Cobbers on the Brain – Page 122 – Student Commentary on the Neurological Sciences

Future Strategy to Treat Obesity and Prevent Damage in the Brain

Posted on December 11, 2016 by / 0 Comment

In recent years, research has been showing the many negative effects that fat and obesity can have in the brain on top of the known effects that fat can have on the rest of the body. For example, obesity has been linked to white matter deficits, which can lead to language, memory, and visual problems, as well as diseases like Alzheimer’s, dementia, and depression.
Researchers are working on understanding the mechanism by which obesity causes problems in the brain. From this, they will hopefully be able to develop new treatments for obesity through targets in the brain. If we could treat obesity outside of the brain, though, we could prevent any negative effects it would have on the brain.
A group of researchers from the University of Pennsylvania decided to take this direct approach to treating obesity. They decided to try to turn white fat into brown fat instead of targeting the proteins or mechanisms in the brain that obesity effects in the brain. They have recently discovered a way to successfully make this conversion by targeting a gene in fat cells.
Before moving on, though, isn’t fat just fat? What is the difference between white and brown fat and why should we care?
When we think of fat, we typically are thinking of white fat, which is involved in the storage of energy in our bodies as triglycerides. It can also produce hormones such as adiponectin, which is involved in making the liver and muscle less sensitive to insulin and is thought to make people less susceptible to diabetes and heart disease. White fat is more plentiful that brown fat, especially in overweight people, and when white fat is in excess it slows or stops producing adiponectin and can have adverse effects on many parts of the body.
Brown fat on the other hand, is thought to be “good fat.” When brown fat cells are stimulated, they are responsible for burning calories through the production of heat. Children and lean people tend to have more brown fat than white fat, and stimulating brown fat keeps people warm and burns white fat. The burning of white fat can prevent diseases such as diabetes, so the discovery at Penn University could be very significant and lead to future treatments of obesity.
The researchers discovered a gene that can start a “browning process” in white fat cells when it is deleted. The protein produced by this gene is called foliculin, or FLCN. It is a known tumor suppressor, and is key for preventing the conversion of white fat into brown.
When FLCN is removed, a protein known as TFE3 can be transported into the nucleus of white fat cells. This is usually prevented by FLCN and another protein, mTOR. Once in the nucleus TFE3 binds to DNA and activates a protein called PGC-1β, which is involved in cell metabolism regulation. After PGC-1β activation a set of genes were transcribed that began the browning of white fat cells. This process is simplistically outlined in the figure below.

This browning process was shown to occur the white fat of mice after the deletion of the FLCN gene, and one of the reasons for this is that the fat cells started producing more mitochondria. These are cellular organelles that are responsible for the production of chemical energy in cells and are responsible for the added heat production in brown fat cells. On top of producing more mitochondria in white fat cells, the deletion of the FLCN gene changed the structure of white fat cells, increased the activity of mitochondria that were present, and changed gene expression.
Although this pathway is not well understood at this point, it is possible that it could be targeted to treat obesity and the diseases that stem from it by converting white fat into brown. Although this treatment wouldn’t directly act on the brain, it could prevent the negative effects that obesity has been found to have on the brain.

Disease/Health

What Does Your Brain Have to Do With Obesity?

Posted on December 10, 2016 by Joseph Kennedy / 0 Comment

Before last week, I rarely thought about obesity. Not because it wasn’t in my life – my Dad and most of my uncles are obese – it had just become so present that I didn’t think anything of it. That all changed when I learned that obesity can be categorized as a brain disease. A main point in this classification is insulin resistance in the central nervous system that arises as a result of obesity and type 2 diabetes. It isn’t a surprise that insulin resistance connects these two diseases, as 90% of people with type 2 diabetes are also overweight or obese.
In the 1970’s, researchers discovered that insulin receptors exist in the brain and that signaling through these receptors regulates feeding behaviors and body weights. When functioning properly, insulin signaling in an area of the hypothalamus called the acruate nucleus (ARC) works to maintain a healthy appetite level. Within the ARC are two subsets of neurons, called the POMC and AgRP. Interestingly, these two types of neurons have opposing effects with POMC decreasing appetite and AgRP stimulating appetite.
Insulin signaling regulates POMC and AgRP through its deactivation of the transcription factor FOXO1. FOXO1, when activated, lowers the expression of POMC and increases the expression of AgRP neurons. The result, then, of insulin deactivating FOXO1 is a stimulating effect on POMC expression that ultimately leads to the decreased appetite from insulin. This is demonstrated in the figure below.

