Name of projectFrom the beginning of my high school career I've known that both community and the outdoors have an important and special meaning to me and knowing this I knew I wanted to do something for my action project senior year that would create a long lasting positive affect on Durango's community. This drive lead me to plan a fundraising event for a local mental health organization - All Forward Wilderness Therapy - and raise money for a permanent space, in the form of a yurt, that will help our local community reach back into nature especially during a time of need and healing.
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While planning the fundraising event I learned how to reach out into the community as I was doing it almost everyday and create communication and connections with local businesses and community members.
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TED TalkA study of PTSD, specifically how it can affect one's physical and mental health and how some cope with PTSD and discussing the differences and reasons of positive and destructive methods of coping.
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Senior thesis paper
What are the impacts of chronic PTSD on cell health and which medical treatments are promising involving the inflammatory impacts specifically in relation to long-term chronic PTSD?
Caity Mulcahy
Senior Project Advisor: Tina Hott
Abstract:
PTSD is a common and debilitating disease. Treatment of PTSD is vital, as the harmful symptoms of PTSD can lead to the development of other diseases. I chose to research how PTSD and its symptoms can lead to other disorders, specifically how chronic stress creates an involuntary immune response that may develop into a secondary disorder after some time. This research’s purpose is to determine the source of the problematic inflammation, and investigate treatments for inflammation and long term PTSD. Multiple studies on symptom reducers, such as EMDR and dietary effects, as well as studies showing what is being effected on the cellular level causing the inflammation conclude that long-term PTSD does induce an inflammatory response, and can cause an immune disorder after time. The most promising treatments found to reduce symptoms are dietary change, EMDR therapy, vmPFC stimulators , and HPA Axis inhibitors. This research is meant to give knowledge to those struggling with PTSD and experiencing these symptoms, to create an understanding of what is happening at a cellular level, and provide multiple choices to consider for treatments. Although the conclusions of this study are broad regarding a PTSD condition with inflammation, they become specific when talking about the general PTSD condition.
12th Grade Humanities
Animas High School
5 March 2018
Introduction
“They carried all they could bear, and then some, including a silent awe for the terrible power of the things they carried.” ― Tim O'Brien, The Things They Carried
In silent awe, we regard those who have carried all they can bear and then some as heroes: veterans giving hope to others. However, this comes at a cost for many as they carry an inescapable suffering: Posttraumatic Stress Disorder (PTSD). PTSD affects about 24.4 million people at any given time in the U.S., almost the population of Texas (PTSD United). About 80% of people who develop PTSD will have symptoms continue long-term - a month or more, causing chronic PTSD (Elements Behavioral Health). PTSD disturbs a person’s behavioral and psychological tendencies. The most common behavioral symptoms for the average patient are an increase in isolationism, self-destructive habits, irritability, loss of interest, insomnia, and nightmares. Psychological changes include an increase in flashbacks, anxiety, emotional detachment, chronic stress, and fear (National Institute of Mental Health). These symptoms take a significant toll on the patient, creating a more challenging day to day lifestyle. Similar to most diseases, chronic PTSD affects more than the person with the disorder. It affects their family, friends, and surrounding communities.
In order to address the full spectrum of chronic PTSD impacts, those afflicted need to become more informed so they are more able help those struggling with the disorder as well as the communities affected. For this reason, studying chronic PTSD and its effects on a cellular level is important to developing a comprehensive profile for the disease and its treatments.
Background Knowledge
As PTSD's effects numerous functions in the brain, and understanding how PTSD leads to these changes is necessary to treating these alterations. PTSD is usually caused by any experience that was shocking, terrifying, or dangerous: such as sexual violence, combat, or any other traumatic event (National Institute of Mental Health). The brain itself is known as the central nervous system and controls all the nerves throughout your body as well as most of the functions in the body. Since the central nervous system controls many systems and function in your body when altered everything else has potential to be affected as well. As for PTSD, there only a few known effects to specific functions and processes in the brain and body.
Some of the central nervous systems PTSD impacts are the Hypothalamus, Pituitary gland, and the Adrenal gland Axis (HPA Axis). These three systems work together to control reactions to emotions and moods - specifically stress - as well as regulate bodily processes such as digestion, the immune system, energy storage and usage, and lastly, the endocrine system. PTSD related dysfunction of the HPA Axis impairs the functions mentioned above, which can cause long-term diseases of varying resilience and severity (Jones and Moller) (Marković et al. 889-904).
In addition to the HPA axis, common systems known to be affected by PTSD are the Ventromedial Prefrontal Cortex (vmPFC) and the Amygdala. The vmPFC is a part of the brain that communicates with the amygdala. These neural groups process risk, fear, decision making, and self-control. The vmPFC and amygdala work together to inhibit emotional responses and cognitive evaluation of morality. The vmPFC of PTSD patients seems to have ‘fallen asleep’ letting the amygdala - mainly known for controlling the flight or fight response - over activate this response and go unchecked as the vmPFC’s function is to processes signals from the amygdala and evaluate how to respond, explaining some of the symptoms PTSD patients experience (Newton).
