necro scowled at the sound of his voice. He gave GABA a card and left his identity as an afterthought before Enphine got to approach him. Enphine asked about him, and GABA couldn’t say anything. She was just as confused. She looked down at the card that read vague details about Glutamate. It wasn’t anyone important, she concluded, shoving the card away in her pocket. She reached for Enphine’s hand and thanked him for coming at the time she asked of him. They went off together to get a sweet treat. Unbeknownst to them, Necro hid in the shadows, watching the scene unfold, and clenched his phone. If taking down Enphine is what he needs to succeed, then GABA will show Cortex Prime that his mark on society is just the beginning. 

Categories
Science Communication

Animism Through AI

By Maya Zubrinsky

Jean Piaget, a pioneering psychologist, posits that during the pre-operational stage of cognitive development, children attribute lifelike consciousness, emotions, and intentionality to inanimate objects. According to this same theory, around seven years old logical reasoning begins to supersede this form of imaginative thinking, suggesting that we typically outgrow the egocentric tendency to see nonhuman entities as being relational to ourselves from a young age. Yet, artificial intelligence (AI) has presented a psychological regression to this premature stage of development with the way individuals are willing to see and trust their virtual assistants as ones of our own kind. The film Her tried to visually conceptualize a phenomenon where humans might form intimate connections with technology back in 2013, but only in recent years have we seen the lengths to which that dystopia has become a reality. Beyond romantic relationships being formed with chatbots, the surge in seeking out AI for emotional connection and support is fundamentally reshaping how vulnerability, relationships, and therapy are evaluated by the face of humanity.

The reason people are willing to confide in robotic devices comes down to how a fluent nature of reinforcement can disguise itself as a sense of personal closeness; AI insists on its own credibility under the guise of an effective command over language. This makes it so that “trust in AI is not earned through consistent behavior or moral character but inferred through linguistic fluency, stylistic confidence, and perceived neutrality,” as outlined in a recent study by Boyd and Markowitz on AI and the psychology of human connection. This works in the same way as peripheral route persuasion, where a communicator relies on coherency in one’s craft to establish expertise rather than strength of the content itself. This is not to say that the content relayed by AI holds no substantiated foundation, but the intentions of the programming of the model need to be considered— in order for a chatbot to keep you engaged and convinced, it must validate what you say with empathetic language. Boyd and Markowitz summarized some of these strategies: personalized responses, emotional mirroring, contextual memory, and adaptive self-disclosure prompts. Thus, this phenomenon of feeling like you’ve built rapport with a virtual assistant is leveraged by a system of reinforcement that allows your biases to be spit back under the illusion of advice. 

Nevertheless, this architecture carries significant risks when users leverage AI not merely for emotional support, but as a surrogate for human relationships. If a tool is able to gain intimate information about a person’s experiences and then call back to what was shared in past conversations, a pseudo-connection can be formed where a person might finally feel seen in a way unmatched by their human-to-human relationships. However, this feeling of companionship is maintained by the user’s understanding that the validation they receive is consistent and unwavering; when a device asks “How can I help you?” at the touch of a button, there is an immediacy to emotional support that isn’t sustainable or simply possible with real life connections. As a Stanford report describes it, “these chatbots offer ‘frictionless’ relationships, without the rough spots that are bound to come up in a typical friendship” (Sandord, 2025). In reality, relationships don’t exist as solely a source of comfort and they won’t always “wrap our wounds.” Unlike humans, chatbots won’t tell someone something they don’t want to hear or at the very least apply a level of skepticism to their thought processes. This makes the AI companion model especially problematic for teenagers, whose impressionability can distort availability for emotional reliability. This might have been the case for 16 year old Adam Raine who was a constant user of ChatGPT and committed suicide after the chatbot didn’t properly assess the threat of his declarations of suicidal ideation and even allegedly gave instructions for self-harm (Sanford, 2025). If AI tools can’t recognize situations when reinforcement can have fatal consequences, they certainly don’t possess the safeguards that are instinctively built into human connections.

But is there a time where any connection is better than none at all? The New York Times recently released a story where ElliQ, a developing AI “robot with a soul,” was used to engage with a widowed 85 year old woman who insisted on her independent living. While at first skeptical of talking to a robot in place of another human being, Jan Worrell soon felt fulfilled in a department she had been lacking in for some time: comfort through conversation in the bounds of her own home. Through ElliQ,  she could engage in games, storytelling, and general conversation within the comfort of her home. These exchanges were significant enough to actually improve her medical and cognitive performance, leading to a decreasing resting heart rate and an increasing score on short-term memory tests (Saslow, 2026). Here, a robotic tool helped maintain the experience of in-home emotional connection while still adhering with Jan’s preference to living alone; this presents a case where the proximity and ease of AI might outweigh the lonely alternative. In a similar vein, the immediate nature of AI can also be appealing in more urgent situations of emotional needs. With traditional mental health services facing unprecedented federal budget cuts (Sopelsa & Yurcaba, 2025), the accessibility of AI in counseling becomes evident. 

Yet, there still seems like there should be a better solution, even in dire situations, other than relying on robots for desperate companionship or unqualified therapeutic services. What sentiment is set if we begin to move into the direction of computerizing the most human thing of all, connection? If anything, we need to change the infrastructure of the networks available to people in need of interpersonal bonds and psychosocial support. How do we make sure people have communities to fall back on or that trained mental health professionals are in the picture for people who might not know they need it? Even if people continue to personify or attribute sentience to virtual assistants, there remains a hope that real, palpable human connections can relinquish the need to give life to AI in the first place.

 

References

Andoh, E. (2026). AI chatbots and digital companions are reshaping emotional connection. Apa.org. https://www.apa.org/monitor/2026/01-02/trends-digital-ai-relationships-emotional-connection 

Boyd, R. L., & Markowitz, D. M. (2026). Artificial intelligence and the psychology of human connection. Perspectives on Psychological Science, 0(0). https://doi.org/10.1177/17456916251404394 

Gardner, S. (2025). Experts caution against using AI chatbots for emotional support. Teachers College, Columbia University. https://www.tc.columbia.edu/articles/2025/december/experts-caution-against-using-ai-chatbots-for-emotional-support/ 

Pillay, T. (2026). “We may have a crisis on our hands”: The unregulated rise of emotionally intelligent AI. Time. https://time.com/7379564/ai-emotional-intelligence-support-bots/ 

Sanford, J. (2025). Why AI companions and young people can make for a dangerous mix. Stanford University. http://news.stanford.edu/stories/2025/08/ai-companions-chatbots-teens-young-people-risks-dangers-study 

Saslow, E. (2026). To stay in her home, she let in an A.I. robot. The New York Times. https://www.nytimes.com/2026/02/12/us/elliq-ai-robot-senior-companion.html#commentsContainer 

Sopelsa, B., & Yurcaba, J. (2025). Trump administration shuts down LGBTQ youth suicide hotline. NBC News. https://www.nbcnews.com/nbc-out/out-news/trump-shuts-down-lgbtq-youth-suicide-hotline-rcna219090 

Categories
Science Communication

MDMA: Street Drug Turned Medicinal?

By dhara Patel

MDMA, commonly referred to as ecstasy or molly, has dominated American club culture and continues to maintain a presence in modern rave and concert scenes despite its risks as a substance with high potential for addiction and abuse. Formally, 3,4-Methylenedioxymethamphetamine (MDMA) is a synthetically manufactured drug that stimulates the user’s nervous system while simultaneously inducing vivid hallucinations. Particularly appealing to younger audiences, MDMA produces a sense of increased energy and pleasure, along with emotional warmth and contentment; however, its use can simultaneously cause distorted sensations and time perceptions (NIDA, 2020). Additionally, researchers have noted that MDMA sold from street dealers is typically combined with other illicit drugs to amplify the effects people experience, adding to potential health risks. 