A decreased appetite in response to insulin makes logical sense when you consider that insulin is released in response to high blood sugar. In essence, the high blood sugar is a signal that the body has an adequate energy store in the form of sugars. And while this system works well in a healthy person, problems can arise when a person becomes resistant to the signaling from insulin.
Insulin resistance arises from a variety of sources. One interesting mechanism involves accumulation of saturated fatty acids in the hypothalamus from high fat diets. These fats can activate receptors on the neuronal surface leading to an inflammatory state in the brain that causes insulin resistance. A general inflammatory state arises from obesity and the subsequent production of pro-inflammatory cytokines can also signal through their own receptors to cause insulin resistance.
What can be stated generally is that obesity and overnutrition can lead to an inflammatory like state that renders the brain “resistant” to insulin signaling. That means that the insulin pathway discussed above, which normally responds to high-energy states by signaling through insulin to reduce appetite and expend energy, is shut down and the body doesn’t properly recognize that its energy needs are met.
One can begin to see how insulin resistance forms a cyclical process where obesity and overnutrition can lead to insulin resistance, which then leads to an unregulated appetite that further contributes to obesity. In the end, it’s a dangerous cycle that already plagues much of the world.
Perhaps the link between the brain and obesity will bring more awareness to the issue and catalyze positive changes to diets and lifestyles. Possibly it will also spur a new age of medicine that treats obesity through the lens of insulin resistance. Time will tell how the scientific and general community reacts to this research, but the fact remains that we must address the obesity epidemic. In my opinion, further research into the brain’s role is a great start.

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Bet’cha Can’t Eat Just One: The Reality of Food Addiction

Posted on December 10, 2016 by / 0 Comment

We’ve all seen the Lays commercials where they “Bet You Can’t Eat Just One” of their amazing chips. And it’s true. It is really difficult to eat just one chip. We call them addicting, just like chocolate or cookies or your favorite flavor of ice cream.
When we say this, we are usually joking. Nobody shoots up Lays potato chips or has to go to potato-chip rehab to quit their addiction. But what if I told you that food addiction is real? As real as drug or nicotine or alcohol addiction?
Well, it is. But to understand how food can be addicting, we need to understand how addiction works in the first place.

The Basis of Addiction

Addicting things – alcohol, nicotine, drugs, sex, exercise, food – are addicting because they make you feel good. They do this by mimicking or causing the release of “feel good” chemicals in your brain like dopamine or endorphins.
In the case of dopamine, substances can cause the release of dopamine in your brain, which binds to dopamine receptors. Other drugs can bind dopamine receptors themselves. Either way, the same “feel good” effects are produced.
When your brain goes through this a lot, it starts to become resistant to it, which we call tolerance. Your brain develops tolerance by decreasing the number of dopamine receptors in your brain, so that you have to do more of the thing that makes you happy to reach the same level of happiness.
This is the common thing that occurs in drug and alcohol use, where your body pushes you to use or consume more and more to get the feelings that cause you to use in the first place.
This same effect can occur with the opioid system of the brain, which is normally activated by endorphins (the feel-good chemical released during exercise), but artificially stimulated by opiate drugs like painkillers or heroin.
But how is any of this related to food?

