Autistic Spectrum Disorder affects thousands of families all over the world. This disease does not have a cure or a reversal treatment but provides medications to help suppress the symptoms. Symptoms can range from impaired social interaction to repetitive activities and behaviors. The spectrum ranges and the severity of these symptoms can as well.
What causes ASD is an open-ended question. The cause changes from case to case from one simple malfunction to multiple impaired functions. A few possibilities outlined in “Advances in understanding the pathophysiology of autism spectrum disorders,” are: neural connectivity impairment, impaired neural migration, dendrite morphology, excitation-inhibition imbalance, impaired immunity, epigenetics, genes and finally, the broken mirror theory.
Autistic Individuals Can’t Learn
While most people can learn using 2-3 various styles most autistic individuals rely on one. These various learning styles are chosen from: auditory learner, visual learner, hands-on leaner, etc. Input is received from all senses in an environment that a person is in. In most schools, the requirement of reading a PowerPoint while simultaneously listening to a teacher is required. An autistic individual may only learn from hands-on experience, permitting them from learning properly in an educational system. Learning styles differ from person-to-person just as each autistic individual needs to be provided with their correct learning style to learn. They have the ability to learn, but might not be provided with the correct tools to learn.
Autistic Children Are Anti-Social
Individuals with autism can be very social and enjoy having relationships with other individuals. However, they may use other forms of communication and may not enjoy being in crowded, loud environments. This does not mean that the individual is anti-social, but rather that they enjoy a more comforting environment. Children with autism can be found to make good connections with individuals who are understanding and patient with the form of communication. Autistic individuals may seem anxious, misread social cues, and need support to communicate, but should not be misunderstood as anti-social personality disorder. In “Emotional Understanding, Cooperation, and Social Behavior in High-Functioning Children with Autism,” the article helps debunk the idea that children with autism are anti-social. They found evidence that children with autism may lack in appropriate behavior and reading of emotions but still have a social behavior just like any other human. With such a broad spectrum, what an autistic patient requires in a social environment changes and their ability to understand as well.
Vaccines Cause Autism
The first vaccination was given in 1796 in England. Centuries of vaccinations were provided before a young red-headed girl brought her case to court about Autism. In 2007, Hannah Poling received a settlement for acquiring autistic-like symptoms after being vaccinated with the MMR vaccine. MMR vaccine is found to fight against measles, mumps and rubella. This vaccine has been vary controversial in the autism and vaccine theory. A study conducted by B. Taylor, E. Miller, C. Farrington, etc al. in took 498 autistic patients and debunked the connected between MMR vaccine and autism. “Our analyses do not support a causal association between MMR vaccine and autism.” Repeated research has been testing the safety of vaccines. No scientific data concludes vaccines cause autism.
(For more information on the case: https://www.nejm.org/doi/full/10.1056/NEJMp0802904)
It is believed that over 1.5 million people in the United States have Autism spectrum disorders (ASD). Individuals that have been diagnosed with ASD typically display symptoms of ritualistic or repetitive behaviors, have difficulty communicating with others, and often have unusual social interactions. As this disease continues to become more prevalent with no known explanation, researchers have begun to try and find a link that may combine the many different theories as to how ASDs develop.
The Puzzle Pieces (Theories):
Imagine the brain as a sophisticated computer complete with many delicate connections, wires, and an instruction manual so thick that it’s impossible to know all of its functions.
“Faulty Wiring”
It is believed that ASD may be the result of improper neuronal connection in the brain. If neurons are unable to connect to each other successfully, they will not be able to communicate properly. As seen in a computer, if the wiring is faulty, the device will not be able to carry out its desired function. This is exactly what occurs in the brains of individuals with ASD. This faulty wiring can happen in many ways:
(1). Too many neurons
If there are too many “wires” in the circuit, it will not function properly due to excess “noise”. This is exactly what happens in brains that have too many neurons. The abundance of neurons impairs the proper functioning of the circuit, or in the case of the brain, the synapse. In a “normal” brain, excess neurons are removed through synaptic pruning, and the remaining neurons strengthen their connections with one another to improve communication via synaptic plasticity. In a brain with too many neurons, such as in ASD, these connections are unable to properly form and remain weak.