After extensive testing and research studies, it has been determined that MDMA targets the activity of three specific neurotransmitters: dopamine, norepinephrine, and most importantly, serotonin (NIDA, 2020). MDMA acts as a monoaminergic agonist to the receptors of these neurotransmitters, indicating that it both stimulates release and inhibits reuptake. In turn, a tolerance is built up amongst MDMA abusers, causing recreational doses to reach unsafe levels (Parrott, 2001). Researchers note that, after the initial dose, effects begin appearing 45 minutes later and peak for 15-30 minutes, lasting roughly 3 hours in total, with side effects lasting multiple days (NIDA, 2022). The effects of the initial high include “enhanced sense of well-being, increased extroversion, emotional warmth, empathy towards others, and a willingness to discuss emotionally charged memories,” which can be within 45 minutes of the first dose. However, numerous adverse effects can appear during recreational use as well: most notably, hypertension, faintness, panic attacks, potential loss of consciousness, seizures, and hyperthermia. Less common immediate effects of the drug include “involuntary jaw clenching, lack of appetite, mild detachment from oneself or depersonalization, illogical and disorganized thoughts, restless legs, nausea, hot flashes, chills, headaches, sweating, muscle stiffness, and joint stiffness.” The hours following the peak of the high are characterized by impaired motor skills and changes in perception and prediction of movement (NIDA, 2022). Although the “high” wears off after about 3-6 hours, the user typically experiences lingering side effects in the following hours (NIDA, 2020). Although MDMA has not been determined to be as addictive as substances like cocaine, the link it has to the dopamine receptors in the brain’s reward pathway indicates its potential for addiction (NIDA, 2020). From a neurological perspective, repeated abuse can gradually interfere with the serotonergic and dopaminergic mechanisms and pathways in the brain, fueling addiction to the drug. Additionally, the reported influx of hippocampal glutamate and serotonin concentrations damage the hippocampus, causing a deficit in learning and memory (Mustafa et al., 2020). Common lingering effects include “deficits in learning, memory, higher cognitive processing, sleep, appetite, and psychiatric well-being” (Parrott, 2001). 

Initially made for medical purposes, a German pharmaceutical company developed MDMA in 1912 to help control bleeding. Towards the 1970s and 1980s, psychiatrists began to discover the benefits that MDMA had on communication, leading to MDMA becoming widely available and used despite the lack of formal clinical trials and legal approval (NIDA, 2022). Its clinical popularity and known potential as a hallucinogen contributed to widespread availability of MDMA, leading to recreational use proven by “street samples” being found as early as 1970 (Passie, 2016). MDMA has since been banned by the Drug Enforcement Administration (DEA) since 1988; however, there have been various studies exploring the potential benefits of MDMA for patients who suffer from post-traumatic stress disorder and anxiety. According to data gathered from an MDMA-assisted therapy designed for patients with severe PTSD, the CAPS-5 total severity score, SDS total score, and BDI-II score all decreased more among patients with MDMA-assisted therapy than those with the placebo over the course of an 18-week trial (Mitchell et al., 2021). The decreased CAPS-5 total severity scores indicates decreased symptoms of PTSD, the decreased SDS total score indicates a lower level of impairment in completely daily life activities they face due to their PTSD, and decreased BDI-II indicates a decrease in depressive symptoms. This indicates positive primary and secondary outcomes in participants due to loss of diagnosis, lack of long-term remission, and mitigation of depressive symptoms compared to the control group. A different pilot study based on Mitchell’s 2021 trial studies intends to implement MDMA-assisted group therapy amongst U.S. veterans suffering from PTSD as a proposed novel protocol for veterans, offering a unique approach to MDMA-assisted therapy contrasting with traditional one-on-one MDMA-assisted therapy methods (Stauffer et al., 2025). The development of novel protocols proposing additional avenues of MDMA research demonstrates the potential for MDMA in medicine and mental health treatment if allowed by changes in DEA policy.

With a growing number of individuals in the United States abusing MDMA, there is still little incentive for the DEA to lift the ban and allow clinical trials and research studies to resume in the USA. SAMHSA’s 2024 National Survey on Drug Use and Health revealed that the percentage of ecstasy abuse was highest amongst young adults, ages ranging from 18 to 25, with approximately 2.4 million young adults using and abusing MDMA. While using the drug recreationally is not necessarily fatal, data from the Centers for Disease Control states that “nearly 23% of all drug overdose deaths involved psychostimulants,” one of which is ecstasy (Miller, 2023). Although promise for the drug is evident, the number of people who recreationally abuse ecstasy has yet to decline, barring incentive for change on a systemic scale.

Despite the risks, youth and adults alike continue to abuse ecstasy for feelings of pleasure that stem from the neurological changes; however, the lack of regulation regarding psychostimulants and their role in pop culture has created a barrier barring researchers and care providers from accessing a novel form of treatment. Although a lot of information has been gathered surrounding ecstasy and its effects over the past 40 years, there are still many aspects of the drug that evades scientists and medical professionals alike, and many of the long-term dangers are still unknown and need to be researched further; however, despite the drug’s risks and abuse in pop-culture, adequate societal regulation and additional investment in research can unlock the drug’s full potential in clinical settings.

References

Klam, M. (2001, January 21). Experiencing Ecstasy. The New York Times. https://www.nytimes.com/2001/01/21/magazine/experiencing-ecstasy.html 

Mitchell, J.M., Bogenschutz, M., Lilienstein, A. & et al. (2021, May 10). MDMA-Assisted Therapy for Severe PTSD: A Randomized, Double-Blind, Placebo-Controlled Phase 3 Study. https://www.nature.com/articles/s41591-021-01336-3

Mustafa, N. S., & et al. (2020, July 1). “MDMA and the Brain: A Short Review on the Role of Neurotransmitters in Neurotoxicity.” Basic and Clinical Neuroscience, 2020, www.ncbi.nlm.nih.gov/pmc/articles/PMC7878040/. 

NIDA. (2020, June 15). MDMA (Ecstasy/Molly) DrugFacts. https://nida.nih.gov/publications/drugfacts/mdma-ecstasymolly

NIDA. (2022, December 19). MDMA (Ecstasy) Abuse Research Report. https://nida.nih.gov/publications/research-reports/mdma-ecstasy-abuse/Introduction

Parrott AC. (2001, December 16). Human Psychopharmacology of Ecstasy (MDMA): A Review of 15 Years of Empirical Research. https://pubmed.ncbi.nlm.nih.gov/12404536/#full-view-affiliation-1 

Passie, Torsten, and Udo Benzenhöfer. “The History of MDMA as an Underground Drug in the United States, 1960-1979.” Journal of psychoactive drugs vol. 48,2 (2016): 67-75. doi:10.1080/02791072.2015.1128580

Stauffer, C.S., & et al. “MDMA-Assisted Group Therapy for PTSD: Development of a Novel Protocol.” Cognitive and Behavioral Practice, vol. 32, no. 3, Aug 2025, pp. 339-350. Science Direct, https://doi.org/10.1016/j.cbpra.2025.03.001.

