It seems that every year more and more children are being diagnosed with a cognitive disorder called autism. Over the past 32 years the number has risen from 1 in 5000 people having this disorder to 1 in 150 having this disorder. There are several different reasons that this could be occurring. One reason that this could be occurring is that there is a broad spectrum of symptoms that are related to autism. When diagnosing autism there are three different broad categories to look for in the child. They are social skills, communication skills, and behavioral skills. If a child has autism they might be more inclined to be an introvert, shy, appear unaware of others feeling and poor social behavior. The communication skills that may be lacking in an autistic kid is that they don’t speak very often, can’t keep a conversation going, and they may repeat phrases exactly as someone else has said them. The behaviors that may develop are a desire for an inanimate object, repetitive movement, or become disturbed at the slightest change in routine. All of these could be confused for a personality disorder or simply the unique personality of the child.
One idea that has come about when talking about autism is that there needs to be genetic screening to see if there is a way to diagnose the disease. The problem with that is there are so many mutations that are prevalent in autistic children is that it is hard to narrow it down to a few that may cause autism. One study showed that there are 130-234 mutation points that may be linked to autism. One of the more interesting mutations that occur happens on chromosome seven. If there is a deletion on chromosome seven in a specific region a child is more likely to develop Williams’s disease. This is a disease that children to me overly friendly to strangers and to be very social. If there is a duplication that occurs in this region, there is a tendency for the child to develop autism. This is interesting because one point in a child’s genome may determine a major characteristic of their personality. Another idea that was tested during study was that the researchers wanted to see why males are more likely to have autism than females. They determined that this is because females are more resistant to these genetic mutations. It takes larger changes in the genome for them to be affected. An importance to figuring out the genetics behind autism is that proper diagnosing can occur. Physicians will be able to figure out whether the child has autism or the have a personality disorder. This would change the treatment process of the neurological disease.
Another cause of autism is the diet that the person has. The diet can affect the molecules that are in the brain and how the brain develops. If someone has a diet that is high in linoleic acid (LA), it will be beneficial to the brain. This is because this acid promotes arachidonic acid (AA) and eicosapentaenoic acid (EPA). Both of these acids will cause brain growth and development. This will cause the correct neurotransmitters to be released in the brain. If the neurotransmitters, such as acetylcholine and serotonin, are not released correctly, the brain will not have correct neuron function and neuronal preservation. This can then lead to autism spectrum disorders.
Can genetics affect obesity and the brain?
There are many negative side effects of being obese. Some of the effects that are not looked at though, are the effects that obesity has on the brain. There are many problems that can occur within neurotransmitters because of high fat diets and obesity. One of the main systems that is affected by a high fat diet is that leptin activity is inhibited. This causes many downstream effects to occur. One of these is that Erk is inhibited and this causes the up regulation of the Gsk-3 pathway. This is detrimental because less BDNF is produce. BDNF is a transcription factor that helps protect the cells and prevent apoptosis. A high fat diet will also increase the chances of having type II diabetes. With type II diabetes there will be insulin resistance within the cell. From one of my previous blogs, it can be seen that insulin resistance will lead to decreased cognitive function. This insulin resistance will also cause the inhibition of leptin activity. Then the cycle that was described earlier will occur in the neurons. Another result from a high fat diet is lipid peroxidation. This causes oxidative stress to occur within the cell. This oxidative stress will disrupt the unfolded protein response (UPR). If the UPR is not correctly working, the cell will end up dying because of apoptosis. This apoptosis will cause a decrease in cognitive function. Another problem that can result from this diet type is disruption in the blood brain barrier. The blood brain barrier is disrupted because of the down regulating the mRNA expression of Claudin-5 and -12. The reason that this is a problem is that harmful chemicals can enter into the brain if the blood brain barrier is not working correctly. It also disrupts the ability of the brain to flush molecules out of the system.
