In the Caron lab, my project has largely been testing new schizophrenia drugs on the dopamine receptors. Because my interests in the sciences have largely revolved around pharmacology and cell biology, I have usually approached the concept of neuropsychiatric disorders as a dysregulation of neurotransmitter systems that can be fixed by the administration of a molecular substance (i.e. drug). This would involve knowledge of the receptor and the subsequent effects it has on the cell. This approach to these disorders focuses on abating symptoms once they are present in a patient (or forced in an animal model), and does not truly examine the causes of such disorders (but merely the effects). Thus, I was quite fascinated to hear about some of my colleague’s labs which focus on proposed causes for certain disorders, like the role of gut microbiota in contributing to depression.
One chalk talk that really grabbed my attention was the one given by Annika Sharma. In the talk, she stressed that experiments transferring fecal matter from a depressed mouse (mice eat poop) into a healthy mouse was able to induce depression in the healthy mouse, suggesting a role for the gut microbiota in facilitating connections with the brain (i.e. the gut-brain access). It is also known that Major Depressive Disorder (MDD) patients have altered microbial compositions and many metabolites which play a role in depression are byproducts of gut microbiota. I was also rather shocked by the way in which her lab generates what it calls the social defeat paradigm. Essentially, to create a depressed mouse, it is left in the company of older, more aggressive mice that beat it up. The lab then extracts fecal matter from the depressed mouse and is able to run any series of tests that they want to determine, for instance, the presence or absence of certain metabolites. Overall, I was just interested in learning the many different ways in which researchers have approached certain disorders.
This week, we had a chalk talk where everybody in the research fellowship gave a general overview of their projects and what they were doing in their projects. The projects in the group spanned from poop to the mechanisms of the brain to immunology and other parts of the sciences. Everyone did an amazing job during their chalk talks and many of the projects got me very excited for the future of the sciences.
One of the projects that I found the most exciting was the one that Anikka is working on that deals with the gut microbiome and its link to depression. I have always been interested in mental illness and the brain but who would have guessed that mental illness and the stomach are so closely connected? I was once watching an ASAP Science video that briefly talked about the link between our guts and who we are. I did some researching online and found that about 80-90% of our serotonin is actually in our gut. This not only makes serotonin a neurotransmitter, but it also means that it is a type of hormone. That is simply amazing. Serotonin affects our mood so that explains why I feel so grumpy when I’m hungry and why I feel so happy when I eat something good or when I’m full.
Anikka’s project was also looking on how fecal transplants could also change the anxiety in rat models. That means, if you took the poop from a rat without anxiety and put it into a rat with anxiety (in an attempt to change the gut bacteria), would the rat with anxiety no longer have anxiety? Believe it or not, these fecal transplants are actually being done on humans in present day. I heard of a project at MIT that was having students donate their fecal matter in order to use it as microbiome therapy for other people.
But if anxiety can be affected by the bacteria in our guts, what else can be affected? Can you change intelligence by changing your gut bacteria? How about the fears that you have? If you take the gut bacteria of someone who loves snakes (like Dr. Grunwald) and put it into someone who is deadly afraid of snakes (like a lot of his students), will that person’s fear of snakes and their sympathetic nervous system response to snakes be different? These are some of the thought that ran through my head as Anikka was giving her presentation. I hope that I can soon find out what some of the results say.
I thought that Iris’ research into Traumatic Brain Injury (TBI) was quite interesting. I was initially interested in the project because I am also doing research in neuroscience. What I quickly discovered through her talk, however, was that her research was much less molecular and much more mechanical. Thinking about the different kinds of acceleration that could damage the brain was a very new experience for me. The idea of thinking of the brain in as a rigid structure that could be thrown and broken was a very new idea.
Rather than repeatedly breaking our prized model subject, Iris first models these assaults in a computer program. I thought it was really cool that they had this predictive power to know what particular injury would occur given a certain type of trauma. I thought this could be of great clinical relevance as a reconstruction of the trauma, quickly ran on a computer, could be a great aid to a surgeon to know where bleeding would occur.