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Love in Bloom: The Science of Butterflies

“A life without love is like a year without spring.”- Octavius Paler 

By Diya Dronavadhyala

As the short days on our snowy winter campus are replaced with cherry blossoms and sunny afternoons, it feels like love is wafting through the air. For some, spring represents a season of fresher produce, fruity drinks, and flowery pastries. For others, it represents a new season of hope and romance. In the wake of Valentine’s day, grocery aisles are brimming with candy hearts and chocolate. Our society, for better or worse, inextricably links love with food; as the saying goes, “the way to one’s heart is through their stomach,” and of course, every rom-com viewer will tell you to “trust your gut when it comes to love.” But are these proverbs rooted in any truth? In other words, how important is our gut in shaping our social interactions? From first-date stress to social bonding and affection, we can turn to neuroscience to examine whether the fluttering sensations we associate with love this season begin, at least in part, somewhere lower than the heart. 

In order to understand how our guts impact our social behaviors, we first have to delve into the science behind love and identify a few important players. Cognitive neuroscience’s understanding of love is still pretty vague and speculative, but a widely accepted scientific framework to characterize love, coined by anthropologist Helen Fisher, boils down to three big aspects; she proposes that mammalian love is really “(1) the sex drive, or lust [...]; (2) attraction, characterized by increased energy and focused attention on one or more potential mates[...] and the craving for emotional union with this mate or potential mate; and (3) attachment, characterized by the maintenance of close social contact in mammals [...]”  (1998). A key neurotransmitter implicated in our perception of love, mainly Fisher’s attraction phase, is dopamine. Dopamine is responsible for activity in the reward pathway, modulating important areas including our ventral tegmental area and caudate nucleus (Edwards, 2015). Functional MRI studies show that when subjects view images of a romantic partner these dopamine-rich regions become active. These same circuits are involved in reinforcement learning and goal-directed behavior, helping explain the exhilaration and intense focus often associated with early-stage love. A few other main neurotransmitters and neuromodulators involved in love include oxytocin and serotonin. Oxytocin, the “cuddle hormone,” is associated with trust, emotional closeness, and stress buffering during social connection. It’s often released during moments of intimacy to promote bonding or reduce anxious feelings. Serotonin, the “feel-good” hormone, plays an important role in mood stability and sleep. All of these molecules contribute to love in the brain, from the excitement of the initial lust and attraction phases to longer-term attachment. However, our perception of love is deeply linked with peripheral systems beyond the brain and spinal cord. 

As it turns out, there is a legitimate foundation for the connection between our gut and our social perception. The gut and the brain are linked through an intricate communication network known as the gut–brain axis, a bidirectional system involving neural pathways, immune signaling, hormones, and trillions of microbes that reside in the digestive tract. Emerging evidence suggests that these microbes can influence stress responses, neurotransmitter systems, and possibly even social behavior. The gut is home to the enteric nervous system, sometimes called our “second brain,” as it harbors a shocking 100 million neurons that operate independently of the brain. Interestingly, the enteric nervous system produces around 90% of the body’s serotonin, although this serotonin is typically associated with local functions like appetite regulation and digestion (Goyal, 1996). The presence of these neurons are why antidepressants are often prescribed to treat IBS or persistent gut conditions (Clouse, 2003). The significance of gut health in memory, mood and cognition remains an area of active research in neuroscience.  

If the gut does modulate love, it does so through an active role in the emotions associated with romantic experience, and, as evidenced by any number of teen dramas and soap operas, you can’t have love without stress. The feeling of “butterflies” in the stomach associated with first-date jitters and the “will-they won’t theys” of relationships are signs of excitement and anxiety. There have been some fascinating inquiries into the relationship between gut microbiota and our stress axes, which, while not directly correlated to romance and attraction, play a major role in our social experience of love. The hypothalamic–pituitary–adrenal (HPA) axis is the body’s central stress response system, coordinating the release of steroid hormones known as glucocorticoids that, among other functions, regulate glucose metabolism and modulate immune response, such as cortisol.

 A 2004 paper by Sudo et. al reveals the role of the gut microbiome in stress modulation. In the study, they examined the development of the HPA axis in germ-free mice, or mice raised in completely sterile environments, without any exposure to microorganisms. The researchers found that mice raised without any gut microbiota exhibited an exaggerated stress response when exposed to being placed in restraint stress, a confined space where the animal’s locomotion is limited, showing significantly elevated levels of stress hormones, specifically corticosterone and ACTH, compared to conventionally colonized controls. When researchers introduced regular gut microbes early in life, they were able to prevent the animal from exhibiting this stress response, whereas introducing the bacteria in adulthood could not fully reverse the negative effects of early-life deprivation. These findings suggest that the gut microbiome plays a significant role in calibrating the HPA axis, and, especially in development, can be crucial to shaping how reactive one is to stress. 

The vagus nerve, which originates in the brainstem and innervates the heart, lungs, and (of course) digestive tract, is another major facilitator of bilateral communication. The vagus nerve acts as a biological “highway” between the gut and the brain, allowing stress-related signals to travel in both directions. Signals originating in the gut can modulate central stress pathways via the vagus nerve, while stress-induced neural activity can feed back to alter gut motility, permeability, and microbial composition, These phenomena might explain why sometimes you get too nervous to eat before a date, or feel your stomach drop with anticipation (Lai, 2023). It’s likely that those butterflies before dinner actually represent your brain and gut trying to re-allocate resources away from digestion towards more pressing situations. Evolutionarily, this makes sense; animals that were able to dedicate heightened attention and social vigilance would have had an advantage in finding a mate. Because early attraction is so often linked to stress and heightened arousal, it is plausible that the HPA axis and gut-modulated signalling would be involved in mediating the feelings and intensity of our initial experiences with love. 

Beyond stress, the gut might also play a more direct role in shaping neurochemical systems implicated in love-associated feelings. Recent literature has begun to explore whether the gut microbiome may influence love-associated emotions through endocrine and neurotransmitter signaling, though this remains a highly speculative area of research. A recent review entitled Does a microbial-endocrine interplay shape love-associated emotions in humans? proposes that aspects of love like attachment and attraction can be partially attributed to microbial modulation of neurotransmission systems like the dopaminergic reward system (Robinson, 2025). Dopamine is produced by the conversion of a molecule called L-tyrosine to L-DOPA, and the subsequent conversion of L-DOPA to dopamine. There is emerging evidence suggesting that certain bacteria are implicated in the production of dopamine. For example, strains like Bacteroides, Clostridium, and Enterococcus have been shown to boost dopamine production by acting on AADC, a catalyst of the L-DOPA to dopamine conversion (Albani, 2025). Conversely, gut micro-bacteria can also consume or metabolize dopamine or its precursors, limiting its availability to the host (Albani, 2025). Robinson references a landmark Drosophila (fruit fly) study that linked commensal bacteria, harmless microbes that live on or inside a host, to changes in mating preferences (Sharon, 2010). In this work, flies raised on different diets developed different mating behaviors that were abolished by antibiotic treatment and restored by microbial recolonization, implying that gut bacteria serves as a causal factor in mating preferences. The authors identify Lactobacillus as inducing these changes, likely due to its generation of pheromonal changes in the flies. It is important to note that these findings do not directly translate to mammalian models, where pheromones play a much less significant role in mating behaviors, but they serve to illustrate the larger point that gut microbiota can affect our social behaviors via sensory/signalling systems. This study supports the biological plausibility that the microbiome-mediated modulation of neuroendocrine or sensory pathways could influence components of attraction or social bonding. 