Figure 1. The image on the left shows a brain unaffected by ASD, while the one on the right shows an increase in neurons found in an individual with ASD. This increase may be the result of the aforementioned failed synaptic pruning. (Credit: Guomei Tang, PhD and Mark S. Sonders, PhD/Columbia University Medical Center) http://www.kurzweilai.net/children-with-autism-have-extra-synapses-in-brain
(2). Neurons in the wrong place
It is believed that during development a mutation in the reelin gene (RELN), responsible for the proper placement of neurons, may lead to neurons developing in the wrong place. If neurons are in the wrong place, they are unable to communicate properly and functioning is impaired; this is the case in ASD.
(3). Too many synapses
A mutation in the MeCP2 gene, a silencer of gene expression, leads to an inability of the brain to properly rid itself of excess synapses within the brain. In addition, an abundance of dendritic spines (the receivers of the message) resulting from defective pruning has also been shown to induce a hyperactivated mTOR pathway. The mTOR pathway inhibits autophagy. As autophagy is responsible for removing excess dendritic spines, synapses, and neurons, these structures remain in the brain and induce further faulty wiring, which inhibits proper communication.
(4). An imbalance of On/Off signals – Excitation and Inhibition
A balance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters, the chemical messengers in the brain, is essential for proper communication. It is believed that this imbalance may be the result of gene mutations, a defective blood brain barrier (BBB), or neuroinflammation, which will be discussed later. When this balance is not maintained, the neurons (wires) may die. This is often the result of excess glutamate in the brain. Under these exitotoxic conditions, further neuroinflammation may occur inducing more cell death.
“Faulty Programming”
(5). Mirror neurons
Mirror neurons and the connections they form are responsible for one’s ability to learn from their environment through imitation. If an individual is unable to recognize, understand, and learn from the actions and emotions of those that they are in close contact with, it is impossible for them to understand how to act “normal” in social situations. Being that two of the main symptoms of ASD are problems with communication and difficulty behaving in social situations, it is believed that faulty mirror neurons may play a role in the development of ASD.
(6). Genes/Epigenetics
It is impossible for a computer to work properly if it is programmed incorrectly. This is exactly what occurs with mutated genes that may cause ASD. As there is no single gene responsible for ASD, through extensive research, scientists have been able to classify the defective genes into three main families:
Genes responsible involved in synaptic transmission
Ex: SHANK3, NXN1, NLGN3/4
Genes related to abnormal cellular/synaptic growth
Ex: Genes associated with autophagy/mTOR: TSC1/2, PTEN, NF1
Genes that control gene transcription and translation
Autism is difficult to define, because it is such a spectrum. From mild to severe cases, every individual may experience different symptoms of the disease. However, the generic idea is that in people with autism experience a decrease in amount of neural communication. The communication error may be the result of three different issues that neuroscientists have looked at.
Neural Connectivity
In autism, the normal process of pruning the unnecessary neurons to promote stronger connections is vital in neural signaling. If there are too many neurons, the amount of low-level signaling is too high, causing “noise” in connectivity which then disables efficient processing of information.
E/I Imbalances
In the brain, GABA is the substrate that inhibits activity, while glutamate is the molecule that excites the brain. The two work together to balance each other out to do the basic functions of the brain. This is all good and dandy until the balance gets out of whack. When the brain uses its spidey senses and detects something is wrong, it tries to fix it. The immune cells in the brain stimulate inflammation, which is great when there is actually something wrong in order to get rid of the “bad guys”. But in this case, there are no “bad guys” and the inflammation only contributes to the difficulty of neural connectivity.
Dendrite Morphogenesis
Remember about that inflammation causing trouble with signaling? That’s probably because the inflammation, during the developmental years (2-4 yrs old), creates little room for the neurons to expand and grow into the correct size and shape. With odd-looking neurons, signaling cannot go as planned.
So how do we fix it?
Unfortunately, there is no cure to autism, yet. Several labs are currently studying the ways that autism can be treated. However, with such a large spectrum, it is hard to find a cure for everyone. Right now, all we can do is treat the symptoms of autism. We can do this using treatments, medicine, or a combination of the two.