Food and Addiction

Everybody knows that fat and sugar taste good, but it’s more than just flavor that makes them addictive. There have been many studies that simulate overeating of fatty or sugary (or fatty AND sugary) foods in mice and how that affects their brains.
One effect seen is a decrease in the number of dopamine receptors with subsequent increases in sugar intake, just like the reduced number of receptors and increased use that we see in drug tolerance.
Additionally, scientists have found a decrease in the number of dopamine receptors in obese humans that correlates with their weight. So, the higher the weight, the less dopamine receptors they have. This means that they would need to consume larger amounts of sugary and fatty foods to elicit the same effect as those foods had in the past.
Another result is the activation of the opioid system caused by sugar intake. When rats were taken off of their sugary diet, they exhibited the same withdrawal symptoms that are typical of opiate drug withdrawals.
Rats who had been on a high-fat diet would traverse a painful and difficult terrain to get to high-fat foods rather than eat low-fat foods that were easily accessed.
All of these results indicate that fatty and sugary foods are, in fact, addicting.

Social Implications

So, since fat and sugar are addicting, it’s not my fault if I eat too much of them, right? Because I’m an addict and it’s out of my control?
Not quite.
Yes, these things are addicting. But the addiction does not just hit you out of the blue. It occurs as a result of over-consumption of fatty and sugary foods, and perpetuates continued over-consumption. So, that means I should never eat anything with fat or sugar, right?
Again, not quite.
Rats who had been consuming a lot of fat and sugar and then were not allowed to fat and sugar binged and relapsed as soon as they were allowed access to fatty and sugary substances. So cutting yourself off completely will likely lead to extreme overconsumption and relapse into unhealthy habits.
So, as with everything that has to do with a healthy lifestyle, consume them in moderation. A few potato chips and a little bit of chocolate won’t make you a full-blown addict, but too much will, so it is important to be aware of how much you consume and what’s going on in your brain in order to help yourself to live a healthy lifestyle.

Community/Health

Insulin’s Role in the CNS

Posted on December 10, 2016 by / 0 Comment

Most people are aware that insulin plays a very important regulatory role within our body. As glucose levels rise within the body, insulin is responsible for breaking the glucose down and turning it into glycogen, thus lowering the levels of glucose within the body and avoiding hyperglycemia. But, insulin also plays many other important roles, specifically within the central nervous system (CNS). It has effects on reproduction, cell proliferation and differentiation, neuro-protective effects, and cognition and memory.
When I first learned that insulin plays a role in reproductive regulation, I was surprised. It does not have a direct role in regulating reproduction, but rather is a contributing factor. Insulin is able to contribute to the control between the reproductive function and metabolic actives that take place during fertility. When the hypothalamus is perfused with low concentrations of insulin, it leads to a stimulatory effect on GnRH secretions. So, insulin has somewhat of a regulatory effect on the reproductive cycle, but other hormones play a larger role within the CNS. (Please refer here for further information on the reproductive cycle)

Insulin also contributes to cell proliferation and differentiation. Insulin increases the levels of ornithine decarboxylase within the CNS, which is an indicator of growth stimulation. It also increases the proliferation of astrocytes, which are supporting cells within the CNS. Lastly, it is able to contribute to the increased stimulation of the PI3K-AKT pathway, which is a pathway that contributes to neuritis growth along with an increase of synaptogenesis. In combination, all three of these stimulatory effects will increase cell growth within the CNS.
Another function of insulin within the CNS is its contribution to cognition and memory. Through an increase of insulin within the hippocampus, improvements in both memory and learning processes have been observed. This is indicated by an increase of insulin receptor (IR) expression and an increase of signal transduction pathways within the hippocampus. Memory is formed through the modulation of long-term potentiation (LTP) and long-term depression (LTD) events. Insulin is able to modulate gluatamatergic neurotransmission at the synapses in order to contribute to this delicate balance by inducing LTD events, therefore contributing to the increase of memory.
One last function that insulin has within the CNS is its neuro-protectivity. Insulin is able to protect against apoptosis, beta amyloid toxicity, oxidative stress, and ischemia. By producing ATP during glycolysis, insulin is able to counteract events that would otherwise produce oxidative stress within the cell. Also, through the stimulation of the PI3K-AKT-mTOR pathway, insulin stimulates growth within the CNS. Through the protein p70SK, one of the downstream targets of the mTOR pathway, insulin is able to avoid apoptotic events. It also is able to avoid cell death through the protection against the formation of beta-amyloid fibrils, which is potential target for the regulation of beta-amyloid plaque formation. These plaques are also found in diseases such as Alzheimer’s and Parkinson’s Disease.
Insulin has far more roles than what most people would think. It is intriguing how one molecule can have effects on so many different processes throughout the CNS. Just being aware of some of its other functions can bring more appreciation for the molecule!