The HPA Axis, amygdala and vmPFC, and the hippocampus are detrimentally affected by PTSD. The hippocampus controls spatial navigation and regulates emotions, memory - usually long-term - and fear response to thoughts, memories, and situations. PTSD affects the hippocampus by impairing its ability to regulate memory. This effect can range from difficulty recalling certain memories, to making memories much more vivid and unforgettable (Wingenfeld, 109–120) (Kolassa et al. 321-325). Another impact of PTSD on the hippocampus is an inability to overcome fear responses to thoughts, memories, or situations that relate to traumatic events. As explained by Wingenfeld: “Stress hormones,( . . . ), influence a wide range of cognitive functions, including hippocampus-based declarative memory performance. Cortisol enhances memory consolidation but impairs memory retrieval” (109-120). Due to the hippocampus’ role in memory and emotional experiences, it is believed to cause some of the trouble with the patient's experiences and responses.
Long-term exposure to stress can affect many executive functions of the body. In the hippocampus, long-term stress can be so damaging that it could cause the region to shrink, as shown in animal studies, as well as in research examining the hippocampus in persons without PTSD compared to those with PTSD through MRI’s. This occurrence is thought to happen due to damage and destruction to cells from the overload of cortisol - a hormone released as a stress response, usually helpful in mobilizing the body in a stressful event.
Studies show that the size of the hippocampus is an indicator of a person's risk for development of PTSD after traumatic events (Gilbertson et al.). A study conducted by Mark Gilbertson and others seemed to prove this theory: those who have a smaller hippocampus are more susceptible to developing PTSD. This study examined twin’s brains, particularly looking at the difference in size of the hippocampus and how trauma affects it. As the investigation concluded,
We found evidence that smaller hippocampi indeed constitute a risk factor for the development of stress-related psychopathology. Disorder severity in PTSD patients who were exposed to trauma was negatively correlated with the hippocampal volume of both the patients and the patients’ trauma-unexposed identical co-twin. Furthermore, severe PTSD twin pairs—both the trauma-exposed and unexposed members—had significantly smaller hippocampi than non-PTSD pairs.
Gilbertson’s study was flawed in that the twins grew up in the same environment making it difficult to tease out the role of nature versus nurture and its effects on development, specifically on the size of the hippocampus. However, this theory still stands as the study was not conducted on twins exclusively. The verdict remains out on the true relationship between PTSD, the hippocampus, the vmPFC and amygdala, and the HPA Axis, as well as how these systems react with the rest of the body in PTSD patients as they are going through these changes.
Psychosomatic is defined as a physical illness or other condition caused and/or aggravated by a mental factor such as stress and/or internal conflict. Chronic PTSD shows signs of psychosomatic impacts, specifically with inflammation in immune cells. Inflammation on a cellular level is known to be a complex response of body tissue to damaging stimuli. It is a protective response involving immune cells, blood vessels, and molecular mediators where the goal of the cells is to eliminate the initial cause of cell injury, clear out the now dying cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.
Research and Analysis
Focusing on symptoms shown from PTSD and isolating them to study them can give insight as to what is causing an increase in inflammation. Once there is more known about the symptom taking what is applicable to the patient and treating as needed is one possibility on how to relate to PTSD.
While PTSD leads to several psychosomatic symptoms, the symptom of PTSD focused on in this paper will be chronic stress. Recent studies and research have proven chronic stress can affect bodily responses, and increase cellular inflammation. This occurrence is due to the constant increase in blood pressure, heart rate, and cortisol also known as a stress hormone, which triggers a response from the endocrine system. The endocrine system releases hormones that can cause damage to muscle tissue, inhibit growth, and suppress the immune system when over-produced (Miller et al.). “When under stress, cells of the immune system are unable to respond to hormonal control, and consequently, produce levels of inflammation that promote disease” (qtd Cohen, How stress influences disease: Study reveals inflammation as the culprit). In relation to PTSD, chronic stress can increase after a traumatic event, thus putting the immune system into a state of high inflammation (Miller et al.). This chronic stress can lead to the development of immune disorders after long periods.
In regards to the psychosomatic aspect, patients can experience a disease caused mainly by their stress levels. Such diseases are extremely difficult to control when dealing with other symptoms of PTSD. In an article by Dewleen Baker and others articulate on the concept of psychosomatic trends in correlation with neuropeptides - a group of compounds that act as neurotransmitters - and immune signaling in cytokine are examined:
As studies show that cytokines, detectable in the fear circuitry, e.g. hippocampus, amygdala and pre-frontal cortex are directly and indirectly involved in fear-related synaptic plasticity via cross-talk with NE [norepinephrine] and cortisol and via interactions with glutamate and GABA [gamma- Aminobutyric acid], their receptors, intercellular signaling pathways and regulators, i.e. the transmitter systems responsible for memory consolidation and reconsolidation (668).