Treatments:
A commonly used treatment for autism is Applied Behavior Analysis (ABA). It is based on the idea of positive reinforcement in order to communicate goal behaviors. The person receives a reward when the goal behavior or skill is performed. It teaches the person that good things happen when that behavior is displayed.
Speech therapy is also very common with people with autism. For non-verbal, low-functioning autistic people, speech therapy can help with basic words and can even spend time working on the teaching of non-verbal communication. For high-functioning autistic people, speech therapy might just be a place where they learn about social and non-verbal cues that happen during conversations.
Both are good to help with interactions and communication.
Medicine:
It is necessary for medication to treat the three main symptoms of autism: communication difficulties, social interaction challenges, and repetitive behavior. Unfortunately, there isn’t a medication on the market that treat any of those things.
There are two main drugs commonly used by those who have autism: risperidone and aripiprazole. They both function by blocking dopamine and serotonin receptors in order to cut back on the “noise” that is being produced by the overactive neuron signaling.
Although not common, autism may be treated with naltrexone, which is an approved treatment for alcohol and opioid addictions. In the same way that it alleviates the addiction, naltrexone helps to disable repetitive and, sometimes, destructive behaviors that may occur with autism.
While not proven, many people with autism elect to take an SSRI, selective serotonin reuptake inhibitor. Some of which include: fluoxetine, escitalopram, and sertraline. It is said that these medications help with social interactions by alleviating anxiety and depression that may develop in autistic people.
That being said, it should be emphasized that AUTISM IS A SPECTRUM! Every person and their situation is unique. What may have worked for one person, may be harmful for another person. Talk to your doctor and see what option is best for you!
Autism Spectrum Disorder (ASD) is an extremely complicated and diverse disorder that presents itself in various ways. This disorder is somehow different in almost every single case, which is why the spectrum is useful in classifying the severity of the disorder. Unlike other diseases and disorders, Autism is not caused by one specific gene mutation or condition that leads to the development of the disorder. It is a combination of a variety of genetic and environmental factors that contribute in various ways to how the disorder is presented in those affected.
The two main themes found in most ASD cases are immune system abnormalities and a Zinc deficiency. Zinc is vital to the development and operation of a functional immune system. Many important enzymes and proteins in the immune system, and found at the excitatory synapses require zinc to function properly. Astrocytes are star-shaped glial cells that promote the recycling and re-uptake of neurotransmitters. They maintain a balance of excitation and inhibition signals in the brain. In patients with ASD, the GABA pathway was found to be one of the most affected pathways. Patients were found to have significantly decreased levels of GABA, an inhibitory neurotransmitter. When these levels are too low, there is not enough inhibitory signaling happening which leads to the overstimulation due to more excitatory signaling occurring. This could be linked to the symptoms experienced by people with ASD being overstimulated by their environment and not knowing how to process and appropriately respond to that stimulus.
In addition to this factor of the imbalance of excitation and inhibition signaling, there are many other factors that could possibly contribute to the development to Autism as well. One of these is the lack of pruning of unnecessary neurons which is called autophagy. In healthy brains, autophagy happens as the brain is developing, degrading the unneeded neurons while new ones develop. However, when this process does not go as it should, it leads to excess neurons which can also be a cause in the symptoms experienced in ASD.
Another common factor in patients with ASD is gastro-intestinal symptoms. The autistic brains were found to be correlated with a less diverse gut microbiome, specifically lacking carbohydrate and fermenting bacteria. It has also been shown that children who are born via C-section and who do not breastfeed are much more susceptible to a microbiota imbalance. In addition to this imbalance of microbiota, an increased permeability in the intestines is found to be common in individuals with ASD. This can be caused by a variety of factors including poor diet, chronic stress or bacterial imbalance. This condition allows unwanted macromolecules and bacteria to escape from the gut into the bloodstream and have the ability to cross the blood brain barrier which could contribute to the development of autism.
Autism is not a disorder with a single cause or treatment. Therefore, it is challenging to find the root of the problem occurring in the brain as each case is unique. It is a puzzle with many parts that come together to present the symptoms in an individual. These puzzle pieces can be any number of environmental and genetic factors that include and go beyond the factors previously mentioned. Autism Spectrum Disorder is extremely unique and difficult to research due to this aspect of the disorder. The spectrum can also be thought to include everyone. We are all on the spectrum somewhere, but the severity varies significantly depending on the symptoms that an individual displays. Each piece of the Autism puzzle comes together uniquely, and there is continuing research trying to solve more and more of this extremely complicated puzzle in the brains of people with ASD.
