Community/Disease

Schizophrenia and Autism: More Alike Than You’d Think

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Distinct differences, striking similarities

Schizophrenia and Autism Spectrum Disorder (ASD) are both well-known developmental disorders involving the brain. At first glance, the two seem strikingly different: when we think of symptoms of schizophrenia, we may think of hallucinations, delusions, or loss of speech and movement. With ASD, we may think of interrupted social and communication skills or repetitive behaviors. ASD is typically evident and diagnosed in childhood, while schizophrenia often doesn’t show up for several decades of a person’s life. However, the two disorders arise from similar molecular causes and even their symptoms are more alike than you might realize.

Both disorders have a genetic component (meaning that children can inherit them from their parents) and an environmental component (meaning the circumstances a person grows up in from conception to adolescence influence their likelihood of developing the disorder). Let’s dive into the genetic and molecular component of these two disorders.

Schizophrenia on the brain

First, let’s look at the way schizophrenia is caused in the brain. It is a developmental disorder, meaning that the brain differences resulting in schizophrenia occur as the brain develops in the womb (even though symptoms usually don’t come about until later in life).

In a non-schizophrenic brain, an important signaling pathway (a cascade of events in a cell) known as the canonical Wnt pathway causes a protein called β-catenin to form and accumulate in neurons (brain cells). When there are high levels of this protein in a neuron, it causes certain target genes to be expressed. This means that the DNA of those target genes is copied and the proteins that the genes code for are made. The genes that are affected by β-catenin are important mostly during development, so the brain doesn’t need them to be at high levels all the time. A protein called GSK3 helps break down and recycle β-catenin so it doesn’t lead to gene expression all the time.

That was a lot of neurochemistry! If you’re interested in reading more, this paper by K. Singh dives even deeper into the pathway and its role in schizophrenia. If not, the big takeaway is that β-catenin is an important molecule during brain development, and GSK3 makes sure there isn’t too much of it. In schizophrenia, GSK3 is too active. This means that it breaks down more β-catenin than it should, so the genes making proteins needed for development aren’t expressed and the brain doesn’t form the way it’s supposed to.

What about ASD?

In ASD, the developmental disruptions resulting in brain changes are very similar. Even the exact same molecule is involved in the same way: β-catenin levels are too low, so genes that should be expressed during development aren’t, resulting in brain abnormalities. In ASD the lack of β-catenin is due to other interruptions to the signaling pathway, but the result is similar.

Can someone have both schizophrenia and ASD?

Yes; and it’s fairly common. When two disorders are frequently present together, the disorders are said to have high comorbidity. An individual’s official diagnosis could more likely be something like “ASD with psychosis”, but they would often display sufficient symptoms to be diagnosed with both disorders.

Additionally, studies have shown that individuals diagnosed with schizophrenia but not ASD still have higher levels of autistic symptoms than control groups. Symptoms of schizophrenia that are less-well known are often similar to characteristics of ASD: social withdrawal and exhibiting lower levels of emotion are two shared symptoms. These schizophrenia symptoms that are more similar or identical to ASD symptoms are called negative symptoms, not because they’re inherently bad, but because they exhibit a lack of something that is expected to be there, like emotional expression. The more well-known symptoms of schizophrenia like hallucinations and delusions are called positive symptoms because they’re adding something that doesn’t exist.

Conclusion

Despite very similar molecular causes involving a lack of the protein β-catenin during development, the differences between schizophrenia and ASD from age of onset to symptoms remain significant. However, knowing the similarities between molecular causes of the developmental disorders may help scientists in diagnosing and treating individuals exhibiting symptoms of both disorders in the future.

Community/Disease/Spirituality

The Voices in My Head: Friends or Foes?

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In America, when we think of hearing voices, most people’s immediate reaction is to think well, that’s crazy! And while auditory hallucinations are certainly a sign of abnormal functioning in the brain, some societies think of them in a different manner: as a gift, magic, or as a sign from a higher being. With this in mind, we will dive deeper into why these hallucinations come to be and how interpretation may be a much more crucial component than we think.

But what causes these voices?