With this information, one can infer that the connection between chronic stress and inflammation would also produce a connection with PTSD and inflammation, as chronic stress is a symptom of PTSD, a common one when discussing long-term aspects.
Moreover, offering a comprehensive view of what is happening on the cellular level during this demanding process of how cytokines interact with cells and how those cells respond, might be of service to understanding what is happening and how the cells are affected. To give an example of such processes can be seen in an immune cell. This immune cell has a receptor protein in its plasma membrane that is searching for a specific compound- its ligand. The ligand is what signals the immune cell’s pathways to activate, once it binds to the receptor protein. As a result, the structure of the receptor protein is the first to undergo the change in the immune cell due to the binding. Proteins that are in the cell then undergo a series of chemical reactions which finally reaches the nucleus. These reactions give instructions to transcription factors to activate specific genes and produce particular cytokines. Cytokines are chemicals used by cells to communicate, commonly known as hormones. The cytokines then communicates with other cells, causing them respond in a certain way; this response could include producing more cytokines or causing the cells to become more relaxed, thus moving out of the way of backup immune cells.
As this pertains to PTSD a study done by Hannah Gola and others “ . . . found evidence for a heightened inflammatory state in PTSD patients when analyzing spontaneous ex vivo cytokine production. Concentrations of IL-1β, IL-6, and TNF-𝛼 in supernatants of unstimulated PBMCs were significantly higher in the PTSD compared to the control groups (4-6).” This study simply states there are no ligands to spark this process in those with PTSD, thus causing a spontaneous creation of certain cells. The cytokines being produced are Interleukin -10 (IL-10), Tumor Necrosis Factor - alpha (TNF-𝛼), Interleukin - 4 (IL-4), Interleukin -6 (IL-6), and Interleukin - 1 Beta (IL-1β). Each of these cytokines produce different interactions between cells. IL-10 is an anti-inflammatory cytokine, which communicates with the cells to inform them that there was enough of an immune response and no more pro-inflammatory cells are needed. IL-6 is a pro-inflammatory cytokine; this cytokine communicates with the cells to inform them to produce more of an immediate immune response. IL-4 is a cytokine that generates what is called a positive feedback loop for the production of T cells. A positive feedback loop is merely an interaction where the output causes the start of the cycle again. T cells are part of the back up immune response that can be alerted by IL-4. The T0 cells sit waiting for IL-4, and when activated they mature to a variety of different T cells, for example, Th2 cells. These activated and mature T cells then produce IL-4 - the positive feedback loop - as well as an immune response to the insult.
Another cytokine researched was IL-1β. An easy way to understand IL-1β, a cytokine involved immune response, is to think of it as a ‘manager’ cytokine. IL-1β functions as pro-inflammatory cytokine, attaching to another cell and activating the production of other cytokines or proteins dependent on what is needed. For example, IL-1β can send out signals including cell proliferation, differentiation, and apoptosis - dependent on the need for more or less of an immune response. IL-1β is produced by macrophages - active immune cells - and, similar to IL-4, when secreted causes a positive feedback loop. TNF-𝛼 can be thought of in the same way as IL-1β, a cytokine regulating an immune response. TNF-𝛼 has the same functions and are produced in the same way as IL-1β, with the exception of the rate of activation. It is important to note this only accounts for a small amount of cytokines that deal with the immune system. These specific cytokines are only a few that my research focused on and are the ones that are most severely affected by PTSD.
The cytokines referenced above showed differing levels of spontaneous production, as spoken to in a study by Hannah Gola and others: “ . . . we found evidence for a heightened inflammatory state in PTSD patients when analyzing spontaneous ex vivo cytokine production. Concentrations of IL-1β, IL-6, and TNF-𝛼 in supernatants of unstimulated PBMCs [peripheral blood mononuclear cells] were significantly higher in the PTSD compared to the control group” (6). The levels of spontaneous production of these cytokines prove a change that is happening, though there is nothing to show how or why there is a spontaneous overproduction of these specific cytokines.
Treatments
There are many treatments for PTSD and its symptoms. This study focuses on chronic inflammation caused by long-term PTSD and treatments specifically for this inflammation, as well as the overall cause of the inflammation - PTSD - rather than looking at a broad treatment plan. This treatment plan is based on research and various studies and is not a diagnosed plan, as I am not a doctor - yet. In the broad spectrum of PTSD this treatment plan is very specific as it only takes into account chronic inflammation in correlation with PTSD. When looking at this specific case, though, this treatment plan can be seen as a base or outline as each case is specific and specialized to what will help the patient best and is based on what they are experiencing. Furthermore, these treatments show proming advancements for clinical trials for the improvement of either inflammation or certain aspects of PTSD itself. Not all of the symptom management for these problems are medications. In reality, many - if not most - are therapy and lifestyle changes.