Autism spectrum disorder, or ASD, is a neurodevelopmental disorder characterized by impaired communication, behavior, and social interactions. The name in it of itself brings us to the first thing you need to know about this disorder: it’s diagnosis and symptoms lie on a spectrum.
Autism is a spectrum You may be asking yourself, what exactly does ‘spectrum’ mean in this case? I’m so glad you asked! With ASD, there are 3 known levels characterized by high functioning (level 1), autism (level 2), and severe autism (level3). The main differences across these levels include the support the person needs, the person’s communication and social skills, as well as their behavior (see image below). But again, remember, it is a spectrum disorder, which means it can be quite difficult to pinpoint which level any given individual might ‘fall into,’ considering their symptoms and how they behave change constantly. ASD is more fluid than most disorders because of this spectrum.
One of the many causes of ASD has to do with neural connectivity. Essentially, what this means is there is an increased number of neurons in the brain, which decreases the connectivity and circuitry of neurons and synapses in the brain. In a normal brain, the number of neurons actually decreases over time, which strengthens the connectivity overall. This impairment in ASD patients has other cognitive effects and plays into other causes discussed further.
The gut-brain axis is next. The gut-brain axis is how the gut, or the gastrointestinal tract, specifically communicates with the brain and CNS. There is still much unknown about the gut-brain pathway, but there has been research that shows that ASD individuals tend to have a less diverse gut microbiome (less carbs) and tend to have higher levels of “bad” bacteria. Along with this, there is also evidence for increased permeability in the intestines, which allow unwanted molecules to pass through the tight junctions. The GBA is so fascinating and plays a big role in epigenetic factors leading to Autism.
Hey, did somebody say epigenetics? The role of epigenetics is crucial to understanding more about ASD. This notion of changes in gene expression leads to interesting findings related to ASD. Rett syndrome is another genetic disorder that has been found to always produce symptoms characterized by ASD. Along with Rett syndrome, is fragile X syndrome, which has genes located on the X chromosome. This could potentially relate to the fact that we find a predominance of males with ASD!
It’s also important to understand the environmental factors associated with ASD. Zinc deficiency and immune dysfunctions can ultimately imbalance the excitatory/inhibitory (E/I) signaling in the brain due to glutamate dsyregulation. These environmental factors lead us right into number 6.
Maternal infection. Along with possible prenatal viral infections, prenatal and perinatal stress, toxins, the mother’s age, and postnatal risk factors, it is important to understand possible maternal infections linked with the onset of ASD among the infant. It has been found that mothers who had children diagnosed with ASD were more likely to have two or more infections during pregnancy, with bacterial infections also leading to a greater risk of ASD.
Another factor that is important to discuss with ASD, especially when it comes to symptomology, is mirror neurons. Mirror neurons help to explain why an individual is more likely to unconsciously copy another individual’s behavior. Think of the common saying, “stop yawning, you’re going to make ME yawn.” That’s right, you probably will, because of mirror neurons! This helps wrap our heads around individuals with ASD and how they behave and act-something isn’t working with their mirror neurons as many lack empathy, or know how someone around them may be feeling.
Defective synapses: oh no! As mentioned above, the increased number of neurons increases the number of synapses and actually the excitability of the synapse itself. Essentially this means something isn’t working quite right and leading to symptoms of ASD. Along with this, come genetic factors such as neurexin, neuroligin, and SHANK. Individuals with ASD may have genetic deletions of the protein neurexin, as well as incorrect linkages between neurexin and neuroligin proteins (causing something to go wrong with synaptic transmission). Finally, SHANK is a protein that regulates dendritic shape, and in ASD, could be disrupted.
It is known that there are elevated levels of cytokines in the brain that lead to inflammation. Cytokines are also linked with damage to the blood brain barrier and increased permeability. There have not been many studies on the link between inflammation and ASD, but it is critical to understand the role of cytokines and other neurochemical pathways outlined in ASD.