One important idea that is associated with the problem is that some people may have a gene that may incline them to be more obese. This gene is known as the fat mass and obesity associated gene (FTO). The gene is for a enzyme that catalyzes the demethylation of 3-methylthymine. This gene has been shown to be upregulated after food deprivation and negatively correlated with the food stimulation of food intake. This gene has been shown to have a greater effect on the person if they have both alleles for it. This means that if both of the chromosomes have the FTO gene, the person has a higher chance of being obese. The problem with this though is that people may try to use this as an excuse on why they are obese. This gene may cause this but it can have no effect if someone diets and exercises properly. Another problem with this gene is that people with it tend to have a tendency to show more symptoms that are commonly associated with metabolic syndrome. These symptoms include higher fasting insulin, glucose, and triglycerides, and lower HDL cholesterol. This may be caused though by the weight gain rather than the gene itself. A final problem that may occur because of this gene is that there is a decrease in the frontal lobe in the brain and an impaired verbal fluency performance. Like I stated earlier, a person may have this gene but it can be a non-factor if some has the proper diet and exercise regimen.
The Basics of Autism
During the week of November 17, my neurochemistry class and I learned about and discussed a very common mental disorder that impacts many families throughout the world. The disorder that I am referring to is autism. Autism is a disorder of neural development that is characterized by impaired social interaction and verbal and non-verbal communication, and by restricted, repetitive or stereotyped behavior. People who have autism have a difficult time making friends because of their impaired social and communication skills. It is one of the three disorders that are recognized to be on the autism spectrum. The other two diseases that are on the autism spectrum are Asperger syndrome and pervasive development disorder, not otherwise specified, which is diagnosed when the criteria for autism and Asperger syndrome are not met. In our particular discussion of this disorder, we primarily talked about the many different mechanisms that are impacted within an affected individual. In this blog, I hope to convey this information as accurately and clearly as possible.
It is believed that autism is a neurodevelopmental disorder that occurs as a result of disjointed information processing in the brain due to alterations in how nerve cells and their synapses connect and organize. Researchers have determined that there are several lines of evidence that point to synaptic dysfunction as a cause of autism. There are rare mutations that may lead to autism by disrupting some synaptic pathways, primarily those that are involved in cell adhesion. The neurolignin genes, which encode postsynaptic adhesion, undergo point mutations and deletions that have been observed in patients with autism. Currently, there are no cures for autism, but the neurolignin genes could potentially be a target for future research regarding a cure for this disorder.
Another system that is negatively impacted in patients with autism is the cholinergic neurotransmitter system. People with autism have neuropathologic abnormalities in the cholinergic nuclei in the basal forebrain, which is an aspect of the cholinergic neurotransmitter system. Within the cholinergic neurotransmitter system, the levels of important nicotinic receptors were significantly lower in autism patients compared to patients without autism. This causes the level of brain derived neurotrophic factor (BDNF) to be higher in the basal forebrain of individuals with autism. These findings suggest that abnormalities of the cholinergic nervous system must exist in autism.
Although there is not currently a cure on the market for autism, researchers are in the early stages of clinical trials of a potential cure. In the meantime, it is important for individuals with autism to utilize the necessary treatment protocols in order to try to improve their social and communication skills. One important treatment that is utilized for autism is to increase the intake of polyunsaturated fatty acids (PUFAs) in the diets of people with autism. PUFAs are essential for brain growth and development and enhance cognitive development and memory. In addition to this, PUFAs inhibit the production of neurotoxic cytokines and enhance nitric oxide synthesis. This prevents neuronal apoptosis and facilitates memory improvement and consolidation. Overall, increasing PUFAs in a person’s diet will increase their social and communication skills.
Since autism is such a common neurological disorder and is even becoming increasingly more common, it is important to know and understand its negative effects on the brain. The disorder doesn’t allow the proper formation of synapses to occur in the central nervous system and it also negatively impacts the cholinergic neurotransmitter system. Overall, it has been very interesting learning about autism and the effects it has within a person’s brain.