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Risk Factors for Autism

Posted on December 6, 2016 by / 0 Comment

Autism is a very common condition. This disorder is characterized by abnormal social behavior and communication. Autism is often caused by genetic factors, however, environmental factors also play a significant role. There are a large number of risk factors that increase the chances of a child developing autism. Some of these include:

Viral infections during pregnancy
Heavy metals
Zinc deficiency
Problems with melatonin synthesis
Stress (before or after birth)
Maternal diabetes
Gastrointestinal irregularities
Older parents
Psychiatric drugs

It should be noted that vaccines are not on this list. Vaccinations do not increase the chances of a child developing autism.
Anyway, the risk factors listed above correlate with higher levels of autism. Genetics also play a role, but these factors somehow cause autism by altering brain development before or after birth.
So how does all this cause autism? Well it has to do with zinc and the immune system. Low zinc levels in the brain are correlated with autism (and might be a cause). Autism may also start with abnormalities in the immune system. There is not one cause of autism. Genes and the environment both play a role in this complicated disease.
Where do these abnormalities with the immune system and zinc levels come from, and what do they do?
Low zinc levels can be caused by a variety of factors. First there is genetics, deletions or mutations in certain genes can cause very low levels of zinc in the body. Gastrointestinal problems can also cause very little zinc to be absorbed into the body. There is also malnutrition (of either the mother or the baby). Heavy metals, especially copper, can also interfere with zinc adsorption in the body.
Immune system deficiencies also have a variety of causes. First of all, zinc deficiency can cause the immune system to not develop properly. Also, genetics can cause abnormalities in the immune system. These abnormalities can also be caused by many of the risk factors listed above such as toxins, stress, psychiatric drugs (taken by the mother), parental age (both parents), and melatonin deficiency.
Melatonin deficiency can be caused by low levels of Zinc. This causes the disturbed sleep patterns seen in autistic children and as stated above has negative effects on the immune system.
Autistic people also have some differences in how synapse are formed. For example some synapses have scaffolding proteins called Neurexin and Neurolinin. These proteins hold the two ends of the synapse together so signaling can occur. If these scaffolding proteins do not work right the signaling molecules may have a hard time getting to their receptors. Some people with autism have mutations to the genes that code for these proteins rendering them nonfunctional. Low zinc levels can also cause these structural irregularities. These structural irregularities can lead to improper signaling, which leads to the symptoms of Autism.
Overall, autism in an incredibly complicated disease. It is widespread and still not fully understood. Still there is progress being made. Understanding what is happening the brain will help medical professionals make better treatments that can improve the lives of autistic people.