Last, but not least, we have the mTOR pathway and autophagy. Critical to understanding ASD and putting the picture all together is the link between this pathway and autophagy. This pathway promotes cell growth and differentiation, however an overactive mTOR pathway leads to inhibition of normal autophagy degradation. Autophagy is the way the brain helps to degrade synapses and neurons, which means the brain is being poorly pruned, thus leading to ASD. Autophagy can also be related to the connectivity and defective synapses that are characteristic of ASD!
Now you hopefully know 10 more things about Autism than you did before reading this post, and are better able to fit the puzzle pieces together for the causes that lead to the disorder.
Welcome to Cobbers on the Brain! This blog is a compilation of student commentary on the scientific articles discussed each week in my CHEM/NEU 475 – Neurochemistry class at Concordia College. Discussions are held each week regarding the scientific understanding of various neurological diseases, as well as the often muddy social, cultural, and ethical implications of this knowledge. Alzheimer’s Disease, concussion, ALS, addiction, anxiety, bipolar disorder, autism and aging are just a few of the topics covered in the course. We learn a lot, have much to say, but rarely have all the “answers” to our questions! I hope you enjoy…
According to the CDC, more than 1/3 of adults in the U.S. are obese. Why is this a problem? Why is obesity rising? Could we blame it on America’s fast-paced society and the growth of processed and fast foods? Sure we could, and those factors do play a role to some extent. Are people just not making conscious healthy decisions anymore? Of course not everyone makes healthy conscious decisions, but can we attribute that solely to the will of that individual? What if some people are not actually controlling their unhealthy decisions? What if their brain has been rewired in a way to promote their actions of unhealthy eating?
I hope you are not surprised when I say YES, scientists have been discovering that brain rewiring may be a huge factor in the obesity epidemic we have not yet considered.
Watching the Hips, Watching the Brain
Saturated fatty acids and other unhealthy components of processed food commonly consumed today pose a danger to the chemical signaling within our brain. These molecules are able to freely cross and accumulate within the brain tissue, leading to the activation of various inflammatory pathways within the brain. Over time, this over-activation of inflammatory pathways in the brain leads to insulin resistance and the inability of the body to properly utilize insulin for energy homeostasis maintenance. So my choice of chips over carrots at the grocery store is not only going to my hips, but is also negatively changing the chemical signaling within my brain that is responsible for regulating my energy and food intake. Awesome..
Obesity and Type 2 Diabetes
Insulin normally plays a role in the body to help store sugars (glucose) in the cells of the body after food consumption. This allows body cells to use that stored glucose for the body’s energy production of ATP, which powers our physical and mental actions, allowing us to go about our daily functioning. Diets high in sugar and simple carbohydrates (or simply just a high caloric diet) lead to insulin resistance because of the excess insulin released when you eat a lot of high-calorie foods. When too much food is consumed (high fat diet), the organelles in your cells become overwhelmed and stressed and inflammation ensues. The resulting activation of inflammatory pathways in the brain then lead to the inhibition of insulin receptors on body cells and ultimately insulin resistance. So, now when food is consumed, the body continues to release insulin, but the insulin receptors on body cells no longer respond to insulin’s binding, and glucose remains in the blood instead of being stored in body cells. Increased blood glucose levels over time is harmful to the body. This is also known as Type 2 Diabetes.
Insulin resistance also leads to the inhibition of POMC neurons in our body. This is of great concern because POMC neurons in our body are normally activated after food intake and tell us to stop eating. Inhibition of POMC neurons leads to the overeating often associated with obesity. Normally when we are hungry, AgRP neurons are activated that tell us to start eating so that we can gain more energy. The activation and inhibition of POMC and AgRP neurons are a vital component of our body’s ability to maintain energy homeostasis. Scientists have found an increased ratio of AgRP:POMC neurons in the brain of obese individuals, as well as an up regulation of inflammatory pathways discussed above.
Obesity is in the brain.