Capping off my Capstone: an Unconventional Chemistry Class
Neurochemistry at Concordia College was unlike any other science course I have ever taken. When most people, including myself, think of science classes, they think of a teacher standing in front of a room of unresponsive students lecturing about topics that are hard to see in a greater context while the students write down as much information as possible to memorize for an exam. Almost none of this occurred in CHEM 475. Neurochemistry was a very unconventional class in many ways, but in the end a fair amount of science, as well as other applicable skills, was learned by everyone, including the professor.
The first unconventional aspect of CHEM 475 was the structure. This class fulfills the capstone requirement to complete the core at Concordia College. The purpose of a capstone class is to be the, “arc of the Concordia Experience,” as said by the college’s president. Some main goals of Concordia’s core curriculum are to integrate writing into all classes and to invite student to become responsibly engaged in the world. These requirements might not seem to fit in with a neurochemistry class, but through the unconventional structure of the class, they definitely were met. There were very few days of actual lecture in this class. The first few periods were lecture simply to introduce the course and some basic background knowledge for the unconventional group of students in the class. Most upper level chemistry classes are strictly taken by chemistry majors only. But CHEM 475 was made up of students from chemistry, biology, neuroscience, and even psychology. The diverse group of students helped create a lively learning environment that perfectly housed the unconventional structure of the class. Like mentioned before, the class was not lecture based. Mondays were devoted to asking questions and discovering what we didn’t understand for the week’s assigned article. Wednesdays were designed for each student to teach a specific topic relating to the article to every other person in the class, including the professor. Fridays were spent discussing the week’s article as a whole. It was a time to put together the small topics discussed on Wednesday to help understand the article assigned for Monday and to see how each specific neurological disorder topic could fit into our lives and society in a new and well informed way. It gave us a day to develop our own ideas on the week’s topic so we could go back and spend the weekend writing a blog articulating what we learned to share it with the world on our online blog,
Along with the unconventional structure of the class came unconventional assignments. Each week were assigned an article relating to a different neurological disorder or concept. For Mondays, our job was to read the article and to write down things we didn’t understand. Usually when scientific articles are assigned in a class, the point is to summarize them or to learn some sort or concept, memorize it, and then be tested on it. This was not the case in CHEM 475. The point of reading the article was to pick specific confusing things, present them to the class, and to ask our peers to help understand them. This class was taught as a team, with each one of us, along with the professor, being an equal and important contributor to the learning of everyone. We all relied on each other for learning. We each did a small portion of research but ended up gaining a ton of knowledge through the help of our classmates. I had never thought to learn this way, but I think it was quite effective. The process of presenting my topic helped me understand it more. When a peer would ask me a question about my topic, I had to use my critical thinking skills to try to answer it to the best of my ability if it wasn’t something I had specifically researched. Sometimes asking questions can be intimidating for me. But asking another peer one on one was a lot easier and very comfortable. I also felt less awkward admitting I didn’t know the answer to a question to just one other person and not in front of the whole class.
The “exams” in CHEM 475 were just as unconventional as the assignments. For our exams, we were given a deconstructed version of a scientific paper with some basic facts and diagrams. We were then asked to use critical thinking and then piece together the puzzle of the molecular mechanism described in the paper using our knowledge of how mechanisms work. Then came the most important part. Analyzing our response in the form of a take home essay in order to evaluate our answer with the actual mechanism proposed in the actual paper. I definitely struggled with the first take home exam, but I was quite impressed with myself when my hypothesis for the second exam was actually pretty consistent with the mechanism presented in the actual paper. I think this was an awesome way to learn. It is very rare that we are the graders of our own assignments. Many times you simply take an exam, see your score, and move on to the next set of material. Not in CHEM 475. Evaluation of your own work was a huge part of the learning process. It caused you to actually think about what you wrote and why you thought it.