Most commonly, auditory hallucinations are tied to a diagnosis of schizophrenia. In short, schizophrenia occurs as a result of a lack of b-catenin transcription, going hand-in-hand with too much dopamine or too little Wnt signaling. Wnt signaling is a crucial component of development, so it’s a major concern when it isn’t working properly. These differences ultimately result in chemical variations in our neurotransmitters, which are essential for communication within the brain. Taken together, there are neurochemical, genetic, and environmental risk factors/implications associated with a schizophrenia diagnosis, ultimately manifesting as the voices people hear in their head.

How are the voices expressed?

To a patient with schizophrenia, these auditory hallucinations—voices—are as real as their mother and father’s voices. In many cases, the voices cause people to do things typically out of their character and are quite troubling, often encouraging their host to perform violent acts. The voices can lead to trouble keeping jobs and maintaining relationships, resulting in difficulty with “normal” societal functioning.

This understanding of voices in one’s head is what we Westerners commonly associate with auditory hallucinations. Think of movies you’ve seen about individuals with schizophrenia: in most movies, auditory hallucinations are commonly portrayed as a negative, insulting, troublesome, and sometimes dangerous aspect of the patient’s life.

What’s incredibly interesting, though, is that this all may depend on cultural context.

What if the voices aren’t bad?

While other cultures’ understanding of schizophrenia may be wildly different, the symptom expression can be almost the exact same—beside one crucial aspect: interpretation. These individuals still have the same major psychotic disorder, but don’t understand the visual hallucinations in the same manner. To Westerners, the voices are most often hostile and scary, but different cultures see those voices as friendly and possibly even magical.

What this suggests, Stanford researcher Tanya Luhrmann says, is that “the way people pay attention to their voices alters what they hear their voices say” (see article below). This is an incredible thought. Essentially, interpretation may have a much bigger role in the voices’ manifestation than we ever considered. In Luhrmann and colleagues’ study, the results showed that while individuals from California, Ghana, and India all reported prevalence of both good and bad voices, not one American reported predominantly positive experiences with the voices, where the majority of the others did. The Americans were more likely to describe violent voices, whereas the Indians and Africans said their voices reminded them of friends and family—more of a companion than an outsider.

What does this mean?

This early research may suggest another method for treating schizophrenia: encouraging patients to develop relationships with their voices to have a more tolerable experience. Because there is no outright cure for schizophrenia, there is still much more to understand and study in order to improve patients’ quality of life. Thinking of auditory hallucinations as friends rather than foes may be the new “drug” of choice for schizophrenia.

Continue reading →

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Anxiety and The Hippocampus

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Role of Hippocampus:

The hippocampus is a region in the brain located between the inner folds of the temporal lobe. This region plays an especially important role in the formation of two specific types of memories. These include spatial relationship and declarative memories. Spatial relationship memories help us derive directions whereas declarative memories are related to the facts and events. These two types of memories help transform short term memories into long term memories and then they will be stored elsewhere. More information on the role of the hippocampus and memory can be found at https://www.positivemed.com/2018/06/02/role-of-the-hippocampus/.

How the Hippocampus Relates to Anxiety:

The hippocampus is an important area to look at when studying anxiety. When an individual undergoes chronic anxiety, they have an increase in glucocorticoids which are hormones that contribute to the flight or fight response. This increase in glucocorticoids causes a raise in cortisol levels which ultimately impairs the fragile hippocampus.

One major impairment to the hippocampus from chronic anxiety is the decrease in this regions size. Many studies have proven that individuals undergo a shrinkage of their hippocampus if they are under sever anxiety. Decreasing of size in any area of the brain is not ideal and, in this case, memory formation becomes extremely hard. When one loses volume in their hippocampus, that means they also lose storage space for all the memories that are within the spatial relationship and declarative memory categories. These memories are often used to pull certain events together and create a memory. Less volume equals less memories formed.

Alzheimer’s Disease and Anxiety:

Following the chain of events within anxiety we can trace our way to Alzheimer’s disease. Individuals with Alzheimer’s disease struggle with memory formation and retrieval. To no surprise the hippocampus is playing a large role in this disease. Those with Alzheimer’s also show a decrease in volume to their hippocampus. It is no coincidence then that individuals with anxiety are more likely to develop Alzheimer’s.