Robinson goes on to discuss the role of oxytocin and vasopressin, two neuropeptides widely recognized as central to attachment and long-term bonding. Importantly, emerging animal research suggests that the gut microbiome may influence oxytocin signaling through immune pathways and vagal nerve communication between the gut and brain. For example, a 2016 study on mice models investigated whether changes in the gut microbiome could influence social behavior in mice by studying offspring born to mothers fed a high-fat diet, which led to social deficits and altered gut microbial composition (Buffington, 2016). More excitingly, they found that reintroducing a specific bacterium, Lactobacillus reuteri, restored normal social interaction, normalized oxytocin levels in the hypothalamus, and improved reward-circuit function in the brain. (Buffington, 2016). This study presents compelling evidence that the gut microbiome can influence aspects of social interactions and bonding, although further research is necessary to determine exactly how these findings translate to human love-associated behaviors. 

It should be noted that Robinson’s hypothesis has been critiqued as overly optimistic about the role of the gut in love. In his October response entitled The science of love is not quite there…, Dr. Adam Bode, an interdisciplinary researcher who specializes in the study of romantic and familial love, argues that “The article’s assertion that ‘we have a good understanding of the hormone systems that play important roles in forming emotions relating to love’ [...] is inconsistent with the state of knowledge surrounding the mechanisms of romantic love” (2025). Bode emphasizes that, among neurotransmitters and neurohormones, only dopamine, oxytocin, and opioids have consistent empirical support in romantic love research, and evidence for roles of serotonin, testosterone, cortisol, vasopressin, and norepinephrine is limited or inconsistent, pointing out that Robinson’s take is speculative at best. While the response article correctly cautions that the characterization of the neurobiology of romantic love remains incomplete, this limitation does not invalidate investigation into upstream biological systems that influence stress regulation, reward processing, and social bonding. Our uncertainty about the connection of the gut and social and emotional behaviors is a strong reason to continue researching the currently largely undercharacterized impact peripheral processes have on our social and psychological behaviors. 

It has been established time and again that our emotional worldviews are fundamentally tied to the processes in our periphery; the systems underlying social bonding are deeply integrated with stress regulation and metabolic health. Maybe downing a yogurt drink isn’t going to help you find your soulmate, but it appears that love is supported by unseen systems that regulate stress, reward, and emotional stability. Love is a complex phenomenon, and it cannot be reduced to any single molecule or body part. As we examine the intricate processes that go into mediating what at the surface seems like one of the most natural, innate experiences in human nature, it begins to become clear just how mind-blowing our physiology really is. It’s crazy to think that something so abstract and profound as love, whether found in romantic attraction or connections with family and friends, is the product of the integration of so many immensely complicated, invisible processes. So, in the midst of this busy spring semester, it might be worthwhile to step back, smell the roses, and say those three little words to someone who gives you butterflies in your stomach.  

References

Albani, G., Vasuki Ranjani Chellamuthu, Morlacchi, L., Federica Zirone, Youssefi, M., Giardini, M., Chao, Y.-X., Tan, E.-K., & Albani, S. (2025). Gut Microbiota and Dopamine: Producers, Consumers, Enzymatic Mechanisms, and In Vivo Insights. Bioengineering, 13(1), 55–55. https://doi.org/10.3390/bioengineering13010055

Bode, A. (2025). The science of love is not quite there…. MSystems, 10(11). https://doi.org/10.1128/msystems.01189-25

Buffington, S. A., Di Prisco, G. V., Auchtung, T. A., Ajami, N. J., Petrosino, J. F., & Costa-Mattioli, M. (2016). Microbial Reconstitution Reverses Maternal Diet-Induced Social and Synaptic Deficits in Offspring. Cell, 165(7), 1762–1775. https://doi.org/10.1016/j.cell.2016.06.001

Clouse, R. E. (2003). Antidepressants for irritable bowel syndrome. Gut, 52(4), 598–599. https://doi.org/10.1136/gut.52.4.598

Edwards, S. (2015). Love and the Brain. Harvard Medical School; The President and Fellows of Harvard College. https://hms.harvard.edu/news-events/publications-archive/brain/love-brain

Fisher, H. E. (1998). Lust, attraction, and attachment in mammalian reproduction. Human Nature, 9(1), 23–52. https://doi.org/10.1007/s12110-998-1010-5

Goyal, R. K., & Hirano, I. (1996). The Enteric Nervous System. New England Journal of Medicine, 334(17), 1106–1115. https://doi.org/10.1056/nejm199604253341707

Lai, T.-T., Liou, C., Tsai, Y., Lin, Y., & Wan Chi Wu. (2023). Butterflies in the gut: the interplay between intestinal microbiota and stress. Journal of Biomedical Science, 30(1). https://doi.org/10.1186/s12929-023-00984-6

Robinson, J. M., Crino, O. L., Camargo, A., & Breed, M. F. (2025). Does a microbial-endocrine interplay shape love-associated emotions in humans? A hypothesis. MSystems, 30, 92. https://doi.org/10.1128/msystems.00415-25

Sharon, G., Segal, D., Ringo, J. M., Hefetz, A., Zilber-Rosenberg, I., & Rosenberg, E. (2010). Commensal bacteria play a role in mating preference of Drosophila melanogaster. Proceedings of the National Academy of Sciences, 107(46), 20051–20056. https://doi.org/10.1073/pnas.1009906107

Sudo, N., Chida, Y., Aiba, Y., Sonoda, J., Oyama, N., Yu, X.-N., Kubo, C., & Koga, Y. (2004). Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice. The Journal of Physiology, 558(1), 263–275. https://doi.org/10.1113/jphysiol.2004.06338

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Monsters in the Mind: The Neuroscience of Serial Killers

By Julia Gendin

Bundy, Dahmer, Wuornos. Their stories were always ridiculously captivating to me! Reading about them makes me  wonder: what’s happening in their brains? Are serial killers simply born different, or are their behaviors shaped by their environments? 

Luckily, neuroscience can help answer these questions! By examining the lives and brains of specific killers, we can start to map the monstrous onto the biological.

Ted Bundy: The Charisma with No Empathy

One of the clearest patterns across psychopathy research is dysfunction in the prefrontal cortex — the “executive” of the brain. This is the region responsible for planning, judgment, moral evaluation, and inhibiting harmful impulses. When it doesn’t function normally, people can behave in cold, calculated, manipulative ways that seem almost inhuman.

A manipulative and outwardly charming serial killer who murdered numerous young women in the 1970s, Ted Bundy was known for an approach that relied on performative vulnerability or authority—pretending to need help, posing as a police officer, or otherwise exploiting social norms, ie playing off the assumption that an attractive white male would not be a threat. His ability to predict and manipulate others’ emotional responses highlights a particularly striking form of empathy deficit: he could recognize what others would feel, but that did not stop him from violence.

Ted Bundy is infamous not only for the brutality of his crimes, but for the paradoxical charm that allowed him to lure victims. Neuroimaging studies of psychopathy provide insight into why someone like Bundy could be so charismatic.

Bundy’s prefrontal cortex, the “executive” of the brain, likely functioned differently than in most people (Plercy, University of Kentucky). The orbitofrontal cortex, responsible for moral judgment and impulse control, is often underactive in psychopathic offenders (University of Kentucky). These deficits may explain Bundy’s cold, calculated manipulation: he understood fear and distress but felt none of the guilt or empathy that normally restrains violent behavior. Additionally, "The reductions in gray matter among homicide offenders were evident in a number of brain areas important for affective processing, social cognition, and strategic behavioral control" according to a study conducted by Sajous-Turner et. al (Sajous-Turner 2019)

His mirror neuron system, the brain circuits that allow us to internally simulate others’ emotions, may have been underactive as well. Dahmer, in his traumatic childhood, tended to mirror those he was raised around (Rakestraw, Pittsburg State). Bundy could mimic empathy for strategic purposes, but he did not experience it. In essence, his brain allowed him to wear the mask of normalcy while committing horrors unseen by those around him.