As a capstone course, this class was supposed to offer an opportunity for all students to build competence, creativity, and character through collaborative learning. I don’t think this sentence could have described CHEM 475 more perfectly. Collaborative is the perfect word to describe the learning that went on in this class. I wouldn’t know even half of the things I learned in this class without the help of my peers explaining specific topics to me. I would have never thought of many of the things talked about in large group discussions if I was to have expressed my opinions in some sort of paper. Learning in CHEM 475 happened as a team of equals, students who were equally confused, equally ready to learn, and equally ready to share our ideas, even if it did take some pushing at first. For me personally, competence was built because prior to this class I knew very little about neurochemistry and neurotransmitters. Creativity was built while piecing together information for take home exams. Character was built through being forced to be independent and take charge of my own learning rather than relying on a professor to spell everything out for me.
Some specific goals of the class were to identify basic properties of neurochemicals and their responses, describe mechanism of common intercellular signaling pathways, learn about neurogeneration and neurodegenerative disorders, and to translate scientific information into general terms for non-scientific audiences. I would say every single one of these goals was accomplished for me in this class. Seeing as I knew close to nothing about the brain and neurotransmission prior to this class, I definitely now know the basic properties of neurotransmitters. Could I tell you every single pathway we talked about this semester? Absolutely not. But I could tell you that THC might not be as bad as some people think, type 2 diabetes can be linked to Alzheimer’s disease, lithium could possibly help treat Parkinson’s disease, the AKT/GSK3 pathway is involved in a ton of signaling, and many other important pieces of information from my semester in neurochemistry. Hopefully, my previous blog posts have proven that I can translate scientific information that myself and 20 other senior college students studying some sort of science could hardly understand into semi-simple ideas that non-scientists can appreciate. Science is cool and all, but if we can’t share it with the general public, it doesn’t do much good. To have a bunch of super educated individuals knowing about science is important, but translating that information to the greater general public is much more valuable.
How do I feel about this class as a capstone? Well to be honest, I was dreading this class. For three years I was planning to take Biomedical Ethics to complete my capstone requirement. Sadly when registering for classes in the spring of my junior year I was informed that class was no longer being offered. Being stuck needing a capstone to graduate, I signed up for CHEM 475. I thought I was unprepared in the class and was ready to feel lost the entire semester. Basically, I was right about both of those things. But I wasn’t alone in that boat. Many others were lost throughout the semester. Working together through our confusion led to even greater learning than we could have done on our own. In this class, we were responsible for the learning of our peers, we were the teachers, and we needed to pull our weight in order to help everyone else succeed. What a better way to become responsible engaged in the world than by taking personal responsibility for the learning of others. That is exactly what we did in CHEM 475. Am I upset I was unable to take my preferred capstone? A little, but I think what I gained from CHEM 475, both in knowledge and experience from a completely unconventional class makes up for my small loss.
A Different Spectrum
Autism spectrum disorders represent a variety of disorders in which neural development is altered, leading to impairment in social interaction and communication. In addition, spectrum disorders are typically characterized by a variety of restricted or repetitive behaviors. Within the spectrum are autism, Asperger syndrome, and pervasive developmental disorder, not otherwise specified. Changes in screening as well as an increase in screening has seen a 600% increase in prevalence over the past two decades. While some of this may be a confounding effect from an increase in screening, it is likely that the incidence of autism is truly increasing.
With strong genetic as well as environmental factors, it is difficult to be certain of autism’s pathology within the brain. Changes have been noted in inflammatory markers as well as synapse formation, nerve transmission, and information processing. Of primary concern is a deficiency of brain-derived neurotrophic factor as well as an altered metabolism of polyunsaturated fatty acids (PUFAs). PUFAs are fatty acids that contain more than one double bond in the backbone and are typically known as the “good fats”. These PUFAs include omega-3 fatty acids which have been shown to lower the risk of heart attacks. PUFAs have been shown to augment levels of BDNF in the brain as well as physically interact with BDNF. With a deficiency in levels of BDNF in the brains of individuals with autism, PUFAs may be necessary to support proper brain function.
