Cobbers on the Brain

When I first enrolled in the Neurochemistry Capstone course, I was a little unsure of what I was getting myself into. But, now that I am quickly approaching the end of the semester and thus the end of this class, I am finding myself a little nostalgic. I have loved every second of this course, as it certainly represents the concept of a capstone course. Concordia’s mission is for students to BREW (become responsibly engaged in the world). Neurochemistry has represented the mission well, as well as aligning with the goals of a liberal education.
Being a biology major, I was a little nervous when I started the course. My general chemistry and biochemistry courses were the only things that I thought would help me out with learning neurochemistry content. However, I found that a lot of the mechanisms and structures that we were learning were things that I was able to understanding fairly well. I really appreciated that I was able to use my foundational skills from other courses to incorporate information across disciplines. I also found out that a lot of neurochemistry involves quite a bit of background from my biology courses. Knowing that I was going to be able to pull previously learned information from my brain made class a lot more enjoyable. Interdisciplinary work is something that Concordia strives for, with neurochemistry not being an exception to their goal for learning.
The concept of BREW was definitely illustrated through this course. Through our Wednesday speed-dating, Friday conversations and blog-posts, I found myself becoming more socially engaged with my peers, many of whom I did not know well at the beginning of the semester. The Friday sessions were pure discussions about the topic that we had gone over for the week. We were able to discuss ethical, cultural, and personal opinions on the topic at hand, an experience I had not had in any previous classes. It was interesting to hear what others had to say about some pretty controversial topics. I also really enjoyed learning new information that I had not known previously. The blog post also gave us another opportunity to showcase our knowledge and opinions about the weekly topic. It also allowed us to connect with the community, spreading knowledge about topics that they may not know much about! Even if not many people read my blogs, I hope that I was able impact some people within the community with my thoughts!
My specific capstone project that I worked on all semester with both neurochem and social work students was on the topic of anxiety. We chose to specifically target the teachers on campus in order to have a “trickle down” effect on the students. I really believe that we were able to succeed with our faculty and staff workshop. This project was challenging, but it allowed me to expand my friendships into other disciplines, while also learning how to navigate through a “real world” issue that exists within our society.
Throughout my entire four years at Concordia, I have fallen deeply in love with learning, so as much to pursue a career that will immerse me in education for years to come. Specifically, neurochemistry has contributed to my love of learning. Learning about topics that are prevalent within the community and may contribute to my work as a physician really stimulated my learning within the course. The environment of students that I have been able to work with throughout the semesters have been phenomenal. Also, having a professor that shares the same passions as you makes learning even more fun and worthwhile. Overall, this was a class for the books. It is hard to find professors that are willing to hold a class in such an environment.

Concordia College prides itself on preparing its students for the real world after their undergraduate experience, and the capstone experience is supposed to be the final addition to the recipe. As my final semester at Concordia is wrapping up and I finish my capstone course, Neurochemistry, I believe I can say that Concordia is doing it right. I hope that I can say the same thing 20 years from now, too, but from where I am now I can.
Concordia has a list of goals for liberal learning that they try to incorporate into their liberal arts education, and at the same time they try to teach the students to become engaged in the world around them. I feel as though Neurochemistry has met these criteria.
The first goal for liberal learning is to instill a love for learning. Although this class has been challenging and a bit confusing at times, the material has been fascinating. I hadn’t taken a neuro class before this, so I thought I might be a little behind and easily overwhelmed. This may have been the case if it was a typical class, but, because we had to learn the material on our own outside of class, I could spend as much time as I needed. It was easy to spend a lot of time understanding some of the articles, but they were so interesting it didn’t matter.
The second goal is about developing skills and transferable intellectual capacities. I think that this goal was probably the most relevant to me because I am going into dentistry, which is a constantly evolving field. I will need to be able to pick up a scientific article years from now have the skills necessary to critically analyze and understand its content, something that I learned reading articles and discussing them in this class.
Developing an understanding of disciplinary, interdisciplinary and intercultural perspectives and their connections is the third goal of liberal learning. Our class had people from many backgrounds, majors, and countries, so we had people with different perspectives weighing in on our discussions. In addition, Dr. Mach did a wonderful job of bringing things to our attention that we maybe didn’t think of or that enhanced our discussion in some other way. Our topics were controversial at times (legalization of marijuana, end of life care, drug addiction, etc.), so it was interesting to see where people were coming from when they had a contrasting opinion.
The fourth goal is to cultivate an examined cultural, ethical, physical and spiritual self-understanding. Neurochemistry satisfied this goal through our class discussions. We were never just memorizing information from a lecture given by our professor. We were asking questions about the implications of a new discovery, discussing if a new treatment option was ethical or not, comparing our views to those of another culture, or looking inside ourselves to formulate our own opinions. Many of us will be professionals in medicine or a related field, so we will face these kinds of issues at some point and will need to deal with it properly.
The final goal of liberal learning is to encourage responsible participation in the world. Our weekly blog posts relaying scientific information to the public were an obvious way that we were participating in the world. In our discussions, we often found ourselves saying, “If only more people knew (fill in the blank).” Because we have the educational background and access to scientific articles, it is our responsibility to do what we can to educate others to make informed decisions.
Overall, this class was a great experience and I would recommend it to any science student that is looking for a capstone. It is challenging, yes, but it is an awesome class and is near the top of my list of engaging, interesting, and rewarding classes here at Concordia.