I was also surprised when Iris said that she would use a dead pig brain to test these forces and strains. As her questions are purely on the forces the brain was enduring, physiological responses are not necessary.
The final thing that was different about Iris’ talk was her ending it with ideas about the potential impacts of her research. While I’m sure my PI must be thinking of these things while writing grants, I had never thought of a reason for my research other than to learn more about the brain. Iris’ specific mention of applications to headgear and neurodegenerative disease, which are implicit in any neurobiological research, were an interesting consideration to make.
All the talks from this past week were incredible; I was so awed by the research everyone was working on and how relevant and meaningful these studies are.
That being said, I believe immunology is such an interesting and riveting field that’s developing so quickly these days. I learned about it briefly in my microbiology class this past semester and thought it was such so fascinating. Maddie O and Cassie’s talks this week really enlightened my understanding of it and how it’s being tackled in different fronts using molecular engineering.
Cassie’s chalk talk on dendritic cells in the mammalian immune system reminded me of the phenomena of antigen-presenting methods that cells practice once faced with a pathogen. Her project’s take on the topic using fluorescent peptides is such a fresh way to tackle the issues of the immunocompromised. Synthesizing these nanofibers from scratch sounds so exciting.
Maddie O’s presentation on epitopes and the immune response with T cells and inflammation really opened my eyes to the way her project can benefit the field. Her study of the major histocompatibility complex really highlighted the importance of testing for these pro-inflammatory or anti-inflammatory responses.
These two chalk talks were very intriguing and gave me some more insight into immunology and where more research can take us into the future.
This past week I have enjoyed listening to everyone’s research. Since all the fellows are in a lab conducting research most of the time, we don’t have that much time to talk about our research, so it was great learning about what others are doing. I enjoyed learning how some of the projects being conducted intertwine into mines and it made me rethink the way I am tackling my research project. I saw some interconnections between my research and others but I enjoyed Iris’s project since it is completely different than mines.
Iris Chang works in Dr. Dale Bass lab in the department of Biomedical Engineering. Iris main goal for her project is to uncover the mechanism of Traumatic Brain Injury (TBI), and discovering what causes such thing to occur. The two schools of thought for TBI is between linear and angular kinematics. Iris is more focus on exploring the role of rotational kinematics via the mechanism of shear shock waves. Studies have shown that injuries can send shock waves through the brain in an undesired direction which causes such tragic brain injury. However, how rotational acceleration works through shear waves is still not well understood.
The way she is tackling such project is by using a computer model that allows her to input rotational kinematics and analyze the strain in the model brain. Her second method is analyzing the damage done to the brain by conducting a pig brain impact testing. Her methods in her project involve methods I have never conducted and it is exciting knowing Iris is doing it. Her research made me wonder if the results from both methods be similar or will they differ? And if they differ, why? Can’t wait to hear Iris explain her lab’s data to us at the poster presentation in a few weeks. The best is yet to come.
When Georgia started presenting her chalk talk on that particularly humid Tuesday morning, I felt myself leave the room for just a few seconds. I was no longer in our room in the LSRC but on the ground level of Bell Tower house in a small projection room with eleven other students and one red-haired professor. It took only a microsecond for me to realize what was going on: I was having a flashback to my first semester Writing 101 class, “Can chimps have culture?”. A class I ultimately got stuck with due to scheduling difficulties and grew to despise, it was an experience I had tried to obliterate from memory yet I was here, dreaming about it. But just like that, I was back to reality and listening to Georgia talk about environmentally-induced stress in yellow baboons. Her chalk talk brought up some old memories and it made me think critically about how I view science outside of my own.