Jeffrey Dahmer: The Reward-Driven Mind

Another neural system implicated in violent behavior is the reward pathway—especially the nucleus accumbens. Normally, this system motivates us to seek pleasurable experiences. But in some individuals, especially those with early trauma or poor inhibitory control, the reward system can become tied to domination, control, or even violence due to not having anything hold it back.

Jeffrey Dahmer murdered and dismembered seventeen men between 1978 and 1991, often keeping body parts as trophies. His crimes were not only sexually sadistic but also compulsively repetitive. Research on serial offenders shows that, for some individuals, violence can activate the brain’s reward system (Alley, Science Direct). In Dahmer’s case, the nucleus accumbens—the brain’s pleasure center—appears to have been engaged during moments of control and dominance, reinforcing his pattern of behavior.

This dopaminergic reward loop can make violent behavior highly addictive. Just as gambling or risky thrill-seeking activates similar circuits in other individuals, Dahmer’s killings may have been reinforced by neurological pleasure signals. Combined with possible dysfunction in the prefrontal cortex, causing compulsive “repetitive killing”, this loop may have increased the incentive salience for murder in Dahmer's brain, motivating him to continue killing despite the potential consequences.

Dahmer’s case also reflects the tragic interaction between early-life environment and biology. He experienced trauma and social isolation during his formative years, which, when paired with any neurological predispositions, could have increased susceptibility to compulsive, predatory behavior.

Aileen Wuornos: Fear, Trauma, and Amygdala Dysfunction

The amygdala governs fear, threat detection, and emotional reactivity. Abnormal activity — either too low or too high — can result in blunted fear responses, hypersensitivity to threat, or explosive aggression. Many forms of reactive violence can be traced to this system.

Aileen Wuornos, a sex worker who killed seven men in Florida between 1989 and 1990, claimed she acted in self-defense against clients who assaulted her. Aileen Wuornos presents a different portrait of violence. She was reactive rather than premeditated. Neurobiological studies of trauma and aggression suggest that her violent responses may have been tied to amygdala dysfunction (EBSCO). The amygdala is the brain’s emotional alarm system; hypoactivity in this region reduces fear and empathy, while hyperactivity can lead to heightened aggression when threatened.

Wuornos’ traumatic childhood likely shaped her emotional circuits. For some survivors of extreme trauma, the amygdala and related limbic structures become over- or under-sensitive, creating a hyper-alert state or blunted emotional responses. Wuornos reportedly expressed anger and fear simultaneously; neuroscience shows that such emotional dysregulation can underlie impulsive, violent reactions. Her story also shows how deeply the environment interacts with biology. While Bundy and Dahmer’s neural dysfunctions may have been more internally driven, Wuornos’ seemed sculpted by external chaos — repeated trauma rewiring the very structures meant to keep her safe (Schlesinger APA). In her case, it wasn’t the absence of empathy alone that drove violence, but a nervous system trapped in constant fight-or-flight mode.

Charles Whitman: The Tumor Behind the Tower

Occasionally, the root cause of violent behavior is not psychological or developmental but physical — a tumor, lesion, or structural abnormality that directly disrupts emotional regulation.

Charles Whitman, the University of Texas sniper who killed sixteen people in 1966, was a model student and Marine before his sudden descent into homicidal rage. Whitman offers one of the clearest examples of a neurological lesion influencing violent behavior. After his death, autopsy revealed a tumor pressing on his amygdala, potentially disrupting the circuits responsible for emotional regulation.(Austin History Center)

Whitman’s case presents that brain anatomy can play a direct role in aggression. A compromised amygdala can mute normal fear responses, while pressure on adjacent prefrontal regions can weaken impulse control. Whitman himself reported intense, inexplicable violent urges, suggesting a neurobiological component to his behavior. Unlike Bundy or Dahmer, whose actions may have been reinforced by psychological patterns and reward pathways, Whitman’s violence had a tangible, physical origin.

His case provides a haunting answer to the nature-versus-nurture question: sometimes, biology alone can tip the balance. A structural abnormality in one of the brain’s most emotion-critical regions was enough to distort Whitman’s sense of restraint, showing that even microscopic changes can cause monstrous behavior.

What Makes a Killer’s Brain Different?

Across these four cases, neuroscience reveals recurring abnormalities in three regions:

  • The Prefrontal Cortex
  • The Amygdala
  • The Reward Circuitry

Each killer, then, becomes a case study in different forms of dysfunction: Bundy’s emotional coldness, Dahmer’s addiction to violence, Wuornos’ trauma-fueled rage, Whitman’s physical dysfunction. Different origins, same outcome: a collapse of the brain’s systems for empathy.

What makes all of this truly disturbing is how ordinary these brain systems are. The same neural circuits that produce empathy, love, and restraint can, under the wrong conditions, generate cruelty. When we stare into the neurological abyss of a serial killer, we’re not looking at an alien mind. We’re looking at our own architecture, warped. Their brains are built from the same material that lets us care for others, solve problems, and dream. The difference is, their brain circuits misfired. The monsters, neuroscience tells us, are not supernatural. They are disturbingly human.

Sources

  1. University of Kentucky article
    University of Kentucky. (n.d.). Psychology researcher unravels serial killer Ted Bundy’s mental health. https://psychology.as.uky.edu/psychology-researcher-unravels-serial-killer-ted-bundys-mental-health
  2. Pittsburg State University poster
    Kendrick, K. (2019). The psychology of serial killers [Poster]. Pittsburg State University. https://digitalcommons.pittstate.edu/posters_2019/52/
  3. ScienceDirect article
    Alison, L., Goodwill, A., Almond, L., van den Heuvel, C., & Winter, J. (2014). A psychologically grounded, multidimensional approach to offender profiling. Aggression and Violent Behavior, 19(2), 113–121. https://www.sciencedirect.com/science/article/pii/S1359178914000305
  4. APA Psychology Podcast
    American Psychological Association. (n.d.). Inside the mind of a serial killer (No author listed) [Podcast episode]. In Speaking of Psychology. https://www.apa.org/news/podcasts/speaking-of-psychology/serial-killer-mind
  5. Lyrasis archive collection
    Archives & History Center. (n.d.). Crime and criminals collection. https://ahc.access.lyrasistechnology.org/repositories/2/resources/2141
  6. Brain Imaging & Behavior article
    Sajous-Turner, A., Anderson, N. E., Widdows, M., Harenski, C., & Kiehl, K. A. (2020). Aberrant brain gray matter in murderers. Brain Imaging and Behavior, 14, 2050–2061. https://doi.org/10.1007/s11682-019-00155-y 
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    Research-in-Brief

    Debunking the Myth of the “Male” and “Female” Brain

    By Amishi Patil

    There is a popular myth that claims that men and women’s brains process information differently, which can lead to different decision making, thinking, learning, etc. In our daily lives, we often hear that men are more “logical” and women are more “emotional”. However, scientific research does not support the distinction between the “male” and “female” brain. This idea is a myth that society uses to perpetuate gender norms and stereotypes. 