 

Can You Grow What Has Been Lost?

After reading about the negative impacts anxiety has on the hippocampus region of your brain, one questions the possibility of healing. When chronic anxiety levels have become so high that physical volume in your brain starts to decrease, what can one do to help? Although treatments are subjective to the individual, researchers passionately believe that you can slowly grow volume size back. Through Exercise one can start to create new hippocampus neurons which ultimately leads to increase of size. Exercising with the balance of a good diet will help increase the hippocampus. Studies also show that challenging yourself with brain training will also help memory function and increase volume in the brain region. More information of the explanation of these “treatments” can be found at https://www.growthengineering.co.uk/train-your-hippocampus/.

 

Conclusion:

Overall, it is evident the severe complications anxiety can cause. With the increase of glucocorticoid and cortisol levels, the hippocampus Is proven to shrink. Shrinkage in this region of the brain leads to memory formation issues which later on can cause further complications such as Alzheimer’s disease. Trying to avoid the difficulties of anxiety can be very tough but one can help themselves which some daily changes.

 

 

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Over the Edge

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Your heart rate spikes and yet you experience a shortness of breath. Your mind is overwhelmed with fear-filled stimulus. Your chest resists expansion and your lungs burn as your muscles ache for oxygen. An unbearable sense of dread floods your entire being. You may be experiencing an anxiety attack, one of many anxiety disorders. These include panic attacks, obsessive-compulsive disorder (OCD), and post-traumatic stress disorder (PTSD). Let’s take a step over the edge into the depths of anxiety.

Ground Level

Anxiety is a result of Intense psychological stress which may induce physical/behavioral alterations as a result of changes in hippocampal brain function brought about by complex molecular signaling pathways.

There are interconnections between stress, behavior, and memory where stress plays an important role in long-term memory formation. Because memory and its formation are critical for our interactions with our environment and crucial to our survival (such as remembering a terrifying experience with peanut allergies from your past), stressful events induce the formation of long-lasting memories. These memories then influence our behaviors within our environment such as avoiding the peanut-butter and jelly sandwich a stranger handed you.

The Depths

Through the usage of rodent models and well-established stress-inducing experiments, the molecular mechanisms governing the observed changes related to stress and memory have been explored.

To briefly summarize the detailed pathways and mechanisms leading to anxiety and the formation of associated long-term memories, these events are closely related to glucocorticoids, MAPK, NMDA, and GABA, neural signaling pathways, which are all related to stress, behavioral changes, and long-term memory.

Recap

Subjection of individuals to traumatic or hyper stressful situations specifically early on in their development makes them more likely to develop anxiety disorders especially PTSD and is a result of an inability to properly cope with intense stresses. The link between stress, behavioral response, and memory is revealed, as aforementioned, through the interactions of glucocorticoids, NMDA, MAPK, and Gabaergic driven neural pathways in the regulation of gene transcription within the limbic system. Any disruptions to these pathways can result in stress-related disorders including PTSD. To summarize, a cascade of molecular interactions between several proteins and their effectors results in an increased Histone mark (H3S10pK14ac) which then encourages the stress induced transcription of two genes fos and erg1 which produces proteins important in the process of memory formation.

Relief

Further exploration and a deeper understanding of these mechanisms could lead to therapeutic treatments for stress-related disorders and shed light on the complex mechanisms that govern the link between stress, behavior, and memory.  the link between psychological stress, the changes in behavior, and the effects on memory is an important subject of investigation as it could yield potential therapeutics with intentions of relieving individuals of their symptoms or the disorder completely.

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Forgetting to Remember: Stress and LTP

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Memory is one of the most useful tools we have at our disposal. I’m sure you can come up with (from memory) countless examples right now of how memory has helped you live a better life than if you didn’t have it. Where did I last put my keys? How do I get to Target from here? What was that person’s name? All of these instances are incredibly useful for navigating everyday life, but there are also some times when memory is hindered, and for good reason. 