This week we asked ourselves a very important question: what comes first, over nutrition or insulin resistance?
In 2013, the American Medical Association (AMA) officially recognized obesity as a disease. According to new guidelines released by the American Heart Association, American College of Cardiology, the World Health Organization, and The Obesity Society, doctors should consider obesity a disease and more actively treat obese patients for weight loss.
With this new diagnosis as a disease, more research is being done on how the brain plays a key role in the way we eat. In a paper published in 2013 we found many things that contribute to this energy imbalance in our bodies.
Normally, the brain responds to many signals from within the body and from the external environment to help it to know when it is time to eat and when eating should stop. We are all familiar with things in our environment that seem to increase our appetites, such as the smells of food nearby, food advertisements, parties with friends, group meals and even emotional triggers, like stress, which can change our drive to eat.
This includes certain neurons in our brain that receive signals from insulin when we have enough energy, to tell us we don’t need to eat anymore. When we over eat these neurons can get desensitized and no longer receive the insulin signal that we are full. This starts a cycle of bad eating and just continues to damage the neuron. Also, research on animals has also shown rats fed a diet rich in sugar and fats are less sensitive to the pleasure-inducing neurotransmitter dopamine.
The other hormone controlling our appetite is leptin and as body fat increases, leptin levels also increase. However, instead of high levels of leptin leading to fullness and decreased appetite, it appears that obese people become resistant to leptin’s effects and it works less and less effectively as body fat increases. This resistance to the effects of leptin may help explain why many obese people have normal or even increased appetite despite having large amounts of stored calories in their bodies in the form of fat.
While scientists and doctors continue to work to better understand what causes obesity and to develop new treatments, there are many things individuals can do now and Diet and exercise and the key to it all.

Autism is seen four times as much in men than it is in women. This is a very odd phenomenon that has been hard to explain since it’s been observed. The reasoning behind it still isn’t well understood, but there were some interesting points brought up.
First off, the article Sex differences in autism spectrum disorders from NCBI discussed a possible diagnosing bias in Autism Spectrum Disorder (ASD). There may be a gender bias in diagnosing ASD that stems from how ASD is identified. ASD is diagnosed with many behaviors that violate traditional social norms and it is possible that males exhibit those signs for diagnosing in a more extreme fashion than females. Their main source of evidence of this was that in patients that fell just short of being diagnosed with ASD, the gender ratio was much more even, closer to 60:40.
After getting beyond this, multiple ideas were discussed to explain the ASD gender ratio. The most interesting one to me was about the role of testosterone and other hormones in the development of Autism and women’s genetic resistance. Since there is such a gender discrepancy, the first culprits looked at are what make us a boy or girl, sex chromosomes. A girl has two X chromosomes and a male has an X and Y chromosome. The first idea is that the Y chromosome is destructive, in that it leads to Autism. On the other hand, it could be that the X chromosome is protective against ASD. More than likely, it’s a little of both. Interesting evidence for this is that people with more than two chromosomes, their rates of Autism make sense in consideration to X being protective and Y being destructive. More X chromosomes and fewer Y chromosomes correlate with lower rates of ASD. This association makes sense in consideration with the role of testosterone in Autism.