One of the most promising treatment for reducing inflammation is simply including blueberries as 8% of one’s diet. Blueberries contain useful antioxidants that inhibit the harmful effects of oxidation of other cells, which is a process that can reduce oxidation thus reducing free radicals. Free radicals are a reactive atom or compound produced by a natural biological process in the body or introduced by an outside source that are missing an electron. These compounds can damage cells and alter their DNA structure. As shown in a study conducted by Philip Ebenezer and others on the anti-inflammatory effects of blueberries in an animal model of PTSD found,
The enhanced levels of free radicals, gene and protein expression of inflammatory cytokines seen in the PTSD group were normalized with a blueberry enhanced diet. Decreased anxiety in this group was shown by improved performance on the elevated plus-maze. These findings indicated blueberries can attenuate oxidative stress and inflammation and restore neurotransmitter imbalances in a rat model of PTSD.
A dietary plan focused around the positive effects of blueberries would include 200 calories per day consumed of blueberries, assuming the average person consumes about 2000-2500 calories per day. The primary benefit of including 8% of blueberries in your diet is so that the antioxidants can rid the body of free radicals in order to restore the neurotransmitter imbalances, with this assumption any food high in antioxidants would suffice, though studies have only been conducted on the effects of blueberries on rats. In related to PTSD, blueberries would only be able to affect the inflammation occurrence and wouldn’t be of use for a solution or symptom reducer for the source of the issue - PTSD - though this dietary change would be a considerable change for a system reducer.
Moreover, another treatment that looks to be promising, but is widely controversial in the medical community, is eye movement desensitization and reprocessing (EMDR). This treatment is a form of psychotherapy that uses eye movement and bilateral stimulation to assist in processing distressing memories and beliefs, thus dampening the charge of emotional memories. Through research done, looking at possible symptom management techniques for PTSD, EMDR appears to be promising in the respect to reducing symptoms, but far from a solution to either the problem of inflammation or PTSD itself. Controversy with this treatment in the medical field is raised in concern to how serviceable it is; however, it is widely used as there are over 20,000 practitioners who have been trained to use EMDR many people in the medical community raise the question as to how applicable EMDR is as a long-term treatment method (WebMD). Many use EMDR because the treatment does not have any known side effects and seems to be a more benign for patients than classical treatment methods. As an article by Christopher Lee and other states,
… EMDR therapy was initially posited to be more “gentle” and therefore amenable for this debilitated population because “distancing” rather than reliving has been found to be correlated with treatment effects,55 and the eye movements used in EMDR appear to immediately cause parasympathetic activation, resulting in physiologic calming. Although the usage on patients has appeared to be effective, there is still little known about how this treatment specifically how it can affect the patient, and if it could help with any other disorders than PTSD or help a psychosomatic approach to these disorders. (Lee et al.)
Furthermore, as PTSD can result in or induce a psychosomatic disorder in the HPA Axis, medications used to treat the HPA Axis has potential to be used as a PTSD treatment. There are a variety of HPA Axis medications that can be put into use to lower the cortisol levels being produced and bring the systems in the body back to equilibrium. The main goal of these medications is to reduce the stress response signals, while still letting other functions - such as digestions - work efficiently and smoothly. As illustrated in an article by Timothy Jones and others, current treatments, specifically selective serotonin reuptake inhibitors (SSRIs) and psychotherapy, could have valuable effects on PTSD patients in terms of the HPA Axis, but there are little to no studies on these treatments in relation to the impact they have on the HPA Axis (Implications of hypothalamic-pituitary-adrenal axis functioning in posttraumatic stress disorder).
An additional target system to consider when examining treatments is the vmPFC, and its interactions with the amygdala. PTSD patients are known to show a decrease in vmPFC function which results in nothing restraining the amygdala. Currently, in the medical field, there are no treatments specific to this situation, although the goal of medication in this instance would be to stimulate the vmPFC, so it responds to the amygdala’s signals, as well as to lower the rate of hormones triggering the amygdala.
Conclusion
In awe we witness those with PTSD as heros, veterans silently carrying all they can bear, rape victims witnessing a terrible power to their silence, and others bearing this silent pain with so much power. PTSD is a debilitating disorder that affects many, and for those affected one of the more fearful aspects of PTSD is how much is unknown. In an attempt to give informative resources to long-term patients affected by the disorder this study is designed to present information on this disorder’s effects on the mind and body as well as provide information on treatments. PTSD is a disorder that affects the central nervous system and compromises various regions in the brain such as the HPA Axis, vmPFC and amygdala, and the hippocampus. These systems affected by PTSD knock the body out of equilibrium and can cause other symptoms associated with PTSD - such as flashbacks, nightmares, intense anxiety and mood alterations.
In addition to the psyche affected by PTSD secondary diseases can by caused by psychosomatic influences of the disorder. One specific example is the spontaneous production of inflammatory immune cytokine in patients with long-term PTSD. This overproduction of cytokine causes various immune disorders in addition to the symptoms patients are already afflicted by from the original disorder - PTSD.