Although there is still so much that is yet unknown about autism and its related spectrum disorders, there are certain things that can be done to support proper brain development and function. Of primary concern is prenatal care. Some studies have shown that maternal infections and inflammation may be implicated in altered gene expression leading to dysfunction of neuronal function and neurotransmitters as well as alteration of the metabolism of PUFAs. It is believed that this may cascade and lead to the development of autism. With this knowledge, it is imperative that mothers receive proper prenatal care. This includes a proper diet that is able to support fetal growth. Specifically, a diet rich in poly unsaturated fatty acids may provide the fetus with the necessary molecules for BDNF function. In addition, it is important that mothers take proper care of themselves during fetal development in order to avoid infections or causes of inflammation. Proper prenatal care not only supports proper brain development, but is also beneficial for the development of the fetus as a whole.
With so much yet unknown about autism and autism spectrum disorders it is difficult to pinpoint a specific solution to the problem. Treatment is usually case specific, focusing on a variety of behavioral interventions that are specific to individuals. There are some medical treatments that include improvement of the diet, vitamin and mineral supplements, and some pharmaceuticals that are proving to be very hopeful. The most promising of these drugs is Suramin which blocks purinergic receptors that have been shown to be implicated with autism. While there is some hope as far as treatments, I believe it is imperative we take the simple steps, including proper prenatal care, to hopefully lessen the prevalence of autism.
Autism: A closer look
For those of you who aren’t overly familiar with autism, it is a neurological disorder in which those afflicted have severe social debilitations, as well as communication and behavioral deficits. Over the past two decades (give or take a year), there has been quite a substantial increase in diagnoses of autism in the US. This is obviously due to all of the vaccinations that children are getting now, right? WRONG, that theory has been debunked, and a new theory is in place. This new theory argues that the autism diagnosis rate is linked to social surrounding of the child. For example, the children of higher educated parents are more likely to be diagnosed. Parents with a higher level of education will probably have a greater awareness for such a disorder, and greater means with which to test, diagnose, or treat their children. Additionally, the diagnosis protocol for autism has changed, which may play a part in the increases of diagnoses.
While we’re on the topic of diagnosis it might be helpful to address how someone is diagnosed with autism. Diagnosis of autism is done with a list of twelve symptoms broken down into three different categories; 1. Social Skills, 2. Communication Skills, 3. Behavior. If someone exhibits six of the symptoms on the list, they are diagnosed with autism. This diagnosis scale is helpful, but leaves some room for error and misjudgement, which could play a role in the rise in diagnosis.
From a biologic standpoint, the cause of autism can be pinpointed to multiple sporadic genetic factors in the form of copy number variants (CNVs) in the genome. These CNVs are duplications or deletions of genes in the genome and can lead to autism. In the brain this translates to dysfunction of cell adhesion. Cell adhesion is the process of cell adhesion molecules enabling cell to cell/cell to extracellular matrix connection. This allows for synapse formation and strengthening of synaptic plasticity. In autistic people, these processes don’t work correctly and can lead to the disease. Due to the diverse nature of autism cases the treatment is varied from patient to patient, and usually consists of behavioral therapy and medicines. While there is no cure for autism, the drug Suramin is being tested as a potential cure for the disorder. This drug increases the expression of certain receptors in the brain that are normally underexpressed in autism, as well as block other receptors that contribute to autism.
It seems that with additional research a determination, a cure for autism may be in sight. This would better the lives of a growing number of individuals diagnosed with the disorder each year.
Is Lithium the Missing Element?