When in immediate danger, things can be a blur, and after the fact it can be hard to remember a  lot of the actual occurrences of the moment. It might seem counterintuitive at first to not be able to remember what transpired during a time of panic, but it does make a lot of sense evolutionarily. Flight or fight activates to allow you to survive immediate danger, and that means escaping or fighting. That doesn’t mean remembering the layout of the prowling tiger’s stripes, or what shade of grey the boulder was that was falling towards you from the cliffside. Memory in itself is important to survive, but if it happens to be the source of hindrance in which other things become more important in that moment in order to survive, it makes sense that it will be temporarily disabled. 

A phenomenon called LTP (Long-term potentiation) is what neurologically allows us to engage in a number of memory-related behaviors. LTP is thought to be one of the main components of storing long-term memories and is present in the brain’s ability to learn. The hippocampus, and specifically the dentate gyrus (DG) within the hippocampal formation, is crucial for memory formation through the use of LTP.

When stress is present, the ability to encode information (memory-wise) seems to be diminished, but several factors have to be addressed in order to further understand the relationship here. There are different types of stress, and which kind it is matters in trying to ascertain its impact on memory. Acute stress and chronic stress are the two main types that are mentioned in research, both names being self-explanitory. When either of the two types are present, LTP is virtually eliminated. There are some differences however: In chronic stress, LTP signalling in the hippocampal area of CA1 is imparied, while it has no effect on dentate gyrus function, though there have been other studies that showed the DG being imparied, specifically with unpredictable stress. In acute stress, signalling is a little more complicated, with some regions being facilitated with LTP, like the ventral hippocampus, while the dorsal hippocampus is inhibited. This speaks to the complexity of the task at hand of trying to discern the effect that stress has on brain systems. 

Animal models for different neurological disorders, such as Alzhiemers disease and post traumatic stress disorder, have been trying to figure out the relation between the two, with interesting results. In AD animal models, there is naturally imparied LTP functioning, simply as a result of the degeneration. What was found with these animal models is that acute stress actually facilitates LTP, which is notable as this the opposite of normal, healthy brains. In PTSD animal models, researchers found that a single prolonged stress (SPS) induced LTP-like deficits in the hippocampus and amygdala, but there was an increase in contextual fear response memory. 

There is certainly more to learn in this domain of research, but enough is known in the present moment to make informed decisions about the links between stress and memory. 

 

Health/Hot topics/Uncategorized

Stressed, Tired, and/or Forgetful? NEW MIRACLE DRUG!!!!

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If I told you that the FDA just approved a new drug that has been shown to dramatically reduce stress, improve quality of sleep, and boost your memory, be honest, would you be interested?

I am happy to report that, indeed, there is just the product already on the market—good, old-fashioned exercise. Yes, folks, you heard me right. Exercise.

You might be saying, Kenny, this is nothing new, we’ve all known for ages that working out is physically good for you, which in turn helps your mental health…why should I be excited? If that’s you, then well done, that’s a great logical argument!

However, recent neurological evidence has emerged which suggests that exercise actually directly affects neurobiology in several key ways. Grant me a few minutes of your time and hopefully, you’ll be on your way to understanding some hot topics in neuroscience that have great potential for self-improvement!


Exercise can reduce stress by re-establishing neurotransmitter equilibrium in brain areas involved in stress-inducing scenarios


Think about the last time you were stressed. Like, really stressed out. You may have felt butterflies, sweaty palms, sick to your stomach, wanted to run for cover, or maybe even hit something. Not fun. But for all the negativity around stress, it can be a natural part of the human experience, and some acute stressors are even good for us! For instance, being a little bit nervous can improve performance on exams. This is all well and good, but stress over an extended duration or of an intense severity can lead to mental health concerns like major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). Clearly, something is going wrong here, what’s happening at the neurological level?

Interestingly, stress-induced disorders (e.g. MDD and PTSD) correlate with low levels of GABA (see table), in a specific part of the brain called the hippocampus, which is critical for making new memories. GABA is the Ying to Glutamate’s Yang, The table below should help explain each neurotransmitter and show how exercise can “bring balance to the neurochemical force” by directly increasing GABA in the hippocampus.