Symptoms reducers for PTSD and resulting secondary diseases discussed in this study are blueberries, EMDR, and SSRIs. These target different aspects of the disorders such as antioxidants in blueberries target free radicals and prevent inflammation and restore neurotransmitter imbalances. EMDR and SSRIs target the psyche aspect of PTSD and try to eliminate harmful mental aspects and neuro imbalances. There are a few treatments available that are alternatives to the traditional medication route. There is a need for more study on PTSD, specifically on the interactions between different processes and the spontaneous overproduction of certain cytokines. PTSD is a disorder rampant in our society and although there has been studies on this disorder and there progress made toward understanding PTSD more research is needed to create a comprehensive treatment plan for PTSD and it’s secondary disorders.
Bibliography
Senior Project Advisor: Tina Hott
Abstract:
PTSD is a common and debilitating disease. Treatment of PTSD is vital, as the harmful symptoms of PTSD can lead to the development of other diseases. I chose to research how PTSD and its symptoms can lead to other disorders, specifically how chronic stress creates an involuntary immune response that may develop into a secondary disorder after some time. This research’s purpose is to determine the source of the problematic inflammation, and investigate treatments for inflammation and long term PTSD. Multiple studies on symptom reducers, such as EMDR and dietary effects, as well as studies showing what is being effected on the cellular level causing the inflammation conclude that long-term PTSD does induce an inflammatory response, and can cause an immune disorder after time. The most promising treatments found to reduce symptoms are dietary change, EMDR therapy, vmPFC stimulators , and HPA Axis inhibitors. This research is meant to give knowledge to those struggling with PTSD and experiencing these symptoms, to create an understanding of what is happening at a cellular level, and provide multiple choices to consider for treatments. Although the conclusions of this study are broad regarding a PTSD condition with inflammation, they become specific when talking about the general PTSD condition.
12th Grade Humanities
Animas High School
5 March 2018
Introduction
“They carried all they could bear, and then some, including a silent awe for the terrible power of the things they carried.” ― Tim O'Brien, The Things They Carried
In silent awe, we regard those who have carried all they can bear and then some as heroes: veterans giving hope to others. However, this comes at a cost for many as they carry an inescapable suffering: Posttraumatic Stress Disorder (PTSD). PTSD affects about 24.4 million people at any given time in the U.S., almost the population of Texas (PTSD United). About 80% of people who develop PTSD will have symptoms continue long-term - a month or more, causing chronic PTSD (Elements Behavioral Health). PTSD disturbs a person’s behavioral and psychological tendencies. The most common behavioral symptoms for the average patient are an increase in isolationism, self-destructive habits, irritability, loss of interest, insomnia, and nightmares. Psychological changes include an increase in flashbacks, anxiety, emotional detachment, chronic stress, and fear (National Institute of Mental Health). These symptoms take a significant toll on the patient, creating a more challenging day to day lifestyle. Similar to most diseases, chronic PTSD affects more than the person with the disorder. It affects their family, friends, and surrounding communities.
In order to address the full spectrum of chronic PTSD impacts, those afflicted need to become more informed so they are more able help those struggling with the disorder as well as the communities affected. For this reason, studying chronic PTSD and its effects on a cellular level is important to developing a comprehensive profile for the disease and its treatments.
Background Knowledge
As PTSD's effects numerous functions in the brain, and understanding how PTSD leads to these changes is necessary to treating these alterations. PTSD is usually caused by any experience that was shocking, terrifying, or dangerous: such as sexual violence, combat, or any other traumatic event (National Institute of Mental Health). The brain itself is known as the central nervous system and controls all the nerves throughout your body as well as most of the functions in the body. Since the central nervous system controls many systems and function in your body when altered everything else has potential to be affected as well. As for PTSD, there only a few known effects to specific functions and processes in the brain and body.
Some of the central nervous systems PTSD impacts are the Hypothalamus, Pituitary gland, and the Adrenal gland Axis (HPA Axis). These three systems work together to control reactions to emotions and moods - specifically stress - as well as regulate bodily processes such as digestion, the immune system, energy storage and usage, and lastly, the endocrine system. PTSD related dysfunction of the HPA Axis impairs the functions mentioned above, which can cause long-term diseases of varying resilience and severity (Jones and Moller) (Marković et al. 889-904).
In addition to the HPA axis, common systems known to be affected by PTSD are the Ventromedial Prefrontal Cortex (vmPFC) and the Amygdala. The vmPFC is a part of the brain that communicates with the amygdala. These neural groups process risk, fear, decision making, and self-control. The vmPFC and amygdala work together to inhibit emotional responses and cognitive evaluation of morality. The vmPFC of PTSD patients seems to have ‘fallen asleep’ letting the amygdala - mainly known for controlling the flight or fight response - over activate this response and go unchecked as the vmPFC’s function is to processes signals from the amygdala and evaluate how to respond, explaining some of the symptoms PTSD patients experience (Newton).