I grew to hate Writing 101 not because of my professor or her teaching quality but the students and the course content. It tore me to shreds and killed me internally every single time I had to force myself to read a research paper about chimpanzees, gorillas, and a number of assorted monkeys and their propensity for culture. I lost more and more hope for my intellectual future as a Blue Devil when I would have to sit in a room full of closed mouths in the middle of a class discussion we were supposed to have. But more than anything it was the primates. I just couldn’t stand reading about them. All the research began to blend together and paper after paper seemed to be talking about the exact same thing. I thought they would never be a part of my life again but they came back with Georgia.
She was describing her research project: analyzing the glucocortisol levels in the fecal matter of yellow baboons in different environmental contexts to assess stress levels. She was talking about primates again and I really thought my eyes were going to roll to the back of my head and not come back until she was finished. But just the opposite was happening: I was interested. I cared about how food conditions and hierarchy could affect yellow baboons in such a way as to induce stress. I was engaged and even asked how this research might pertain to humans: due to the fact that the two species share more than 90% of their DNA, understanding stress responses in yellow baboons might allow us to understand them more in humans. At the end of it I realized that other than that memory of Writing 101 at the beginning, I had managed to pay attention to the whole talk.
Why was that? Why was I suddenly engaged and interested in an area of research that I despised just a few months ago? I didn’t know it but the answer was simple: I had been engaged effectively in this research for the first time. While my professor had taken us through stacks of research articles in the study of primates, I had always felt detached from the research. I knew about all these studies and their impacts but I was struggling to see the “So what?” in what I was studying. Georgia changed that for me. She had contextualized interesting research in primates for me and made me understand that it was a real, living scientific field with important implications in the real world. I couldn’t feel detached from this research anymore because it was staring me in the face. Someone was finally talking about it with excitement in their voice and vigor in their conviction. For this, I thank Georgia. In the future, I now know that I can avoid the pitfall of detaching and even resenting a field of scientific research just because I think it isn’t interesting. It’s a matter of going to people that know how to communicate their science and have them show you just why their work is interesting, a lesson for all.
Last week, all seventeen BSURF fellows presented 8-minute chalk talks to explain their research to the class, and wow, everyone had such interesting research questions. My assignment at the end of all of the presentations: to write about one of my peer’s research.
Every person convinced me of the importance of their research question, which made me really want to know the answers to their questions. Of course, in the research world, answers cannot be obtained within a few seconds from existing data on the Internet. The answers are yet to be discovered. That said, as I listened to the diverse methods that have been formulated in an attempt to answer the overarching research questions, I thought long and hard. How does one devise experimental methods that take into account all possible confounding factors?
One of the many presentations that piqued my curiosity is that of Annika, whose lab focuses on how microbiomes of mice are affected by chronic social defeat. Previous research indicates that gut bacteria are important in brain development and function. What interests me the most is her explanation of the social defeat paradigm, which is used to induce social defeat (as a model for depression) in mice. The method her lab uses involves combining aggressive mice and subject mice in the same cages to encourage the aggressive mice to attack the subject mice. Once the subject mice are, I would assume, terrorized, the subject mice and aggressive mice are divided, but kept in close proximity to each other for 24 hours so that, although the aggressive mice cannot physically abuse the subject mice, the subject mice can still see their attackers. Imagine what it would be like to live in the same room as a bully who had just abused you, with only a glass divider to separate both of you. Now that’s a frightening thought. In the experimental method, the subject mouse must go through the same process ten times, with a different aggressive mouse each time. By the end, the hope is that the subject mice will experience “social defeat” and show symptoms of depression and anxiety. Interesting, right??
Annika’s lab in particular is working on comparing two different methods of extracting DNA from fecal samples and determining the best method. The fecal samples are collected and analyzed from the subject mice before and after they are socially defeated. I wonder how the microbiomes of socially defeated mice compare to the microbiomes of regular, happy mice! I will be excited to have Annika explain her lab’s current data to me at the poster presentation in three weeks. Until then, I must sit here and patiently ponder…
I really enjoyed last week’s chalk talks and definitely learned a lot. One of my favorite parts of chalk talk week was seeing how everybody’s research was so different yet somehow shared connections to another peer’s project. It just goes to show how science has many varying forms but there is always a common thread amongst it all.