Exercise can improve sleep by significantly reducing sleep apnea


Sleep apnea is defined as having too many pauses in breathing happen during a night’s sleep. This leads to lower blood oxygen levels, which can be very harmful for cognition, learning, memory, and vascular and respiratory health. However, there is some good news! A new research paper (July 2020) provided evidence that exercise lowers the rate of sleep apnea! Because this paper is so new there’s a lot more work that needs to be done looking at what’s happening in the brain to support these changes. Given that stress increases the prevalence of sleep apnea, one hypothesis is that the same stress-relieving effects of exercise mentioned above are also at work here, that lowering the stressful “flight-or-fight” response leads to more restorative sleep!


Exercise bolsters memory and learning by strengthening local neural connections in areas of the brain key for memory formation



Last, and (at least for me) the coolest new finding of exercise’s outsize role in modulating neurobiology is that exercise makes us remember better.

Another July 2020 report that reviewed 13 studies found that exercise (2 minutes- 1 hour) produced short term advantages in many different memory tests! This is a super interesting finding because it shows how changeable our brains are, and how what we choose to do with them impacts our health at a very fundamental level.

Again, though it’s currently unclear exactly how this effect is caused, several potential explanations are given. One in particular focuses on a neat saying in neuroscience “neurons that fire together wire together”. This literally means neurons that are close to one another and firing in the same rhythm do in fact “wire together” becoming more likely to fire again if the other is stimulated. This complex process, called Long-Term Potentiation (LTP) is foundational for neuroplasticity. The researchers point out that physical activity could activate the proteins involved in LTP, thus “priming the pump” to better capture and store memories after the workout.


Thank you all for making it through my spirited defense of the newest and coolest Superdrug on the market right now! Unlike other drugs there is no doctor’s referral necessary, all you need is a little time and space. 🙂


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Bringing Together Memories under Pressure

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Can you remember the last time you were in a high stress situation? Perhaps it was before a major test, or the last time you had to speak in public.  We can all relate to that heart pounding and nerve-wracking feelings that seem to grip your entire body. I like to use the example of walking up to bat in a key situation in a baseball game. You feel the anxiety  and your heart pounding with every step as you inch move closer to the plate. You step up to bat, zone in, and do your best to perform at your highest level.

After not only this event, but any anxiety provoking situation is over some unique and fascinating things happen with your memory. Regardless of the outcome, If you’re like me sometimes you walk away and remember every vivid detail. On the other hand sometimes you walk away, especially when you’re really feeling excess pressure,  and you say to yourself, “what happened out there? I can’t remember a thing it all just happened so fast”.  Interestingly, there is neural evidence supporting this phenomenon,  and a wealth of information exists on how your memory if affected by anxiety provoking situations.

Spatial episodic memory is enhanced

This type of memory refers to your ability to remember what you saw, heard, and what happened.  The main stress hormone cortisol floods into your brain’s memory center causing increased brain activity when faced with a stressful situation. This increased activity helps you bring together the information into one, coherent story. Overall, this type of memory Memory consolidation, is increased when stress is added.

Memory recollection is hindered

Wait a minute, if your ability to form memories is stronger how can your ability to remember them be weaker? Although these memories are stronger, they are a little harder to get at. This is a protective mechanism caused by the coding of these events in the first place. The same activity that helps encode these memories simultaneously hurts retrieval. You don’t want to relive the stress of these events over and over and have them be at the forefront of your thoughts at all times.  In fact, there is evidence that when this process is chemically imbalanced, and these memories are played on repeat in the brain, there is a higher risk for PTSD.

Working Memory is hindered

Most parts of your memory are improved when stressed, but your working memory is hurt. Working memory is your ability to take in new information and use it in an ongoing task. The fact that working memory is hindered fits with that feeling of being “zoned in”. If you are only working on one thing this is your brains way of telling you to focus on this one important item and ditch the rest.

How much stress is too much?

Now this is where that feeling when you walk away from the event and say, “what just happened out there”. When your brain is flooded with too much cortisol (stress hormone) s your memory is hindered. This process follows the curve shown below. Some stress is good and improves your memory as it follows a curve leading up to ideal consolidation. However, there is a point where this consolidation begins to slope down and increased stress/cortisol has an adverse effect.