Finals week, Stress Eat
STRESS EATING IS REAL PEOPLE. And SURPRISE, it originates in the brain. So this is why I gain 5 pounds during finals week. When your body is stressed and then food is consumed, insulin is released and it increases the firing rate of dopamine neurons. The dopamine neurons then release a lot of dopamine, which is the molecule responsible for the reward pathway and the brain’s ability to make us experience “pleasure.” This is why you feel happy and satisfied after eating something yummy during finals week, like pizza. Over time, the brain starts to remember how satisfied you feel after stress eating, because your brain lays down information and forms memories more when the body is under stress. The next time you are under stress, the brain’s memory station, the hippocampus, and the reward system in the brain activate and have the ability to override any other signaling in the brain responsible for maintaining energy homeostasis. This is why we tend to stress eat, even when we are not hungry! So this brings up the question of whether or not people are actually responsible for the unhealthy decisions they make.
What do you think?
Goodbye Leptin, Hello Hunger
Normally leptin serves the function of telling the brain that it is not hungry and does not need any more food. However, as one consumes more food, body fat accumulates and leptin concentration increases in fat cells throughout the body. This disrupts proper leptin signaling and prevents leptin from telling the brain that it is not hungry anymore. Thus, the brain thinks it is starving, leading to increased food consumption and further body fat accumulation. This pathway continues to spiral out of control unless diet is altered.
Holiday Tips
With Christmas quickly approaching, one can only help but look forward to of all of the goodies to be eaten throughout the holiday season. I mean, you cannot resist eating all of the yummy food at family Christmas meals, right? Take into consideration these few tips to help you and your loved ones to stay ON TRACK this holiday season:
Keep in mind the holiday season is about BEING WITH FAMILY, not eating food
Suggest bringing a healthier dish to meals (sweet mashed potatoes verses mashed potatoes)
Help yourself to the yummy food of the holiday season, but in MODERATION (get your fruits in with breakfast and make sure vegetables have a place on your dinner plate)
Have ONE cookie instead of FIVE cookies
Drink 16 ounces of water before each meal (it will help you feel fuller and decrease your food intake)
Get your daily workouts in (walk the dogs, family walk after dinner, family gym session)
Take this time to CATCH UP on SLEEP
If you would like to learn more about obesity in the brain, please visit:
https://www.sciencedirect.com/science/article/pii/S1043276012002044 Images From:
http://diabetes.diabetesjournals.org/content/63/12/4016
https://www.menorahpark.org/
https://www.pinterest.com
Obesity and over-nutrition are two of the most prevalent health problems facing Americans today. Although more people in the United States are trying diets and exercise programs than ever before, the problem seems to be getting much worse. In fact, 86% of Americans are expected to be overweight by 2030 (1). With that staggering number, there must be more to this problem than what initially meets the eye.
Over-nutrition, which is the excessive consumption of food, can have a variety of effects on the human body on the cellular and neurological levels. For example, consistent over-nutrition over a long period of time can result with oxidative stress in the mitochondria of neurons, which can then promote pathways that lead to the expression of TNFa, a transcription factor associated with over-eating (2). TNFa can also promote ER stress and inflammation, leading to overeating, which can in turn lead to more oxidative stress in the mitochondria and start the cycle over again (2). This promotes a positive feedback cycle causing the person to keep on eating more and more.
Artstract depicting mitochondrial dysfunction and ROS.
Obesity can also lead to changes in the brain’s physiology, such as insulin and leptin resistance, both of which can further promote over-eating and inhibit the pathways in the brain associated with appetite suppression (3). The large amounts of nutrients consumed during over-eating can also stimulate the brain’s reward system and trigger a large release of dopamine, making the brain susceptible to an over-eating addiction over time (3).
However, over-nutrition alone cannot explain the rise in obesity. Food additives may also contribute to the obesity epidemic. Over the last century, about 4000 new artificial chemicals and substances have ended up in our food, and not enough research has been done on these substances to determine what effects they may have on human physiology and behavior (1). Examples of these additives are:
Artificial colors
Emulsifiers
Added sugars
Artificial sweeteners
Pesticides, which end up in our food unintentionally.
Some research has shown that many of these compounds can contribute to obesity and related health problems. For example, MSG, a common food additive, was found to promote fat accumulation in rodents, and some organopesticides have been associated with the onset of Type II diabetes, (1).
Obesity is one of America’s biggest health challenges, and if we don’t change what we’re putting into our food, then this problem won’t go away any time soon.