Elevated levels of fetal testosterone and throughout development are seen in many who exhibit ASD. The exact role of testosterone in Autism isn’t well understood, but an interesting connection was made by the authors. Testosterone functions, on some levels, in a positive feedback loop. Testosterone inhibits the enzyme that changes is to estrogen. So naturally, the accumulation of testosterone leads to the inhibition of its own breakdown, leading to further accumulation. This is relevant to the gender discussion because, not only does the Y chromosome create more testosterone comparatively, but the X chromosome codes for the enzyme that changes testosterone to estrogen. This understanding might explain part of the gender story, as females with less natural testosterone and more enzymes to handle high amounts of it are more resistant to ASD. The most interesting piece of evidence for this hypothesis involves the siblings of those with ASD. When compared, siblings of a girl with Autism exhibit more symptoms of ASD than those with a brother with ASD. All these little pieces of evidence support the idea that women are resistant to ASD in a way that involves their additional X chromosome. An interesting analysis that comes to a funny conclusion, women having lower rates of ASD is due to their additional X chromosome or lack of a Y. Which is effectively saying, women are resistant to ASD because they are women, nonetheless, testosterone’s role in ASD will be important in the future for understanding and treating ASD.

The aging process is one we’ve studied as a people for as long we’ve existed. And extending our lives has always been a major motivation in those studies. Our current understanding of aging at a cellular basis is one of oxidative stress and mitochondrial damage. Over time, our cells create more and more reactive oxygen species (ROS) that cannot be broken down before doing their damage, which lead to the generation of more ROS. I’ll break down the concept and introduce a few interesting ideas from our class discussions.

The mitochondria, the most well-known organelle in the cell. It gets its memorable nickname the “Powerhouse of the Cell” from its function, creating energy. The mitochondria can be thought of as a factory, but it can be better visualized as a furnace. Just like any bomb or engine, sugar breakdown is a combustion reaction. A carbohydrate reacts with oxygen and breaks down to water, carbon dioxide, and energy. So in the mitochondria, sugar is broken down and the heat/energy given off is utilized to generate energy molecules for the cell. However, this process isn’t perfect. Instead of becoming carbon dioxide, the oxygen molecules can be changed to reactive oxygen species, like superoxide.
These ROS are dangerous, a given with the name reactive. They damage DNA, proteins, and membranes. The damaged DNA works less efficiently and increases the chances for mutations. The proteins that are damaged dysfunction and/or accumulate. Membrane damage along with protein damage are important for their impact on the mitochondria. The ROS generated by the mitochondria, turn around and cause it to generate even more ROS. This positive-feedback loop would lead to the accumulation of a lethal amount of ROS. Our body takes care of this with proteins that neutralize ROS. As stated above, ROS damage proteins as well. Over time, our body loses the fight against ROS generation. Leading to disease and aging.
How does this concept apply to us? Calories basically equate to energy for the mitochondria. Meaning that, calories, by virtue, lead to ROS as well. The oxidative stress of calorie consumption is a natural part of life and the aging process. Overnutrition exaggerates that stress. When our body takes in too many calories over a short or extended period of time, it generates more oxidative stress. How relevant is this to the aging process? That’s where we need to learn more.
There is interesting evidence in support of that. Rats have been shown to live longer if their amount of proteins neutralizing ROS are increased. That doesn’t hold true 100% of the time, though. Sometimes the opposite effect happens with similar proteins. The current hypothesis is that ROS are damaging, however, they do have a necessary function in the cell that can be disrupted. The most interesting idea I came across was that reducing caloric intake extended life span.
It has been shown in many experiments with varying mammals that reducing caloric intake by 30-50% below what the animals would eat if they had no restrictions, leads to a significant extension in lifespan. This idea is very interesting for thinking about extending life, but it’s also very applicable on the opposite side of the spectrum, overeating and reduced lifespan. Overeating is obviously a concern in many countries throughout the world and its effects on aging and possible controlling those effects calls for more investigation. Life-extenstion is also very interesting, but those studies called for reduced feeding during development. Reducing calories that far is hard to do in the first place, but its negative effects on even an adult’s body wouldn’t be worth any hopeful benefit in lifespan. Going forward, it will be interesting to see how the role of oxidative stress and overnutrition becomes a factor in preventing and treating illness.