I really enjoyed hearing about Ulises’ research concerning inflammatory breast cancer (IBC). I never realized how aggressive of a form of cancer IBC is and how high the mortality rate is for those diagnosed with IBC. Many times doctors misdiagnose those with IBC, so often times the cancer is not caught until much later stages. Furthermore, a lot of information is left to be elucidated concerning the pathways leading to the onset of this disease and thus the best mechanisms required for its treatment.
Ulises is looking to better understand the role of polycyclic aromatic hydrocarbons (PAHs) in IBC. PAHs are organic compounds released into the environment through processes such as the burning of coal and are known to be carcinogenic. Thus Ulises’ hypothesis is that an increase in concentration of PAH exposure to tumors will lead to an increase in the proliferation of these cancer cells. This information can help better understand some of the mechanisms behind IBC in order to eventually lead to better development of therapies and drugs for patients diagnosed with this disease.
I’m looking forward to continue learning more about my peers’ research in the weeks to come. It will be exciting to see what else my peers learn during the poster session in three weeks.
First off, I want to thank everyone for doing such a great job presenting their chalk talk last week. I know that public speaking is a struggle for me and I’m sure I’m not alone. Everyone did a wonderful job and is on their way to becoming a great scientist!
A highlight of the chalk talk series for me was getting to see my roommate Georgia convey her science. Georgia has become a good friend of mine throughout the program, but I haven’t been able to talk to her about her project as much as I would’ve liked. Her talk was a great example of basic science and how scientists are working across the world to learn more about various organisms. Georgia’s lab studies baboons from Kenya and then analyses their fecal matter all the way in Durham, North Carolina. They then work to correlate the organism’s biochemistry with their behavior and ecological conditions in Kenya. I find it fascinating that something as natural as heavy rain can increase the level of glucocorticoids in a baboon’s system. I think that often there is a large gap in the minds of scientists between organismal activity at the molecular level and then at the level of the entire organism, but Georgia’s research does a nice job of bridging that gap to show how significantly an organism’s biochemistry can change as a result of something in their environment. This type of research is unfortunately often overlooked compared to research that has direct biomedical applications, and with the current political climate could face challenges with funding. I think Georgia did a great job of explaining why her research is good science, interesting, and deserving of public support.
Echoing what everyone else has been saying: The chalk talks this week were great and I really enjoyed learning about everyone’s different labs! I felt like this was a good way to see the scope of BSURF with (almost) everyone working in different labs on a variety of topics. One big theme throughout the talks was the brain. Alie’s research in the Dzirasa lab was in this theme, using a technique called social defeat on the mouse model. This technique induces depression in the mouse model, the mice are treated with antidepressants, and then the brains are dissected to see if a certain protein is present. If this protein, EmCP2, is present in a brain treated with antidepressants and the model does not show signs of depression, this could be a big breakthrough in treating depression in humans! Mental illness is a difficulty many people face, and it was especially interesting to see the different ways researchers at Duke are tackling this issue. We also got to hear from Annika who is researching depression in the mouse model using the social defeat technique from a different angle: the gut. Specifically, Annika is looking at how the micro-biome in the gut may lead to lower levels of serotonin in the brain, which may be a cause of depression. Both viewpoints on depression allow us to see the body as an intricate system and allows us to see how these systems interact, which I thought was very interesting. The two talks also made me think of my own research with baboons (explained in my last blog post), as we start with behavioral data and work backwards to hormone concentrations in the organism. In both Annika and Alie’s lab, they seem to be starting within the subject and seeing how an internal change may affect the external behavior. Again, I really enjoyed hearing all the chalk-talks, and they really broadened my view as to what research can be! Thank you for the time and effort everyone put into their talks, and I really look forward to hearing more during the poster sessions!