For those of us science nerds out there Lithium is known simply as an alkali metal with the atomic number 3. In the medical world, however, lithium has served as a clinical treatment for bipolar disorder for over 50 years. The question that is now being posed is whether lithium is the missing element in the treatment of a wider set of neurodegnerative diseases. Bipolar disorder, also known as manic-depressive disorder, is characterized by extreme mood swings between depressive and manic states. Lithium is effective in treating acute manic episodes as well as preventing relapses. While we do not have a full understanding of lithium’s actions in the brain, it has been suggested that lithium has a neuroprotective/neurotrophic property. It acts in a variety of pathways in the brain, eventually leading to the inhibition of apoptosis, or cell death. In addition, those pathways devoted to cell proliferation are stimulated, leading to a neurotrophic effect.
With lithium’s success in the treatment of Bipolar disorder, some researchers are beginning to wonder if it might be effective in a variety of other neurodegenerative diseases. The neuroprotective role of lithium seems promising in considering diseases that lead to cell death. In addition, lithium has been shown to protect against a variety of pathologies that are present in neurodegenerative diseases. Glutamate-induced excitotoxicity is noted in diseases such as stroke, Huntington’s disease, amyotrophic lateral sclerosis, brain trauma, cerebellar degeneration, spinal cord injury, Alzheimer’s disease, as Parkinson’s disease. Lithium has shown to protect against the detrimental effects of glutamate-induced excitotoxicity. In addition, lithium has been shown to protect against endoplasmic reticulum stress, which is common in many neurodegenerative diseases. While animal models have been successful in utilizing lithium to treat a variety of neurodegenerative diseases, the difficulty comes in seeing if these results will transfer to human trials.
Although lithium has been shown to have beneficial effects, it’s important that proper studies are done prior to its widespread clinical use. As previously discussed, lithium acts within a variety of pathways in the brain. In addition, we haven’t yet elucidated all of its effects in the body. By acting in a variety of pathways, lithium presents the issue of unwanted side effects. In a clinical setting, it may be necessary to consider the benefits along with the side effects to see if the overall outcome is worth the negative effects. While it has been effective in the treatment of Bipolar disorder, more research is necessary for its use as treatment for other diseases. That being said, it seems as though lithium just might be that “missing element” for treatment of a variety of neurodegenerative diseases.
Which is worse?
Amyotrophic lateral sclerosis (ALS) is disease in which motor neurons in the brain degrade and eventually die. This leads to the loss of motor and muscle control resulting in muscle spasms, loss of motion in muscles, potential loss of speech, and even loss of respiratory function. This disease affects 20,000-30,000 people in the US with about 5,000 people being diagnosed each year. This disease progresses quickly and the average lifespan of a person diagnosed with ALS is roughly 3-5 years. The main cause of this disease is unknown, but there are genetic factors that make some people more likely to experience it than others. In this particular blog, I decided to go into a bit more detail about the “disorder of the week” for class since it became apparent in discussion that many people were quite uninformed about ALS prior to reading the assigned article.
The article of the week, Calcium-dependent protein folding in amyotrophic lateral sclerosis, sheds some light on how disturbances in calcium homeostasis and protein mis folding could be related to ALS. In general, dishomeostasis of calcium and mis folded proteins can lead to neurodegeneration. Specific proteins are found in cells in order to ensure that other proteins are folded correctly. The folding regulation proteins are usually regulated by calcium. This creates a distinct link between calcium levels and levels of mis folded proteins. Low calcium leads to low regulation of corrective proteins, which leads to high levels of mis folded proteins. Both of these events can lead to neurodegeneration.
The article tried to make a strong argument for how calcium levels and mis folded proteins can cause ALS. The article did a great job explaining how calcium is able to regulate the proteins that check for mis folded proteins in cells, but I don’t think it made a convincing argument for the cause of ALS. It did have some really great points, for example it explained why motor neurons are most affected by calcium. Motor neurons are more permeable/sensitive to calcium compared to sensory or other neurons. This makes their argument very strong to show why loss of muscular control would come from this imbalance of calcium and mis folded proteins. But in my opinion, explaining the motor neuron loss isn’t quite enough to prove that it is a cause of ALS. I think with further research into how this mechanism is related specifically to ALS and not just motor neuron loss in general would make the paper’s argument more convincing.