Memory as it relates to stress and anxiety is a complicated process with enough neuroscience to make your head spin for years. The next time you find yourself in a stressful situation, maybe take a second to take a deep breath, find your ideal between Zen and freaking out, and thank your memory for zoning in and helping you function at your highest level.

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Contextual Fear Conditioning and Exposure Therapy

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Contextual Fear Conditioning

There are various types of conditioning experiments that have been used across scientific disciplines, nearly everyone has heard of Pavlov’s dogs, and classical conditioning. A different type of conditioning exercise comes in the form of fear conditioning where mice or rats are placed in an unfamiliar environment, and subjected to an aversive stimulus, such as a mild shock to the foot.  After typically just one session, there is a long-lasting change in the animals behavior when presented with this novel environment.  This type of conditioning is called “contextual fear conditioning”.   Whenever the mice or rats are subjected to this environment associated with the shock, they “freeze”.  The act of freezing shows access to a “state dependent memory” based on the context of their current situation.  A state dependent memory is a memory that can only be accessed or triggered by the current mind state of the organisms. This discovery based on mouse models is now being seen as a use for humans against PTSD in the form of Exposure Therapy.

 

EXPOSURE THERAPY

Exposure therapy is the act of exposing a patient to a source of their anxiety, in a similar context, without any intention to create danger or ability to harm the patient physically.  This therapy relies on state dependent memory to access memories that the patient’s brain may have withheld in an attempt to protect them, which later could lead to an underlying cause of the individual’s PTSD.  Examples include virtual reality scenarios, such as swimming in the ocean for someone who was attacked by a shark, driving through a battleground for a combat veteran, or something as seemingly innocuous as petting a dog for another individual. The point is to access these memories by manipulating the brain into this specific arousal state.  By repeated exposure to these situations, it helps take the power that these situations have to cause stress and gives it back to the individual.

 

Is It For Everyone?

Right now, while everyone suffering from anxiety, or PTSD can be treated by exposure therapy to some point, it is important to note it is not as effective for some groups of people. For example, it has been found that combat veterans do not respond as well to treatment as other groups who have undergone trauma.  Sexual assault traumatized individuals demonstrated the most positive outcome from their treatments.  With the premium that is now being placed on mental health, and the support that can be garnered for individuals seeking treatment for PTSD, anxiety disorders, and depression; exposure therapy and it’s future evolution could play an important role in the treatment of mental health disorders.

Disease/Health

Why do only some people develop lasting symptoms of PTSD?

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A snowy evening…

During my sophomore year of high school, I narrowly missed a head-on collision with a semi. I was driving after school to a cello lesson in a neighboring town about 40 minutes away. It was late February, snowing, and the roads were terrible. Coming into a curve on the narrow two-lane highway, a semi crossed the center line into my lane. Quickly trying to avoid the crash, I swerved to avoid the truck and ended up fishtailing before sliding off of the highway into the ditch. I was shaken up, but physically ok. While this experience was traumatic and definitely taught me the value of snow tires and driving slowly, I did not develop any lasting symptoms. So why do some people develop lasting symptoms after traumatic experiences while others do not?

Inside the Brain

While our brains are truly remarkable machines in so many respects, they’re fundamentally focused on finding the way to keep us alive while expending as little energy as possible. So, when you experience a stressful, sudden event, your brain activates the fight or flight response. A rush of hormones including adrenaline and glucocorticoids is released to help you survive. In my case, the adrenaline kicked in, and before I’d even processed that I was in danger, my foot was on the brake and I was pointed towards the ditch. At the same time, glucocorticoids were released in my hippocampus, a brain structure critical in memory formation, so that my brain could form a memory of the event. These glucocorticoids help trigger memory formation by beginning a cascade of signals within neurons resulting in modifications to histones, a family of proteins that help store and organize your DNA. These modified histones expose specific regions of your DNA to allow for glucocorticoid-induced transcription of Immediate-Early genes (IEGs), resulting in protein synthesis. These IEG proteins play critical roles in memory formation, though exactly how that works is still not fully understood. Interestingly and critically, the level of glucocorticoids released in the hippocampus directly relates to both how many IEG proteins are made and how strong of a memory you make of that stressful event. Through a process known as long-term potentiation (LTP), your brain changes and adapt to your own life experiences. Making memories of dangerous and stressful events is important because it can help keep you alive in the future by reminding you of past events. However, when these memories are too strong, sustained LTP activation of stressful memories can result in lasting symptoms of PTSD.