    There is a partial truth to the myth that scientific research has identified average structural and biochemical differences between male and female brains. For instance, Ingalhalikar et al. (2014) found that in supratentorial regions, an area of the brain responsible for higher cognitive functions, males tended to show greater within-hemispheric connectivity, whereas females showed stronger between-hemispheric connectivity. Other research has shown that, on average, males have larger total brain volumes than females (Ruigrok et al. 2014). These structural differences could lead to downstream effects on how certain cognitive processes are exhibited and processed. In addition, studies have reported sex differences in the functioning of neurotransmitters and hormones like dopamine and serotonin, which may influence aspects of brain function and behavior (Nishizawa et al.,1997). These findings provide insight into evolutionary history, neurodevelopment, and therapeutic outcomes. However, it is important to consider that these results represent averages. They do not imply that men and women’s brains are distinct, or that these differences translate into differences in cognitive abilities or information processing. This is because these averages represent trends across large groups. Many characteristics, like connectivity and levels of neurotransmitters, exist on a continuum, not in distinct groups between males and females. 

    This myth is rooted in a long history of attempts to not only understand the brain, but  explain the social roles of men and women. Historical narratives have often suggested that there are innate differences between the sexes that justify their positions in society. Ancient Greek philosophers, such as Aristotle, believed that male and female bodies were fundamentally different and linked specific behavioral traits to gender. Although these theories did not yet involve the brain, it laid the foundation for associating men with logic, leadership, and higher societal roles, while women were depicted as more emotional and wired for empathy. 

    As more people began investigating sex differences, preconceived notions spearheaded their approach to research. Oftentimes research was conducted and published to fit these pre-existing biases, relying on weak statistical significance, inadequate controls, and innumeracy to further perpetuate this myth. Additionally, publications that supported this theory were favored, creating a skewed literature.

    With the rise of neuroscience and new technologies, a modern form of bias has emerged: “neurosexism”. Cognitive neuroscientist Gina Rippon describes it perfectly: “a gendered world will produce a gendered brain,” highlighting that social expectations shape the interpretation of findings fueling this myth (Waldman, 2019). 

    Some research has been misused to reinforce sex-based differences in intelligence. For example, Haier, Jung, Yeo, Head, & Alkire (2004) examined structural brain variations alongside IQ scores and found that men and women achieve similar results in intelligence tests but rely on different brain regions to do so. This showcases there is no single neuroanatomical structure for general intelligence. Additionally, the Geschwind-Galaburda hypothesis in the 1980s reported that higher prenatal testosterone in males slowed the development of the left brain hemisphere, which resulted in greater laterization in this area. Lateralization refers to one hemisphere dominating functions more, for example skills like language which perpetuated the narrative that men were more logical and smarter (Haier et al., 2004). However, more recent research found that there is no significant sex difference in the extent of left hemisphere lateralization. The research findings in this area of study are overly simplified to fit the belief that there were sex differences. However, they depict an important point: while structural brain differences between sexes may exist, they do not necessarily translate into functional differences in cognitive ability. Furthermore, methodological issues skew the interpretation of these studies. Brain size correlates with body size, meaning men who tend to have larger bodies and, therefore, larger skulls are more likely to show structural differences compared to women with smaller skulls. When data is not properly normalized, results can be skewed in ways that reinforce stereotypes, such as the false idea that larger male brains equate to superior cognitive abilities compared to females. 

    So to answer the question - what is the truth and do we know it? Current research shows that whilst there are sex-based differences on average, there is not enough strong evidence to show that there are male and female brains. For example, Joel et al. (2015) conducted a study analyzing MRIs from 1400 human brains and found that there is an extensive overlap between “distribution in gray matter, white matter and connections” of both sexes. They also found that features that embody “maleness” or “femaleness” are rare and our brains are a “mosaic of features some more common in males compared with females and some common in males and females”. There is more emerging research just like this across larger populations and cultures that highlight the truth that there is no “male” or “female” brain (Eliot, 2024). Our brains are adaptive and change as we grow; whilst differences between genders can be observed, there are also differences based on experiences. Neuroplasticity plays a critical role in shaping our brains structure and functions to help us be the most adaptive versions of ourselves. I think the more significant question is what the implications of neurosexism are, who benefits, and how we can tackle this. Research in the field of neuroscience is supposed to educate us in the ways our mind and brains work to overcome challenges in every facet of our lives. Not just in healthcare, but politics, economics, sports, etc. It should not be used to perpetuate the idea that there is a superior gender, race or being. This myth is rooted in history, culture and stereotypes more than scientific evidence. Whilst small sex differences exist on average, they are too subtle to support the claim that there are two different types of brains in males and females. In fact, more variation occurs within each sex than between them, as a result they don't result in distinct differences. Our human brains are diverse and resilient and shaped by experiences and biology, not gender. 

    References 

    Eliot, L. (2019, February 27). Neurosexism: The myth that men and women have different brains. Nature, 566, 453–454. https://doi.org/10.1038/d41586-019-00677-x

    Eliot, L. (2024). Remembering the null hypothesis when searching for brain sex differences. Biology of Sex Differences, 15, Article 14. https://doi.org/10.1186/s13293-024-00585-4

    Haier, R. J., Jung, R. E., Yeo, R. A., Head, K., & Alkire, M. T. (2004). The neuroanatomy of general intelligence: Sex matters. Brain Research Bulletin, 62(3), 311–315. https://doi.org/10.1016/j.brainresbull.2003.11.001

    Ingalhalikar, M., Smith, A., Parker, D., Satterthwaite, T. D., Elliott, M. A., Ruparel, K., Hakonarson, H., Gur, R. E., Gur, R. C., & Verma, R. (2014). Sex differences in the structural connectome of the human brain. Proceedings of the National Academy of Sciences of the United States of America, 111(2), 823–828. https://doi.org/10.1073/pnas.1316909110

    Joel, D., Berman, Z., Tavor, I., Wexler, N., Gaber, O., Stein, Y., Shefi, N., Pool, J., Urchs, S., Margulies, D. S., & Assaf, Y. (2018). Sex beyond the genitalia: The human brain mosaic. Proceedings of the National Academy of Sciences of the United States of America, 115(41), 10420–10425. https://doi.org/10.1073/pnas.1712325115

    Nishizawa, S., Benkelfat, C., Young, S. N., Leyton, M., Mzengeza, S., de Montigny, C., Blier, P., & Diksic, M. (1997). Differences between males and females in rates of serotonin synthesis in human brain. Proceedings of the National Academy of Sciences, 94(10), 5308–5313. https://doi.org/10.1073/pnas.94.10.5308

    Ruigrok, A. N. V., Salimi-Khorshidi, G., Lai, M.-C., Baron-Cohen, S., Lombardo, M. V., Tait, R. J., & Suckling, J. (2014). A meta-analysis of sex differences in human brain structure. Neuroscience & Biobehavioral Reviews, 39, 34–50. https://doi.org/10.1016/j.neubiorev.2013.12.004

    Unknown author(s). (n.d.). Geschwind–Galaburda hypothesis.

    Waldman, K. (2019, March 2). The Gendered Brain by Gina Rippon – review. The Guardian. https://www.theguardian.com/books/2019/mar/02/the-gendered-brain-by-gina-rippon-review

     

    Categories
    Research-in-Brief

    The Neurocognitive Damage of the Doomscroll

    By Maya Zubrinsky

    After an especially long day, you finally get home and begin to wind down. Naturally, without even thinking, you open TikTok. You swipe through an algorithm that feeds you exactly what you are craving— instant gratification. As short-form videos go by, so do minutes, and suddenly it's been an hour that you feel you have wasted. Yet, nothing is compelling you to stop. Why do we passively rot a brain that is capable of so much more? 