35% of adults age 20+ are obese. This is becoming a severe problem, especially in the United States. What is causing this spike in obesity? How does obesity become an issue in the body? I would like to discuss the background related to this topic. Inflammation and obesity:
The issue with obesity usually begins with the body becoming insulin resistant. The resistance is caused by overnutrition. Overnutrition or overeating causes stress in the body, particularly in the organelles like the mitochondria and the endoplasmic reticulum which are devoted to breaking down the foods we eat and creating proteins in the body. In overnutrition, these organelles become overwhelmed which leads to activation of the JNK pathway. This is a pathway normally implicated in the stress response, therefore, it acts to inhibit the insulin receptor substrate and causes inflammation. This in turn leads to more inflammation and more shutting down of the insulin receptor and insulin receptor substrate. Insulin Resistance:
The shutting down of the insulin receptor and insulin receptor substrate makes it increasingly hard for insulin in the body to do its job. Normally, when we eat food, insulin is released in the body and it signals POMC and AgRP neurons in the hypothalamus which tell the body to stop eating. However, in overnutrition the shutting down of receptors causes the body to not react to the insulin being released. The beta cells in the pancreas are responsible for making insulin and as insulin resistance begins they are able to make increasing amounts of insulin to try to combat the resistance. However, at some point a threshold is reached and the body cannot produce enough insulin. This leads to hyperinsulinemia and usually the onset of type 2 diabetes. Onset of obesity:
Eventually, the insulin is not sufficient to produce a response in the body. Therefore, the body cannot recognize that you’re consuming too much food and will constantly signal to keep eating. The stress continues and just potentiates the problem and causes obesity. This is just some of the pathology behind obesity. With the excess of food and availability of food that we have now, it helps to explain the reason why obesity is such a problem right now. Finding a solution is increasingly important as obesity and type 2 diabetes have very negative impacts on the body.
Onset of Obesity from: http://www.life-enhancement.com/images/LEM1211chart211.gif
For more information about obesity and its pathology read: https://moodle.cord.edu/pluginfile.php/625315/mod_resource/content/0/2013%20CNS%20insulin.pdf
Featured image from: https://d2s9xe8pzxi1js.cloudfront.net/wordpress/wp-content/themes/Marks-Daily-Apple-Responsive/images/blog/obesitycrisis.jpg
Obesity is a common and serious health issue in the United States. According to the CDC, more than 1/3 of US adults have obesity and it’s on the rise. Obesity puts someone at a higher risk of heart disease, stroke, type 2 diabetes, and certain types of cancer. So why is this such a rising issue and what is really happening biologically with obesity?
Obesity Science
Normally, when we eat food, there are two types on neurons in our brain that regulate our appetite. POMC-neurons tell us to stop eating and AgRP-neurons tell us to eat. Eating causes release of the hormone insulin, which activates POMC-neurons to get us to eventually stop eating. However, when obesity is present, we eat too much. This over eating causes our neurons to become stressed and overworked, which makes the normal insulin regulation work incorrectly. The POMC-neurons are unable to tell us to stop eating and the AgRP-neurons are over activated. This in combination with the reward system of our brain that responds positively to our favorite foods is no match for any sort of will power anyone may be able to muster.
Rethinking Obesity
Society paints this picture of obesity as this condition people have because they have no self-control around food and are lazy, living a sedentary life. This however isn’t the case for most people suffering from obesity. Obesity is a biological disease that effects how our brain functions. Take that in combination with many of the foods and food additives present in our society not being healthy and adding to the problem, basically a person is helpless against all odds. Treatment for obesity can be a lifestyle change, but also may require medication or surgery to reset the neurological imbalance that is present. As research into obesity continues, maybe we’ll be one step closer to finding effective treatments and even preventative treatments for obesity. For more on the science behind obesity:www.sciencedirect.com/science/article/pii/S1043276012002044?via%3Dihub
Feature Image: https://www.medicalnewstoday.com/articles/317546.php
Obesity aspects image: https://www.learnhowtobecome.org/make-a-difference-careers/obesity/
Food friends image: https://www.oyewiki.com/health/obesity-a-friend-or-an-enemy-6-9-2017