The HPA Axis, amygdala and vmPFC, and the hippocampus are detrimentally affected by PTSD. The hippocampus controls spatial navigation and regulates emotions, memory - usually long-term - and fear response to thoughts, memories, and situations. PTSD affects the hippocampus by impairing its ability to regulate memory. This effect can range from difficulty recalling certain memories, to making memories much more vivid and unforgettable (Wingenfeld, 109–120) (Kolassa et al. 321-325). Another impact of PTSD on the hippocampus is an inability to overcome fear responses to thoughts, memories, or situations that relate to traumatic events. As explained by Wingenfeld: “Stress hormones,( . . . ), influence a wide range of cognitive functions, including hippocampus-based declarative memory performance. Cortisol enhances memory consolidation but impairs memory retrieval” (109-120). Due to the hippocampus’ role in memory and emotional experiences, it is believed to cause some of the trouble with the patient's experiences and responses.
Long-term exposure to stress can affect many executive functions of the body. In the hippocampus, long-term stress can be so damaging that it could cause the region to shrink, as shown in animal studies, as well as in research examining the hippocampus in persons without PTSD compared to those with PTSD through MRI’s. This occurrence is thought to happen due to damage and destruction to cells from the overload of cortisol - a hormone released as a stress response, usually helpful in mobilizing the body in a stressful event.
Studies show that the size of the hippocampus is an indicator of a person's risk for development of PTSD after traumatic events (Gilbertson et al.). A study conducted by Mark Gilbertson and others seemed to prove this theory: those who have a smaller hippocampus are more susceptible to developing PTSD. This study examined twin’s brains, particularly looking at the difference in size of the hippocampus and how trauma affects it. As the investigation concluded,
We found evidence that smaller hippocampi indeed constitute a risk factor for the development of stress-related psychopathology. Disorder severity in PTSD patients who were exposed to trauma was negatively correlated with the hippocampal volume of both the patients and the patients’ trauma-unexposed identical co-twin. Furthermore, severe PTSD twin pairs—both the trauma-exposed and unexposed members—had significantly smaller hippocampi than non-PTSD pairs.
Gilbertson’s study was flawed in that the twins grew up in the same environment making it difficult to tease out the role of nature versus nurture and its effects on development, specifically on the size of the hippocampus. However, this theory still stands as the study was not conducted on twins exclusively. The verdict remains out on the true relationship between PTSD, the hippocampus, the vmPFC and amygdala, and the HPA Axis, as well as how these systems react with the rest of the body in PTSD patients as they are going through these changes.
Psychosomatic is defined as a physical illness or other condition caused and/or aggravated by a mental factor such as stress and/or internal conflict. Chronic PTSD shows signs of psychosomatic impacts, specifically with inflammation in immune cells. Inflammation on a cellular level is known to be a complex response of body tissue to damaging stimuli. It is a protective response involving immune cells, blood vessels, and molecular mediators where the goal of the cells is to eliminate the initial cause of cell injury, clear out the now dying cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.
Research and Analysis
Focusing on symptoms shown from PTSD and isolating them to study them can give insight as to what is causing an increase in inflammation. Once there is more known about the symptom taking what is applicable to the patient and treating as needed is one possibility on how to relate to PTSD.
While PTSD leads to several psychosomatic symptoms, the symptom of PTSD focused on in this paper will be chronic stress. Recent studies and research have proven chronic stress can affect bodily responses, and increase cellular inflammation. This occurrence is due to the constant increase in blood pressure, heart rate, and cortisol also known as a stress hormone, which triggers a response from the endocrine system. The endocrine system releases hormones that can cause damage to muscle tissue, inhibit growth, and suppress the immune system when over-produced (Miller et al.). “When under stress, cells of the immune system are unable to respond to hormonal control, and consequently, produce levels of inflammation that promote disease” (qtd Cohen, How stress influences disease: Study reveals inflammation as the culprit). In relation to PTSD, chronic stress can increase after a traumatic event, thus putting the immune system into a state of high inflammation (Miller et al.). This chronic stress can lead to the development of immune disorders after long periods.
In regards to the psychosomatic aspect, patients can experience a disease caused mainly by their stress levels. Such diseases are extremely difficult to control when dealing with other symptoms of PTSD. In an article by Dewleen Baker and others articulate on the concept of psychosomatic trends in correlation with neuropeptides - a group of compounds that act as neurotransmitters - and immune signaling in cytokine are examined:
As studies show that cytokines, detectable in the fear circuitry, e.g. hippocampus, amygdala and pre-frontal cortex are directly and indirectly involved in fear-related synaptic plasticity via cross-talk with NE [norepinephrine] and cortisol and via interactions with glutamate and GABA [gamma- Aminobutyric acid], their receptors, intercellular signaling pathways and regulators, i.e. the transmitter systems responsible for memory consolidation and reconsolidation (668).