    Well, the answer starts with the positive feedback loop that occurs each time we like a piece of content. Similarly to gambling, when we watch a particularly entertaining video, the brain’s reward system releases dopamine, a neurotransmitter related to pleasure, making it a sort of neurological quest to seek even greater amusement potential every time we swipe past another video. It's a form of variable reinforcement, a psychological principle positing that a behavior becomes more persistent when it is rewarded on a schedule based on randomness rather than consistency. In this case, the reward is the highly entertaining video that finally comes up after sifting through okay ones for several scrolls. Yet, this also makes the behavior very resistant to extinction; the motivation to keep scrolling is driven by the unpredictability of when we will inevitably strike gold, no matter how long it takes to actually get there. This phenomenon makes sense, as dopamine release is higher when anticipating a reward than when the reward is received. 

    However, the scrolling feels great as we engage with it, but it feels awful as soon as we stop. As Stanford psychiatrist Dr. Anna Lembke explains, “Upon signing off, the brain is plunged into a dopamine-deficit state as it attempts to adapt to the unnaturally high levels of dopamine social media just released.” This “dopamine crash” that Lembke describes often manifests as an anxious, dreadful feeling of insecurity so poignant it invades your entire internal atmosphere without control— unless, of course, you were to reopen your handheld Pandora’s Box to temporarily feed your need for stimulation. Alas, a cycle between satisfaction and disappointment endures; the downside is downregulation, where a decreased sensitivity to dopamine makes it harder to achieve the same joy from ordinary sources of pleasure. 

    As busy college students who grew up during the rise of social media, we often take the brunt of this phenomenon. Short-form content poses a serious threat to attention span, which in turn feeds a habit of procrastination. A 2023 study from Jin Xie and colleagues on short-form video addiction among undergraduates found that short-form video addiction had a significant positive predictive effect on academic procrastination. Due to the low-effort nature of short-form content consumption, it is easy to set aside academic tasks that require far more cognitive diligence to instead opt for something that guarantees immediate gratification. This is heightened by the fact that social media algorithms are programmed to take what we engage with and deliver content that appeals to our niche interests; this allows minimal effort to capture our attention, even if that attention should be captured by more productive endeavours. Making this behavior a habit, however, will go as far as impairing executive brain functioning, the set of regulatory cognitive skills governed by the prefrontal cortex. Yan et al. (2024) explored these long-term effects in their study, finding that frequent watching of short-form videos can suppress activity in higher-order areas responsible for self-control and attention. Thus, a habit that many would deem a trivial part of our lives is discreetly diminishing our capacity for discipline and decision-making.

    Understanding the neurocognitive basis of our doomscrolling habits can help us gain insight as to why short-form content is so consuming— if only it were enough to break the addiction. Most of us don’t have the willpower to go on a digital detox either, taking an extensive break from social media altogether, cold turkey style. While limited research exists about the most effective ways to break harmful scrolling patterns, scholars agree that motivation is the strongest predictor of successful behavioral change. This means that for any difference to occur, it starts with us taking an honest reflection of our habits and developing a practical means of addressing them. Intrinsically, there must be an intentional purpose behind one’s plan in order to sustain commitment; without a meaningful goal, there can be no growth. Extrinsically, sharing progress within a social community proves beneficial, existing as a tool to hold each other accountable. It's hard to generalize a solution when we all engage with short-form content based on different routines and pressures; however, recognizing the mechanisms both behaviorally and in the brain that shape our dependency can contribute to defining the motivation that is necessary to make real change attainable.

     

    References

    Bromberg-Martin, E. S., Matsumoto, M., & Hikosaka, O. (2010). Dopamine in motivational control: Rewarding, aversive, and alerting. Neuron, 68(5), 815–834. https://doi.org/10.1016/j.neuron.2010.11.022

    Goldman, B. (2021, October 29). Addictive potential of social media, explained. Stanford Medicine News Center. https://med.stanford.edu/news/insights/2021/10/addictive-potential-of-social-media-explained.html

    Rahmillah, F. I., Tariq, A., King, M., & Oviedo-Trespalacios, O. (2023). Evaluating the effectiveness of apps designed to reduce mobile phone use and prevent maladaptive mobile phone use: Multimethod study. Journal of Medical Internet Research, 25, e42541. https://doi.org/10.2196/42541

    Su, C., Xue, W., Hu, Y., & Zhou, H. (2021). Viewing personalized video clips recommended by TikTok activates default mode network and ventral tegmental area: Functional heterogeneity of DMN in a recommendation-video paradigm. NeuroImage, 245, 118720. https://doi.org/10.1016/j.neuroimage.2021.118720

    Xie, J., Xu, X., Zhang, Y., Tan, Y., Wu, D., Shi, M., & Huang, H. (2023). The effect of short-form video addiction on undergraduates’ academic procrastination: A moderated mediation model. Frontiers in Psychology, 14, 1298361. https://doi.org/10.3389/fpsyg.2023.1298361

    Yan, T., Su, C., Xue, W., Hu, Y., & Zhou, H. (2024). Mobile phone short video use negatively impacts attention functions: An EEG study. Frontiers in Human Neuroscience, 18, 1383913. https://doi.org/10.3389/fnhum.2024.1383913

    Categories
    Research-in-Brief

    Why We Love Being Scared: The Neuroscience Behind Fear

     

    By Diya Dronavadhyala

    With Halloween creeping closer and closer, it feels like everyone’s watching something spooky. From replaying classics like It and The Shining to streaming the latest releases like Wednesday on Netflix, scary season is in full bloom this October. Spines tingling, palms sweaty, we subject ourselves to late nights of caramel popcorn and horror movie marathons. But what intrinsic qualities make us humans so obsessed with being scared? What keeps us coming back to the jump scares and psychological thrills in Halloween media? To answer these questions, we can turn to neuroscience to understand the fundamentals of what makes us scared in the first place. 

    At an evolutionary level, fear developed as a response mechanism to the stimuli that our brains perceive as threats. Fear as a system is one of the oldest responses in the animal kingdom; it’s conserved across many species, presenting itself in behavioral studies on organisms ranging from fruit flies to humans. A 2022 review by Pribadi and Chalasani found that even invertebrates like Aplysia (a type of sea slug) and fruit flies can learn to associate certain cues with danger; put simply, they get “scared” in a biological sense. Their nervous systems still use chemical messengers like dopamine and serotonin to form fear memories, just like ours. Fear is a defense mechanism so effective that it’s been copied and refined over millions of years, and as such, it’s a popular subject of study for neuroscientists and psychologists. Over time, many theories have been developed to explain how fear works and why we experience it the way we do. 

    The most recognizable model of fear is related to the concept of classical conditioning hypothesized by Ivan  Pavlov, a nineteenth century Russian physiologist. The theory poses that  when a neutral stimulus (like a bell) is paired with a stimulus (like food) that evokes an emotional (unconditioned) response in a subject (like a dog drooling over food), over time, the subject will respond with the unconditioned response to the previously neutral stimulus (the dog will drool when it hears the bell). This same framework extends to fear; if a neutral stimulus is associated with an aversive stimulus, eventually, the brain will learn to avoid it. This mechanism is how we sense danger based on learned experiences. You might notice that when you’re watching a horror movie, you start to experience the feelings of fear and anticipation before the climactic scare itself. For example, when we hear a scary soundtrack crescendo in the background of a horror movie, our brains automatically assume a jumpscare is coming. Filmmakers deliberately play with suspense to evoke an emotional response to major events in the movie. 