During the discussion of ALS in class, one interesting question came up about which would be worse: To have a neurological disorder that leave you cognitively impaired but physically fine, or one which leave you cognitively functioning but physically very ill. This question really made me think. I thought instantly about Alzheimer’s disease as it would compare to ALS. I personally have never known anyone with ALS, but I have seen AD in multiple people. Both diseases are extremely hard for both the patient and the family, but difficult in what seems to be different ways. I think it would be incredibly frustrating to be cognitively functioning normally but unable to control my body movements or speech like an ALS patient. It would also be frustrating to be physically functioning fine, but be afraid or confused by my own family members due to the memory loss associated with AD. If I had to choose one of these diseases, I think I would prefer to be physically functioning normally but cognitively dysfunctional. I think losing the ability to perform simple tasks on my own and have control of my body would too difficult, especially if I was able to comprehend and perceive the world in the same was as myself “pre ALS.”
This specific disease made me think about neurodegeneration in a new way. Previously, most of the diseases we discussed in class had to do with cognitive decline due to neurodengeration. Even the topic of obesity led to cognitive decline, which to me wasn’t an obvious connection. I think the fact that the brains of ALS patients remain able to think and learn correctly even when their motor neurons are have experienced extreme damage. It is quite interesting how the motor neurons seem to be the only ones effected in ALS, but that seems to be explained by dysregulation of calcium which leads to the buildup of mis folded proteins in the brain. Usually in my blogs I end with some sort of suggestion as to what can be done to prevent the “disease of the week.” Unfortunately this week I don’t have much advice since the exact cause of ALS is unknown. But as usual, everything in moderation will help keep a natural balance in your body.
One to sum it all up
The past semester has gone crazy fast, and I ended up taking away a lot more from this class than I thought I would. Although there were a few topics in this course that were less exciting than others, I found myself drawn to a few key ideas. One topic I found very interesting, and relevant to many topics discussed, was our diet. I knew it was important to watch what I ate, but I was unaware of just how much my diet dictated my mental health. The physical outcomes of eating healthy are obvious, but the not so obvious benefit is our neurological health. I was unaware of how important our diet is in determining how our brain functions, and its ability to retain information. It made me reflect on what I was doing to my short and long term health; not only on being visibly healthy, but being healthy within too. Many of our discussions incorporated some sort of imbalance within the body, and came to the conclusion that if we have everything in moderation we should be able to keep ourselves mentally and physically healthy.
There were a lot of terms and pathways I was not familiar with, but after my classmates helped me through some of the ideas I was struggling with, I was able to take away a lot more from what we were reading. At first it was difficult to take away information that was presented, but after we found a technique that worked, it worked well. Not only was I learning information pertinent to neurochemistry, but I was able to take what others had told me and use them in conversations in other classes or with my peers. After reading many of these articles, I was able to discuss some aspects of them with my friend who is majored in dietetics. Granted we have oddly intense conversations occasionally, but it was fun to use something that I learned in a class in a casual conversation.
One great part of this class is that we were able to have these mini-learning sessions that classes that are large would not be able to do. It took a little while to warm up to each other, but eventually we were able to create an atmosphere where people could ask questions that would never be asked in a large lecture setting. On Fridays we were able to discuss ideas relevant to our week’s topic, but take those concepts and run with them. We often ended up going on tangents, and for me, lots of it came back to what we were putting into our bodies that dictated our mental health among many other things.
Another aspect of this class I greatly appreciated was our “exams.” They were more like puzzles we had to figure out using information given to us. I was forced to think critically and put together a collection of tidbits from a paper, which would (hopefully) represent the hypothesis from the research article. Along with this, we were given an out-of-class portion where we were given the research article. We had to evaluate what we had put together in-class, and discuss how we were either right or wrong. From this, I learned how to effectively read a research article and pull out important information.