With this information, one can infer that the connection between chronic stress and inflammation would also produce a connection with PTSD and inflammation, as chronic stress is a symptom of PTSD, a common one when discussing long-term aspects.
Moreover, offering a comprehensive view of what is happening on the cellular level during this demanding process of how cytokines interact with cells and how those cells respond, might be of service to understanding what is happening and how the cells are affected. To give an example of such processes can be seen in an immune cell. This immune cell has a receptor protein in its plasma membrane that is searching for a specific compound- its ligand. The ligand is what signals the immune cell’s pathways to activate, once it binds to the receptor protein. As a result, the structure of the receptor protein is the first to undergo the change in the immune cell due to the binding. Proteins that are in the cell then undergo a series of chemical reactions which finally reaches the nucleus. These reactions give instructions to transcription factors to activate specific genes and produce particular cytokines. Cytokines are chemicals used by cells to communicate, commonly known as hormones. The cytokines then communicates with other cells, causing them respond in a certain way; this response could include producing more cytokines or causing the cells to become more relaxed, thus moving out of the way of backup immune cells.
As this pertains to PTSD a study done by Hannah Gola and others “ . . . found evidence for a heightened inflammatory state in PTSD patients when analyzing spontaneous ex vivo cytokine production. Concentrations of IL-1β, IL-6, and TNF-𝛼 in supernatants of unstimulated PBMCs were significantly higher in the PTSD compared to the control groups (4-6).” This study simply states there are no ligands to spark this process in those with PTSD, thus causing a spontaneous creation of certain cells. The cytokines being produced are Interleukin -10 (IL-10), Tumor Necrosis Factor - alpha (TNF-𝛼), Interleukin - 4 (IL-4), Interleukin -6 (IL-6), and Interleukin - 1 Beta (IL-1β). Each of these cytokines produce different interactions between cells. IL-10 is an anti-inflammatory cytokine, which communicates with the cells to inform them that there was enough of an immune response and no more pro-inflammatory cells are needed. IL-6 is a pro-inflammatory cytokine; this cytokine communicates with the cells to inform them to produce more of an immediate immune response. IL-4 is a cytokine that generates what is called a positive feedback loop for the production of T cells. A positive feedback loop is merely an interaction where the output causes the start of the cycle again. T cells are part of the back up immune response that can be alerted by IL-4. The T0 cells sit waiting for IL-4, and when activated they mature to a variety of different T cells, for example, Th2 cells. These activated and mature T cells then produce IL-4 - the positive feedback loop - as well as an immune response to the insult.
Another cytokine researched was IL-1β. An easy way to understand IL-1β, a cytokine involved immune response, is to think of it as a ‘manager’ cytokine. IL-1β functions as pro-inflammatory cytokine, attaching to another cell and activating the production of other cytokines or proteins dependent on what is needed. For example, IL-1β can send out signals including cell proliferation, differentiation, and apoptosis - dependent on the need for more or less of an immune response. IL-1β is produced by macrophages - active immune cells - and, similar to IL-4, when secreted causes a positive feedback loop. TNF-𝛼 can be thought of in the same way as IL-1β, a cytokine regulating an immune response. TNF-𝛼 has the same functions and are produced in the same way as IL-1β, with the exception of the rate of activation. It is important to note this only accounts for a small amount of cytokines that deal with the immune system. These specific cytokines are only a few that my research focused on and are the ones that are most severely affected by PTSD.
The cytokines referenced above showed differing levels of spontaneous production, as spoken to in a study by Hannah Gola and others: “ . . . we found evidence for a heightened inflammatory state in PTSD patients when analyzing spontaneous ex vivo cytokine production. Concentrations of IL-1β, IL-6, and TNF-𝛼 in supernatants of unstimulated PBMCs [peripheral blood mononuclear cells] were significantly higher in the PTSD compared to the control group” (6). The levels of spontaneous production of these cytokines prove a change that is happening, though there is nothing to show how or why there is a spontaneous overproduction of these specific cytokines.
Treatments
There are many treatments for PTSD and its symptoms. This study focuses on chronic inflammation caused by long-term PTSD and treatments specifically for this inflammation, as well as the overall cause of the inflammation - PTSD - rather than looking at a broad treatment plan. This treatment plan is based on research and various studies and is not a diagnosed plan, as I am not a doctor - yet. In the broad spectrum of PTSD this treatment plan is very specific as it only takes into account chronic inflammation in correlation with PTSD. When looking at this specific case, though, this treatment plan can be seen as a base or outline as each case is specific and specialized to what will help the patient best and is based on what they are experiencing. Furthermore, these treatments show proming advancements for clinical trials for the improvement of either inflammation or certain aspects of PTSD itself. Not all of the symptom management for these problems are medications. In reality, many - if not most - are therapy and lifestyle changes.