What can be done?

For people living with PTSD, there are effective, research-supported treatment options. Pharmacologically, selective serotonin reuptake inhibitors (SSRIs) are commonly used. This class of medication blocks the reuptake of serotonin, allowing for more serotonin to be present in the brain for a longer period of time. While decisions about how to treat PTSD should always be made in consultation with a physician or therapist, some common non-pharmacologic treatments are:

  • Prolonged Exposure
  • Cognitive Processing Therapy
  • Cognitive-Restructuring Therapy
  • Eye Movement Desensitization and Reprocessing

Conclusion

While this does offer some explanation for why some people do or don’t develop PTSD symptoms, much more research is needed. Science does not have all the answers but does have a dearth of unexplored questions and new avenues of investigation to help unearth more data and find answers.

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Prescribing Exercise

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Anxiety: who it effects and what is offered to help?

Anxiety disorders have been diagnosed to millions of American adults showing their effects in diverse ways to each who are affected. Disorders such as Generalized Anxiety Disorder, Panic Disorder, Social Anxiety Disorder, Obsessive Compulsive Disorder, and so many others effect around 40 million or 18.1% US adults each year. With such prevalence, there are a multitude of treatment medications that can be prescribed to those affected based on their needs. These include medications such as:

  • Benzodiazepines: https://pixabay.com/users/tumisu-148124/
    • Xanax
    • Librium
    • Valium
    • Klonopin
    • Ativan
  • SSRIs
    •  Lexapro
    • Prozac
    • Paxil
    • Zoloft
  • Buspirone
  • Tricyclics

There are even more options than the ones mentioned above, but the list of side effects that can occur with taking these medications may be an even more extensive list. Some of the most common side effects include nausea, dizziness, headaches, diarrhea drowsiness, and benzodiazepines can even become addicting and cause memory problems if used for too long. These medications work by chemically balancing neurotransmitters in the brain such as serotonin, norepinephrine, and GABA. Balancing these neurotransmitters helps to reduce the effects of anxiety with the risk of experiencing side effects.

The benefits of a non pharmaceutical treatment for anxiety

One other non pharmaceutical technique that can be utilized to help with the effects of anxiety disorders: exercise. Some doctors even try to “prescribe” their patients suffering from anxiety constant and consistent exercise as a co treatment that goes along with anti anxiety medications. Exercising has been shown in clinical studies to increase the amount of GABA or gamma-aminobutyric acid. GABA is an inhibitory neurotransmitter that inhibits neurons in the amygdala and its receptor modulators are down regulated in anxiety related pathways. Exercising is a natural way to increase the GABA concentration in the brain that has the chance of decreasing the effects of anxiety. When one experiences a traumatic event, glucocorticoid levels in the brain increase and interact with the MAPK pathway and initiate histone conformation that leads to gene transcription. The gene transcription creates event-associated memory consolidation. This can be modulated by the inhibition of dentate gyrus neurons by GABA. GABA can be naturally increased by exercising. When rats are exercised, they have been shown to come to the decision that their environment is safe quicker than rats who are not exercised. The sedentary rats roam their cage longer insinuating that they are unsure whether their environment is safe or not.

The effects of increased GABA caused by exercise has also been seen in humans through electroencephalograms and magnetic resonance spectroscopy. After doing some type of exercise, whether that be yoga, cycling, running, etc., GABA concentration was increased correlating to a decrease in the symptoms of anxiety. One study looked specifically at doing yoga and how this type of exercise could help to increase the amount of GABA seen in the correlating brain regions. The study found that yoga practitioners had a 26% increase in thalamic GABA and “yoga-naive” subjects had a 13% increase in thalamic GABA after a 60 minute yoga practice.

Although those with different anxiety disorders may need to seek out different methods to treating their anxiety, it seems as though that through more intensive research, prescribed exercise may become more common or at least more common as a co treatment along with medication to help to decrease one’s risk of experiencing the side effects of taking anti anxiety medications.

 

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