Tobacco and weed have both been used for thousands of years by many different peoples, and yet the past 100 years in America have been a time of equating cannabis to heroic and other narcotics. Odd that tobacco which has been shown to strongly associate with cancer and other health issues many years ago (what a struggle that was against the cigarette corporations) is legal in today’s society when weed illegal even though it’s identified negatives are far below that of tobaccos. Some of the stereotypical negative effects cited by the first website to appear in google include memory issues, reduced reaction time, lower iq, impaired thinking, relationship issues, antisocial behavior, financial difficulties, increased welfare dependence, and greater chance of being unemployed. The effects are marijuana are poorly understood because it hasn’t been studied in the US due to being treated like a narcotic rather than potential medicine. So where do these drug effects come from if not from scientific studies? That’s the story of why weed is illegal.
It’s true that weed has negative effects. One you’re smoking, bad no matter what and damages the lungs. Two you’re introducing high amounts of outside chemicals to your body, may not harm too bad but can’t really be good for you either. And thirdly, weed and other drugs should never be used by those still in development, youth. However, side effects like relationship issues, antisocial behavior (stealing, lying) and the financial issues and welfare have a basis outside of science. Those trends might be seen in today’s world, but they were determined to be true long ago.

Marijuana was legal in the use into the 1900’s, however, the Mexican revolution occurred in 1910. Following that event, many Mexican immigrants began to cross the border and with them came weed. Pretty much immediately, state governments began criminalizing marijuana (just like heroin) due to it’s association with the Mexican immigrants. Newspapers publicizing this said things like “Marihuana influences Negroes to look at white people in the eye, step on white men’s shadows and look at a white woman twice.” At the time, regulating drugs like the FDA does now wasn’t constitutional, which is why an amendment was required to ban alcohol. The next stage in our story involves that, prohibition ending in 1933. After prohibition ended Harry J. Anslinger (head of federal bureau of narcotic) being an ambitious man sought to expand his influence by demonizing weed. Using racist publications already in place to justify its demonization and coming up with own, like “….the primary reason to outlaw marijuana is its effect on the degenerate races”. In the end, he was able to bring enough “evidence” to Congress from various racist journals and many from his friend William Hearst, who was the owner of a chain of newspapers with a hate for Mexicans. He was able to convince Congress to pass tax penalties on marijuana against the wishes of Dr. William C. Woodward, Legislative Council of the American Medical Assoc. The doctor called for more primary research before this decision but was ignored and the Marijuana Tax Act of 1937 was passed.
The tax act was found unconstitutional years later, however, the Controlled Substances Act in the 1970’s struck weed down once again. Nixon and the war on drugs, we now know it was resounding failure that we still cling too. Regardless, when the three classes of drugs were defined, weed was placed in schedule 1 initially so that a commission appointed by Nixon could determine its danger. The commission recommended removal from schedule 1 and possibly not consider it illicit at all. Nixon completely ignored this and classified it as schedule 1. Why would Nixon do this though? Not shocking that it was a shady political power move (no way Nixon). Nixon had two main political enemies in America, the Blacks and the Anti-War hippies. As one of Nixon’s aides (John Ehrlichman) opened up about, you can’t just target the pacifists and blacks directly, you have to punish them indirectly. In this case, criminalize the main drugs of use of these populations so that raids and busts can be used to disrupt political organization against him. This racist and political use of drug enforcement continues to this day, just look up the weed usage rates by race and the weed arrest rates by race. I bet you can guess you gets off easy and who doesn’t.
 

Short answer, overall not signifiantly. More complicated answer is that in some individuals in the obese population, leptin might help with the return of normal weights.
Leptin is a hormone that is secreted by fat cells in your body that signal for the brain to have a decrease in appetite. Because of this, abnormal production of this hormone has been associated with obese individuals.
Specifically in the body, leptin interacts with specialized leptin receptors to inhibit excess feeding. In obese individuals though we see very highly elevated levels of this hormone. So why isn’t it working?
Well, in the typical Western high-fat diet, both rodents and humans have shown in various studies to demonstrate a non-response to leptin. This is a problem for being able to use leptin as a weight-loss hormone, as the already high levels of this hormone in obese individuals are already having no effect.
But, that doesn’t mean that looking into further uses for leptin aren’t going to prove beneficial. Although many obese individuals have high levels of leptin, there is about 10% of obese individuals that have very low levels of leptin instead.
In these individuals, there is potential therapies akin to insulin treatment of patients with type 2 diabetes in the form of leptin therapy. In these individuals with truly low levels of leptin, this therapy has shown to induce a sustained increase in weight loss.
This is good news to show that although leptin therapy is not for everyone, if you are overweight or obese it might be well worth it to go get a check up to view your blood-leptin levels to see if this is a potential reason for your obesity.