First of all, I would like to say that everybody did a great job with their Chalk Talks and I really enjoyed this week of morning meetings. I know that we have gone in circles a lot of times telling people our names and our favorite animals and what lab we are working in, but this was the first time we got to talk about our research in depth with everybody in BSURF. I think one of the reasons that BSURF is such a cool program is that there are so many different types of research being done by everybody in the program so we can really get a good idea about what kind of research opportunities there are just within Duke. These talks really showed that there is so much to learn and do in the world of science.
Alie’s talk was particularly interesting to me because she works in a neuroengineering lab, and as a Pratt star of course that would peak my interest. Alie’s lab focuses on using psychiatric neuroengineering to study and provide potential treatments for mental illnesses and Alie’s particular project is looking at the involvement of MeCP2 in anti-depressant treatment of socially defeated mice. Alie is trying to figure out whether MeCP2, which is necessary for the proper function of nerve cells, is phosphorylated when mouse models are given imipramine (an antidepressant drug), because the phosphorylation of MeCP2 is shown to have antidepressant effects. Alie explained that she is using the social defeat method to make mice depressed and then treating mice with different amounts of imipramine to see if they are less depressed and whether their MeCP2 levels increase. I think Alie did a great job with her presentation (as did everybody!!) and I really liked learning about her work.
I also did some of my own googling to learn more about Alie’s lab because I was so interested and the work they do there is pretty damn cool. Her PI, Dr. Dzirasa, has this goal of making a pace maker, which is typically used for hearts, for the brain to treat psychiatric disorders. This is the kind of work that is using engineering to solve medial problems in the work that made me interested in biomedical engineering in the first place.
I loved listening to everyone’s chalk talks this week, especially because we got to learn much more than just a sentence or two about everyone’s project. The project I decided to reflect on this week was Rebecca’s!
Rebeca’s project focused on the effect of an olfactory gene (or47B) in fruit fly courtship. She explained the behavioral aspects of fruit flies that was interesting and a seemed a little silly. We got to better understand the role of the olfactory genes and the fruitless gene that seems to be tied to courtship which was cool! I found Rebecca’s talk interesting because in my neuroscience class last semester we talked vaguely about olfactory genes and pheromones but didn’t speak much about it since pheromones occur mostly in other animals.
I’m interested to see how the rest of her fruit fly watching goes for the rest of the summer, and if the fruit/or47b mutant will not learn the expected courtship behavior of the fruit fly!
Nice job to everyone with their talks this past week!
I remember recently reading an article by The Onion (warning: a bit graphic; mildy NSFW) about a flies mating. In summary, it’s about flies mating on a pile of rotting meat and how it enhanced the experience. To humans, this putrid smell may offset the mood. Little did I know that The Onion was sort of scientifically right: smell plays an important role in the courtship of flies.
Rebecca’s chalk talk, The Role of Or47b in Drosophila Courtship Learning Behavior, further explained the science behind smell and mating. For some context, there’s a gene called the fruitless gene (fru for short) that is key to courtship. When a frumutant fly (meaning a mutant fruitless gene fly) is coupled with another fly, it won’t do the courtship behavior; however, it can learn the behavior after being around normal fru flies.
There’s also a type of gene called an orco gene that’s involved in the olfactory, or smell, of the fly. When a fru (no mutation) AND orcomutant (can’t smell) fly is coupled with a normal fly, it also does not court and it can’t learn to court when around normal fru flies.
Rebecca’s research investigates a specific olfactory gene: Or47b. This gene is a more specific subset of the orco gene. Her hypothesis is: a fru AND Or47b mutant will not learn to court and she tests this by watching them mate for a few hours every day!
Maybe she can do another experiment to see if certain smells cause flys to mate sooner or more often (maybe rotting ground beef as The Onion suggests).