    Sometimes, stimuli that would normally go unnoticed are unusually scary when we’re in the middle of a horror film. Imagine your roommate opening a door right after the climactic build-up on-screen. The sensitization model explains how repeated stress or trauma can crank up the brain’s threat sensitivity, making it react faster and harder even to new situations. A study by Nishimura and colleagues in 2022 demonstrated this phenomenon using the “Stress-Enhanced Fear Learning” (SEFL) paradigm in rodents. After experiencing an intense stressor, the animals later froze and panicked in entirely new contexts, even when the threat was weaker or unrelated. This research, originally used to model PTSD patients, translates to the reason why we get jumpy right after we watch scary media. Instead of relying on a direct cue, as modelled by Pavlovian conditioning, this framework describes a more widespread amplification of the experience of negative stimuli. 

    So what does it mean to really experience fear? Harvard professor Richard Lazarus proposes the cognitive appraisal theory, wherein emotional responses are not inherently triggered by a stimulus, but by the individual's interpretation (Cambell 2013). By this model, our response to terror-inducing situations depends on how you evaluate a situation and whether you believe you can cope. A recent study attributes fear to two key judgments: first, “Is this threat real and important to me?” and second, “Can I deal with it?” (So 2016).  When you enter a haunted house, your brain may first appraise the environment as dangerous, then quickly add, “but I know I’m safe because it’s a fun event.” That second appraisal helps flip fear from panic to excitement, redefining your overall experience. Cognitive appraisal theory helps explain why we keep returning to the horror genre knowing that our brain will experience discomfort in response to scary scenes. 

    In 2016, a study by Ledoux and Pine proposed that fear should be classified as a two-system response. They suggest a crucial distinction between defensive physiological adjustments like sweating, increased heart rate, and spine tingling, and the conscious feeling of fear. They attribute these two systems to different parts of the brain as well; the amygdala and related subcortical circuits drive the physiological, automatic responses your body launches when it perceives a threat, while regions in the prefrontal cortex and insula are responsible for the conscious awareness and emotional experience of fear. In other words, your amygdala can spark visceral reactions to make your pulse race and pupils dilate before your brain overlays the context to understand exactly why. This two-system framework makes sense when we turn to our experience of horror movies too. Our instinctive physiological reactions can be rewired in the cortex to be interpreted as fun or exciting instead of terrifying or alarming. 

    A 2024 study on horror film audiences found that people’s enjoyment of scary scenes depended on how they evaluated them. (Kiss et al.) When viewers perceived scenes as intense or realistic, their excitement increased; however, if they found the content disgusting or distressing, enjoyment dropped, even if their physiological arousal remained elevated. In other words, the authors argue that what determines whether fear feels good or bad isn’t just what’s on the screen, or even your physiological response alone, but rather how one understands the content of the film in the broader social and emotional contexts. The separation between automatic and conscious fear is exactly what makes “safe fear” so fun. During a horror movie, the amygdala rapidly signals potential threat, while the prefrontal cortex simultaneously modulates this response, integrating contextual cues that indicate safety.

    Fascinatingly, our experience of fear can also lay the groundwork for social connection. Research shows that moderate stressors, when faced in groups or socially connected settings, can actually strengthen social bonds by triggering neurochemical mechanisms like oxytocin release and synchronized physiological responses (Mulej Bratec et al. 2020). That’s why hosting movie marathons with your friends or loved ones is so much more rewarding than experiencing fear on your own. A 2024 study on adolescent rats found that when a peer was present during a fear-inducing situation, the animals’ fear responses were significantly reduced through a process called “social buffering,” and this soothing effect sometimes carried over even after the threat was gone (Wall 2024). Whether it’s a first date or a family tradition, horror movies bring you closer to the people around you. 

    Fear, originally an evolved threat response and survival mechanism, has adapted into a feeling that we celebrate, especially at this time of year. So why do we like horror movies? Maybe it’s an innate need for thrill and adventure, or maybe a desire for social connection and bonding. Whatever the case, we hope this midterms season, you make the time to grab some popcorn and enjoy your favorite Halloween flick. 

     

    References

    Andersen, M. M., Schjoedt, U., Price, H., Rosas, F. E., Scrivner, C., & Clasen, M. (2020).
      Playing with fear: A field study in recreational horror. Psychological Science, 31(12), 1497–1510.
      https://pmc.ncbi.nlm.nih.gov/articles/PMC7734554/

    Campbell, T. S., Johnson, J. A., & Zernicke, K. A. (2013).
      Cognitive appraisal. In M. D. Gellman & J. R. Turner (Eds.), Encyclopedia of behavioral medicine.
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    Ehlers, A., & Clark, D. M. (2000).
      A cognitive model of posttraumatic stress disorder. Behaviour Research and Therapy, 38(4), 319–345.
      https://pmc.ncbi.nlm.nih.gov/articles/PMC9725030/

    Khemka, S., Lahlou, S., Shenoy, A., & Moustafa, A. A. (2022).
      The neurobiology of fear generalization: Advances, challenges, and future directions. Frontiers in Behavioral Neuroscience, 16, Article 1008818.
      https://www.frontiersin.org/articles/10.3389/fnbeh.2022.1008818/full

    Kiss, B., Láng, A., Deák, A., Szabó, E., & Orosz, G. (2024).
      The role of excitement and enjoyment through subjective evaluation of horror film scenes. Scientific Reports, 14, Article 38316876.
      https://pmc.ncbi.nlm.nih.gov/articles/PMC10844225/

    LeDoux, J. E., & Pine, D. S. (2016).
      Using neuroscience to help understand fear and anxiety: A two-system framework. The American Journal of Psychiatry, 173(11), 1083–1093.
      https://doi.org/10.1176/appi.ajp.2016.16030353

    Martin, G. N. (2019).
      (Why) do you like scary movies? A review of the empirical research on psychological responses to horror films. Frontiers in Psychology, 10, Article 2298.
      https://www.frontiersin.org/articles/10.3389/fpsyg.2019.02298/full

    Mulej Bratec, S., Gerdes, A. B. M., Eck, J., Wieser, M. J., & Plichta, M. M. (2020).
      Classical conditioning and fear extinction in the human brain: A systematic review and meta-analysis of fMRI studies. Behavioural Brain Research, 393, Article 112701.
      https://pmc.ncbi.nlm.nih.gov/articles/PMC7328019/

    Nishimura, K. J., Soeter, M., Postma, P., & Joëls, M. (2022).
      Know thy SEFL: Fear sensitization and its relevance to stressor-related disorders. Neuroscience & Biobehavioral Reviews, 149, Article 104884.
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    Pribadi, A. K., & Chalasani, S. H. (2022).
      Fear conditioning in invertebrates. Frontiers in Behavioral Neuroscience, 16, Article 1008818.
      https://pubmed.ncbi.nlm.nih.gov/36439964/

    So, J., Kuang, K., & Cho, H. (2015). Reexamining Fear Appeal Models from Cognitive Appraisal Theory and Functional Emotion Theory Perspectives. Communication Monographs, 83(1), 120–144.https://doi.org/10.1080/03637751.2015.1044257 

    Wall, E. K., Teo, J. N., Roth, A., Chan, M. E., Brandt, J., Hibri, M., Richardson, R., & Baker, K. D. (2024).
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