Disease

Our Immune Systems and Autism Spectrum Disorder

Posted on December 6, 2016 by / 0 Comment

Often when we think about our immune system we think of it helping us survive and fight off disease, but rarely, unless it affects us directly, do we think of our immune system harming us. When this happens, it is called an autoimmune disease. This is when a person’s immune system has a response against self-antigens involving T-cells, B-cells, or autoantibodies, all of which are specialized immune cells in our bodies.
This immune response can cause systematic injury or attack a specific organ system, resulting in diseases such as rheumatoid arthritis, lupus, or inflammatory bowel arthritis. I wouldn’t be surprised if a lot of people had no idea that these are autoimmune diseases.
These autoimmune diseases are more prevalent than we might think, though. According to the Centers for Disease Control and Prevention, autoimmune diseases are the third most common category of disease behind heart disease and cancer, affecting about 8% of our population (22 million people), maybe many more in a minor capacity. More than 75% of these people are women.
Because of this, it is extremely important that researchers have linked autoimmune diseases and immune dysfunction to Autism Spectrum Disorder (ASD). Research has shown since the 1950s that autoantibodies produced by a pregnant woman with an autoimmune disease can harm the neurodevelopment of the embryo. More recently, though, this hindrance of neurodevelopment has been shown to cause ASD.
The autoantibodies mentioned above are specialized antibodies (proteins that are produced by the cells of the immune system to identify and neutralize pathogens) that are directed against the individual’s own cells. The production of these autoantibodies is the cause of many autoimmune diseases, and the fact that they attack the individual’s own cells is what causes many of the symptoms associated with the disease. In the case of ASD specific autoantibodies, anti-brain autoantibodies, are thought to cause ASD because they attack proteins and cells in the brain of the developing embryo. They have been shown to attack proteins such as lactate dehydrogenase A (LDH-A) and B (LDH-B), stress-induced phosphoprotein 1 (STIP1), guanine deaminase, collapsin response mediator proteins 1 (CRMP1) and 2 (CRMP2), Y-box binding protein 1, and others (Figure 1), all of which have important roles in neurodevelopment.

A study published in 2009 studied the prevalence of ASD in 700,000 children born in Denmark, finding that type 1 diabetes, rheumatoid arthritis, and celiac disease (all of which are autoimmune diseases) correspond to increase risk of ASD. Another study showed that maternal autoimmune diseases were linked to a 34% increase in risk for developing ASD.
The antigens recognized by maternal autoantigens are significant because several of the targets of the autoantigens are critical for normal brain development, specifically processes essential for neuronal migration and neural network formation. The studies that show links between maternal autoantibodies and ASD were performed in humans, so the mechanism of how these autoantibodies cause ASD is still not completely understood. Animal models are currently being studied intensely to hopefully discover the etiology of ASD in relation to immune dysfunction.
Murine and primate models have been used to study the clinical significance of maternal autoantibodies to show that they are not just correlative. To do so, primate mothers were injected with IgG, an autoantibody, and their offspring were studied. Social behaviors in these offspring were different than normal primates and stereotypical of patients with ASD. Similar studies were carried out in mice and the findings were similar to those found in the primate studies ().
Other research groups have also linked the presence of anti-brain autoantibodies to other behavioral disorders such as schizophrenia, Tourette syndrome, and obsessive compulsive disorder. Unlike the autoantibodies found in the brains of individuals with these diseases, the autoantibodies found in the brains of patients with ASD have been shown to preferentially bind to fetal targets instead of adult targets, which could be the reason that they hinder neurodevelopment in the way that they do.
There is still much unknown about autoantibodies, but researchers hope that by discovering the mechanism by which autoantibodies hinder neurodevelopment they will be able to implement therapeutic interventions that could prevent ASD and other neurodevelopmental or psychiatric disorders.

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Autism at a Glance: Two Factors Increasing Risk of Autism