Thanks for the insight, Rebecca!
Rebecca’s not really a matchmaker in the lab, but that’s the first thing I thought of when she described her project to us during her chalk talk.
Rebecca’s looking into how certain genes (or lack of) may impact the ability of fruit flies to learn courtship behavior. Specifically, she’s looking at a particular olfactory gene called Or47B, and how knocking this gene out might affect a male fly’s ability to learn courtship cues from other flies. A lot of her lab work seems to consist of raising these knockout flies (and others) and putting each male together with a group of females. Then at specific times she takes each male, puts them alone together in a chamber with one female, and sees whether they’ve picked up on how to pick up a lady from their time interacting with the group.
One thing that struck me during Rebecca’s talk was how this courtship behavior of flies, which I thought was an intrinsically innate instinct, could potentially be “erased”. But then again, what does innate mean? In Rebecca’s case, she’s working with things on a genetic level, literally going down to the DNA that defines a fruit fly, and seeing whether removing/adding components to this molecule changes anything about the whole organism. If we say that any behavior stimulated by characteristics/physiological traits encoded in DNA is innate instinct, then I guess fly courtship behavior still counts. This behavior is apparently learned through things such as olfactory receptors; and when you take away the right olfactory receptors, you block the pathway to learning the behavior. Not only was this project an interesting discussion of what counts as innate and if we can alter innate behavior; it’s also a really interesting example of how behavior and physiology/genetics can be, essentially, directly linked (though I assume that the actual relationship is far more complicated than I just stated!)
Speaking of the link between genetics and behavior, I’ve always been fascinated by how genetics studies often have to utilize both ends of the spectrum in order to gather data. For example, a study like Rebecca’s can start out by deciding what genes they want to leave in or out (resulting a control group and other experimental set-ups). But then, to determine what the presence/absence of this gene signifies, they have to observe the resulting phenotype(s), which includes a physiological and/or behavioral change. Again, this link between what has happened at the molecular level and what is going on in the whole organism fascinates me. I’m sure that elucidating the exact nature of genotype-phenotype relationships is not always (if ever) clear-cut. But it’s still an interesting way to try to learn more about different genes and the roles they play, whether in flies, humans, or across a whole range of Earth’s organisms (we all share some bit of DNA after all!)
Thanks Rebecca for sharing your project with us, and great job to everyone on their awesome chalk talks!
Since choosing a chalk talk to write about was so hard (everyone’s projects are so cool), I decided to go with the topic I found most intellectually intriguing. Martin Acosta’s presentation on ‘Rapid Tryptophan Depletion: Sex-mediated Differences in Rats’ stuck with me because of the parallels between our projects.
Tryptophan is an important amino acid which we obtain through our diets and which is metabolized into serotonin (an important neurotransmitter) in the brain after passing through the blood-brain barrier (BBB). Martin’s project offers an alternative to the social defeat (SD) paradigm to induce depression in rodents since SD is not effective in females and hence cannot be used to study sex-differences in depression. In their protocol, the Kuhn lab feeds rats a mixture of several large neutral amino acids (LNAAs) or a mixture of LNAAs & tryptophan. LNAAs compete with tryptophan molecules to pass through the transport proteins in the BBB. Therefore, rats fed only LNAAs have a higher proportion of them which prevent tryptophan from passing into the brain and being converted into serotonin (serotonin deficiency is associated with depression).
Although preliminary results from Martin’s study (which measures the levels of various metabolites in the rats’ blood and brains) have shown no differences in how male and female rats are affected, this is not the aspect interests me. Tryptophan plays an important role in the gut-brain axis—some bacteria are known to use up tryptophan leaving less to be metabolized by our bodies, while others produce it. Additionally, the kynurenine pathway is another important pathway for tryptophan metabolism. Kynurenine is produced from tryptophan and can be further metabolized in two ways with opposite effects—the end product of one pathway is neuroprotective while the other is neurotoxic. Altogether, tryptophan and its metabolites seem to play an important role in depression and are an important signaling pathway between the gut and brain. This is where my project comes in: I can’t wait to see the bacterial DNA sequencing results from the feces of the SD mice in my project to determine whether the bacterial species which are more/less abundant are implicated in the tryptophan pathway.