The class setting was much more relaxed than other chemistry classes, but I found myself just as involved. It allowed me to see my science peers in a different light, and I enjoyed being able to do so. This class challenged me to think in a different way because I had to teach concepts instead of being taught them. This class incorporated many of central aspects of a liberal art learning, and I believe that by taking this capstone I can be more responsibly engaged in the world, especially with being more aware of how to try to prevent many of these diseases we studied and trying to inform others of what I learned. Over Thanksgiving, I tried to start with my family, and just as we assumed in class, you can give someone information, but it may take a while for them to actually believe you and take their health into more preventative measures. However, it is now my responsibility to tell those I love the information I know, and what they do with it is up to them (but my constant nagging may influence their response a little).
This class was both informational and fun. I learned a lot about the pathways within our brain, and how these pathways can be affected by what we do, or don’t do, by what we eat, and by what mothers do/eat while pregnant. Not only did I learn, but I had fun being able to see a completely different side of my classmates, and being able to use what I learned in conversations outside of class. This experience incorporated the goals of Concordia, and I believe that it allows me to be even more responsibly engaged in the world.
Obesity: A growing problem
“Welcome to McDonalds, what can I get for you?”
“Yeah I’ll get a number 1 with a large fry and a large Coke.”
“Alright, anything else for you today?”
“Yeah…can I get a medium Oreo McFlurry too?”
“Of course, we’ll have your total at the first window.”
Above is an occurrence that happens all too frequently everyday in the US, and at 1,970 calories, this meal is nearly enough for a whole day’s nutritional needs. This may seem obscene, but it’s what we have become accustomed to in recent years. This week in class we talked about obesity, and it’s effects on the brain and body of those individuals who have it. We have, however, begun to ask the question, “Is it their fault?” This week’s paper looked at the neurological pathways involved in the disease and discovered that, in fact, there are neurological ties to obesity, and it isn’t just overeating and laziness, as some people view it. In a sense, the article argues that we have no control over our natural inclination for a high fat diet or overeating. It turns out that when a baby is in the womb, their mother’s diet plays a huge role in the inherent disposition for the child’s eating habits. If the mother eats a high fat diet, the child will also be inclined to eat a high fat diet. This was tested and confirmed in a mouse model study. To get into the technical nitty gritty (for just a minute), there are two neuron types in the brain: the POMC and the NPY/AGRP. The POMC stimulates appetite and is overactive in obese people, and the NPY/AGRP suppresses appetite and is underactive in obese people. Other hormones and proteins play a part as well like grehlin (appetite stimulant), insulin (appetite suppressant), and leptin (appetite suppressant).
So we know that it’s not our fault if we’re fat, but that doesn’t change the fact that there are a multitude of negative consequences. Take Type II Diabetes for instance, or heart disease. Those both suck. How about Alzheimer’s? Studies show that those who are obese are at higher risk for Alzheimer’s, as well as other neurological diseases. The real question that remains is what can we do about it? How can those who suffer from obesity fight the negative effects of obesity? Two different strategies were investigated in class, both of which seem to have beneficial effects towards fighting obesity, and both are simple to implement in everyday life. The first is eating the right kinds of foods. A diet composed of high fibrous food such as root vegetables (or really any fruit or veggie) has many advantages. These types of food fill you up faster and make you feel fuller for a longer period of time, because they slow down gastric emptying. Additionally these signal the upregulation of GPl1 and PYY, two hormones that curb appetite. The second strategy is to get more, a regular, sleep. Our society promotes the fast a frantic non-stop lifestyle that usually leads to unpredictable sleeping patterns. This has consequences on the circadian rhythms in cells. Ultimately, irregular sleep can lead to decreased metabolic function and weight gain.
I think that the most important thing is to be aware of what you are taking into your body. While there does seem to be a neurologic predisposition to obesity, if we as a society make smarter choices and regulate our consumption and sleep patterns (just to name two possible solutions), we can curb obesity and fight the growing epidemic.