Posted on December 6, 2016 by / 0 Comment

According to our article,” Environmental Factors in Autism”, their definition states Autism as neurodevelopmental disorders characterized by impairments in communication and social behavior, and by repetitive behaviors.
There are so many factors out in today’s society that are possibly the reason why we are seeing more and more autism cases today. Autism usually appears in the first three years of a child’s life by certain signs like no big smiles or other warm expressions by six months or like no words being spoken by 16 months.
In this blog, I want to talk about two factors that may be causing higher chances of having a child with autism—maternal diabetes and toxins.
First, let’s talk about maternal diabetes. According to our sources in our article, if a mother is pregnant and has diabetes, her child has a two-fold increases risk of obtaining Autism. Current research has proven links between obesity in the mother and her having higher chances of giving birth to a child with autism. However, other metabolic conditions like hypertension or diabetes really only showed trends for the risk of autism.
Secondly, toxins threaten developing fetuses which can cause birth defects. Two main agents are on scientists lists and they are called valproic acid and thalidomide. Valproic acid, when administered in utero, delays and lifelong deficits in motor performance, social behavior, and anxiety. For thalidomide, it regulates cytokine levels and macrophage inflammatory function. It was first used as an antiemetic in the 1950s but was found to cause birth defects shortly after. Finally, one study found that women who were early in pregnancy and were in close range to organochlorine pesticides which were sprayed on fields, had several more times likely of giving birth to a child with autism. These are all toxins that are shown to increase chances of birth defects and possibly cause autism but as of current research now, the concordance rate isn’t 100% and therefore, suggests genetics must play some role for a toxin to act as a trigger.
Science has shown that genetics play a role in autism spectrum disorders, but it also has revealed that genetics cannot fully account for all ASD cases, and thus that’s were many factors come into play like maternal diabetes and exposed toxins.

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Genetic Mutations and Pica in Autism

Posted on December 6, 2016 by / 0 Comment

Autism is a very complex disorder that has a wide spectrum of severity. Some of the broader symptoms used to diagnose autism, per The National Institute of Mental Health, are:

Ongoing social problems that include difficulty communicating and interacting with others
Repetitive behaviors as well as limited interests or activities
Symptoms that typically are recognized in the first two years of life
Symptoms that hurt the individual’s ability to function socially, at school or work, or other areas of life

Individuals with autism can also suffer from a variety of physical ailments, such as difficulty sleeping and digestive trouble.

Pica in Autism

Due to the physical and mental effects of autism, some individuals eat objects with no nutritional value, such as dirt, which is a disorder called pica. Pica is prevalent among individuals with autism, although there are no concrete numbers about the percentage of autistic individuals with pica.
There are a variety of theories as to why pica is so prevalent in individuals with autism. One thought is that, especially in cases of severe mental deficit, the individuals have difficulty discerning edible objects from inedible ones. Another theory is that individuals are lacking certain vitamins and minerals because they cannot tolerate some foods or because their bodies are unable to properly absorb nutrients from their food, which is why they would eat mineral-rich things like dirt.

Zinc Deficiency in Autism

Many individuals with autism have a deficiency in zinc, but it has a very complicated role in autism. Some studies attribute zinc deficiency to the development of autism while others cite it as a result of improper diet in individuals with autism.
Zinc could lead to autism because it is a key mineral for growth and development as well as immune function, so deficiency could lead to improper development, leading to autism. It could be a result of autism because of the gastrointestinal distress discussed earlier. Scientists have also found a genetic mutation that could contribute to zinc deficiency, and, therefore, to autism.

Mutations in ATP7B Gene

There is a gene called ATP7B that, when it is faulty in both copies of the gene, leads to Wilson’s disease, which is a disease of copper toxicity. When only one of the copies of the gene is mutated, there is less significant pathology, but it is hypothesized that copper overload of babies in utero could inhibit brain development and lead to autism.
The ATP7B gene codes for a channel that moves copper in and out of cells, and when it isn’t working right, copper can’t leave the cells. Copper and zinc compete for binding spots in the cell, so when there is excess of copper, it binds all of the spots and leaves zinc just floating in the cell.
The cell sees the zinc as being in excess, because it is not bound to anything, and excretes it. This leads to loss of zinc, which leads to the zinc deficiency that could cause improper development of the brain, which could lead to autism.
This zinc deficiency would not only be present in utero, but throughout the individual’s life. This genetic mutation, coupled with gastrointestinal difficulty and/or an inability to discern edible objects from inedible ones, could contribute to the prevalence of pica in autism.