P.S. Tryptophan is one of my new favorite sounding words—try saying it, it’s addicting!
Everyone did such an amazing job with their chalk talks this week, given that no one had really done one before. New knowledge has been acquired from all of this. Success! To be honest, it was a bit nerve-racking, especially since public speaking is not a forte of mine and for some others. The thing about a chalk talk, it seems very informal, but then you realize that everything in the experiment must be pretty much understood, and then, in my case, you realize that there are a lot of holes to cover up and a lot of jargon scattered about. It’s an informal, yet you must be very prepared, kind of presentation. Also, the time limit. Not a fan of that pressure.
Out of all the great talks and the great experiments, I’ve decided to write about Maddie Go’s experiment, The effect of Spine Morphology on Puncture Mechanics.
So, what really interested me in her experiment was the definition of “spine”. Like what Maddie said at the beginning of her chalk talk, when I hear “spine” I think of our backbones, but I learned that the actual definition of a biological spine is “a rigid structure that comes to a point” (taken from Maddie). I hadn’t thought of it like that before. The examples that Maddie provided kind of blew my mind, because of how different each spine was. She also mentioned that these spines all have similar functions despite the diversity (I don’t usually correlate a rose and a sting ray together). These spines are so different in their structure, yet they essentially have the same function (puncturing things) so how does this difference in structure change the way it is used (Maddie’s question)? Just got to say, science is pretty cool in this way; the way that depending on the environment things can develop so differently, yet have a similar function to other things/organisms and vice versa.
The applications that Maddie brought up were also really intriguing. I wouldn’t have thought that this type of research would be so important in, for example, the medical area, because I don’t usually think about how this research is considered when trying to make maybe a needle to increase its ease for puncturing the skin and then coming out. I think I just assume that the medical area has all of that kind of figured out? However, there’s always room for improvement. It’s some nice brain food to mull over.
Thank you, Maddie, and thank you to everyone else for sharing their research projects!
When one of my friends first mentioned that he literally did not want to leave his bed sometimes in winter and could have a case of seasonal depression, I was awfully confused.
Seasonal depression? In my mind, depression couldn’t be seasonal; there wasn’t a switch where one could turn “on” or “off” depression.
So, curious, I looked into it, and found that during winter, the change in hours of light can modify one’s biological clock and therefore shift hormone levels of serotonin and melatonin (regulators of mood and sleep, which are correlated with depression) (Lieber). I thought it was fascinating that our own environment could change our bodies and how we feel.
I drew upon this memory when listening to Georgia, a fellow B-SURFer, on her talk Stress and Weather: Environmental Factors Affecting Glucocorticoid (GC) Levels. Her lab studies baboons and how not only their social rank but also their environment in Africa contributes to stress. They extract hormones from baboon fecal samples in order to analyze how the environmental factors recorded correlate to glucocorticoid levels (and therefore stress). Her hypothesis was that GC levels would increase as environmental factors became more extreme, and I completely understood when she referred to the different types of food distributions: scramble and contest. In my senior year of high school, I participated in an international written and oral debate contest on the topic of global food security. Through all the research on global food security and relating topics, I understood the food access, availability, and distribution issues that are quickly rising in the world today. With such different food models dispersed around the world and the advent of climate change, stress levels could vary greatly. I’m very curious as to how exactly these increased stress levels will create side effects that weren’t originally conjectured—perhaps in reproductive stress/hormones? Our levels of health, like seasonal depression? I was very enlightened with Georgia’s work and hope to hear about results or possible new leads soon!