Disease/Health

Autism: A Classroom Perspective

Posted on December 6, 2016 by / 0 Comment

If a kid doesn’t participate in class, they get a bad grade. If they act out or are disrespectful, they get sent to the principal’s office.
There is typically a pretty fine line between right and wrong, and they should know better right?
In my opinion, teachers have one of the most difficult jobs these days. They put in long hours, although they’re not paid by the hour; more often than not they take their work home with them; it is both physically and emotionally draining maintaining energy and keeping a group of students’ focus, let alone getting them excited about a subject; not to mention, teachers have to appease parents, students, administration…sounds like a whole ton of fun.
Now, on top of all of that more and more students are being diagnosed with learning problems, behavioral problems, etc. And teachers are expected to know about these and be sensitive to them, when in many cases they don’t even know much about them.
Such is the case with autism.
According to a study done in 2010, the U.S. Centers for Disease Control and Prevention (CDC) estimated that ASD prevalence was 1 in 68 among children age 8 years.
Now, I’m not a school teacher, but I have been a camp counselor, dance instructor, and Sunday school teacher and have worked with kids with both learning and behavioral problems.
Let me say this: it is nearly impossible give each student individual attention, while still being able to accomplish a lesson – and that’s when a teacher doesn’t have a student with a learning or behavioral problem.
Autism is now officially referred to as autism spectrum disorder (ASD). Which means, much as it sounds, that its level of severity ranges – on a rather broad – spectrum. Some individuals can remain high functioning, where other’s may be severely impaired.
Regardless of its severity, science has made one thing very clear. ASD is a disorder. Whether as a result of environmental or genetic factors or both (jury’s still out on that one), distinct brain abnormalities can be observed in the brains of individuals with autism. Decreased signal transduction, improper synapse formation and decreased plasticity can lead to a slew of problems, hence the wide array of symptoms and levels of functioning seen in ASD.
Yet all too often we fail to remember this. We view people as weird, or socially awkward. They’re being disrespectful, they’re acting out to get attention. We think they’ll “grow out of it.” We attribute it to bad parenting or lack of social interaction and we think that a little tough love will fix everything. And when it doesn’t; when we finally turn to medicine to see if maybe it was more than we thought, we are overwrought with guilt. We feel so ashamed to have wasted so much time blaming them for something they had no control over all along.
This is something that happens in our school systems as well and it is detrimental to the education of these young children with autism.
In fact, it wasn’t until 1992 that schools began to include autism as a special education classification. However, even now, schools either don’t have the funding, or the mindset to support this.
Whether the result of teachers, administration, or lack of funding, students with autism are not getting the education or accommodations they need.
To be honest, I’m not a fan of the term accommodations. It sounds like an entitlement given to undeserving individuals, but here that is definitely not the case.
Student’s with autism DO need special accommodations. This is a fact, and it is also a fact that their needs are rarely being met. Many students with ASD can’t focus properly. They are easily distracted and may need isolation for a test or quiz to be able to focus. On top of that, many individuals with ASD are anxious in social settings, which can also contribute to poor performance when forced to work in such conditions.
But it’s more than letting a student take a test in another room. Student’s with ASD throw tantrums; they need to be somewhere they can do this without interrupting class and also without fear of repercussion for something that is out of their control. Student’s with ASD also may have difficulties confronting or interacting with others, resulting from their social anxiety. This means any accommodations they may need, they can’t or won’t even ask for. And in many cases, there is no one else to speak for them.
It is becoming an increasing demand that schools have a special environment for individuals with ASD, as well as instructors specifically trained to work with them and help them reach their goals. This would not only be beneficial for these students, but for the other students in the school as well as the other teachers.
That being said, it is also important for these individual students with ASD to remain as part of the school and not be isolated. Social encounters are highly beneficial for individuals with ASD.
How can we manage this? In many cases, it is a problem of funding. However, in a situation as critical as this, I find it difficult to believe that there are not less important issues that funds could be diverted away from. If it is the case of administration or teacher resistance, they must be educated and from then on held accountable for their actions on behalf of such students.
It’s time we stop labeling individuals as weird or awkward. Tough love may have worked on the kid who was shooting spitballs in the lunchroom, but not here. We need to start identifying the problem and working to solve it, rather that denying its existence or expecting it to just “go away.”

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Searching for Answers About Autism

Posted on December 6, 2016 by / 0 Comment

Autism Spectrum Disorder (ASD) is something I have grappled with trying to understand for much of my life. I think I grew up with the idea that autism was a consistent disorder between everyone with the diagnosis–that they all have severe issues functioning independently and learning in school. In high school, someone I had worked with in a theatre production shared that they had autism about 2 months after I had known him–I would have never thought this was the case.
This friend had a milder diagnosis of ASD called Asperger’s, and this is when I learned that Autism did not manifest the same in all people.
This realization became an extra challenge when I started researching the biochemical and environmental factors that cause the development of autism. In one paper by Andreas Grabrucker, titled “Environmental Factors in Autism,” he identified eight risk factors that impact neurological functioning leading to the development of autism.

Prenatal viral infection–Maternal infection, autoimmune disease, and/or allergy could change the immunity of the fetal brain and the fetal immune system
Zinc deficiency–Maternal or early development zinc deficiency might give an explanation of gene/environment interaction
Abnormal melatonin synthesis–Melatonin regulates the circadian rhythm, is an antioxidant, is involved in the immune response, and regulates synaptic plasticity
Maternal diabetes–Diabetes in the mother during pregnancy increases autism risk by 200%
Prenatal and perinatal stress–Prenatal stress activates the HPA axis resulting in abnormalities in postnatal immune function
Toxins–Certain pesticides may contribute to autism as well as psychiatric drugs taken by the mother during pregnancy
Parental age–Advanced maternal age might contribute through increased pregnancy complications and maternal autoimmunity
Postnatal risk factors–Gastrointestinal or immune system abnormalities, allergies, and exposure of children to drugs, infection, certain foods or heavy metals have been proposed a s risk factor for autism

There is a strong role of the placenta, in regards to what passes from mother to fetus that may lead to development of autism. Here are some examples of substances that can pass through the placenta during pregnancy.

If all of these explanations weren’t complicated enough on their own, Grabucker describes many of these risk factors being related to each other, and an interconnected model of risk factors is proposed with zinc deficiency and immune system abnormalities placed in the center.
To eloquently provide a hypothesis that incorporates how all of these factors work together would be extremely helpful reducing rates of autism.
Here are some 2016 facts from the Centers for Disease Control and Prevention about current autism rates in the U.S.:

1 in 68 children have ASD
Boys are 4.5 more likely to have ASD diagnosis than girls
Until recently, rates have risen since the 1960s
Rates have are unchanged from 2 years ago

As researchers continue to try to prevent the development of autism, it is important for our entire society to think about how to best care for individuals and families affected by autism.
Starting in the 1970s, federal guidelines supported the inclusion of children with special needs into mainstream schooling, mandating that these students be placed in the least restrictive environment for their education. Eileen Bailey, a health guide for Health Central, outlines the benefits and disadvantages of mainstreaming students with ASD.
Benefits:

Prepares students for life outside of school–learning how to interact with different types of people
Early inclusion may help increase IQ scores of ASD students
Neurotypical students provide an example of appropriate social behavior for ASD students

Disadvantages:

Teachers don’t have training or time to tend to needs of ASD students
ASD students may require nontraditional classroom instruction
May subject ASD students to be bullied

The juxtaposition of these benefits and disadvantages illustrates the ambiguity of mainstreaming ASD students in classrooms.
All in all, as I continue to seek answers in my study of autism, I seem to end up with additional questions and a more complex idea of it all. From the many interconnected risk factors for its development, to the uncertain societal solutions for supporting individuals with autism.