One of the most promising treatment for reducing inflammation is simply including blueberries as 8% of one’s diet. Blueberries contain useful antioxidants that inhibit the harmful effects of oxidation of other cells, which is a process that can reduce oxidation thus reducing free radicals. Free radicals are a reactive atom or compound produced by a natural biological process in the body or introduced by an outside source that are missing an electron. These compounds can damage cells and alter their DNA structure. As shown in a study conducted by Philip Ebenezer and others on the anti-inflammatory effects of blueberries in an animal model of PTSD found,
The enhanced levels of free radicals, gene and protein expression of inflammatory cytokines seen in the PTSD group were normalized with a blueberry enhanced diet. Decreased anxiety in this group was shown by improved performance on the elevated plus-maze. These findings indicated blueberries can attenuate oxidative stress and inflammation and restore neurotransmitter imbalances in a rat model of PTSD.
A dietary plan focused around the positive effects of blueberries would include 200 calories per day consumed of blueberries, assuming the average person consumes about 2000-2500 calories per day. The primary benefit of including 8% of blueberries in your diet is so that the antioxidants can rid the body of free radicals in order to restore the neurotransmitter imbalances, with this assumption any food high in antioxidants would suffice, though studies have only been conducted on the effects of blueberries on rats. In related to PTSD, blueberries would only be able to affect the inflammation occurrence and wouldn’t be of use for a solution or symptom reducer for the source of the issue - PTSD - though this dietary change would be a considerable change for a system reducer.
Moreover, another treatment that looks to be promising, but is widely controversial in the medical community, is eye movement desensitization and reprocessing (EMDR). This treatment is a form of psychotherapy that uses eye movement and bilateral stimulation to assist in processing distressing memories and beliefs, thus dampening the charge of emotional memories. Through research done, looking at possible symptom management techniques for PTSD, EMDR appears to be promising in the respect to reducing symptoms, but far from a solution to either the problem of inflammation or PTSD itself. Controversy with this treatment in the medical field is raised in concern to how serviceable it is; however, it is widely used as there are over 20,000 practitioners who have been trained to use EMDR many people in the medical community raise the question as to how applicable EMDR is as a long-term treatment method (WebMD). Many use EMDR because the treatment does not have any known side effects and seems to be a more benign for patients than classical treatment methods. As an article by Christopher Lee and other states,
… EMDR therapy was initially posited to be more “gentle” and therefore amenable for this debilitated population because “distancing” rather than reliving has been found to be correlated with treatment effects,55 and the eye movements used in EMDR appear to immediately cause parasympathetic activation, resulting in physiologic calming. Although the usage on patients has appeared to be effective, there is still little known about how this treatment specifically how it can affect the patient, and if it could help with any other disorders than PTSD or help a psychosomatic approach to these disorders. (Lee et al.)
Furthermore, as PTSD can result in or induce a psychosomatic disorder in the HPA Axis, medications used to treat the HPA Axis has potential to be used as a PTSD treatment. There are a variety of HPA Axis medications that can be put into use to lower the cortisol levels being produced and bring the systems in the body back to equilibrium. The main goal of these medications is to reduce the stress response signals, while still letting other functions - such as digestions - work efficiently and smoothly. As illustrated in an article by Timothy Jones and others, current treatments, specifically selective serotonin reuptake inhibitors (SSRIs) and psychotherapy, could have valuable effects on PTSD patients in terms of the HPA Axis, but there are little to no studies on these treatments in relation to the impact they have on the HPA Axis (Implications of hypothalamic-pituitary-adrenal axis functioning in posttraumatic stress disorder).
An additional target system to consider when examining treatments is the vmPFC, and its interactions with the amygdala. PTSD patients are known to show a decrease in vmPFC function which results in nothing restraining the amygdala. Currently, in the medical field, there are no treatments specific to this situation, although the goal of medication in this instance would be to stimulate the vmPFC, so it responds to the amygdala’s signals, as well as to lower the rate of hormones triggering the amygdala.
Conclusion
In awe we witness those with PTSD as heros, veterans silently carrying all they can bear, rape victims witnessing a terrible power to their silence, and others bearing this silent pain with so much power. PTSD is a debilitating disorder that affects many, and for those affected one of the more fearful aspects of PTSD is how much is unknown. In an attempt to give informative resources to long-term patients affected by the disorder this study is designed to present information on this disorder’s effects on the mind and body as well as provide information on treatments. PTSD is a disorder that affects the central nervous system and compromises various regions in the brain such as the HPA Axis, vmPFC and amygdala, and the hippocampus. These systems affected by PTSD knock the body out of equilibrium and can cause other symptoms associated with PTSD - such as flashbacks, nightmares, intense anxiety and mood alterations.
In addition to the psyche affected by PTSD secondary diseases can by caused by psychosomatic influences of the disorder. One specific example is the spontaneous production of inflammatory immune cytokine in patients with long-term PTSD. This overproduction of cytokine causes various immune disorders in addition to the symptoms patients are already afflicted by from the original disorder - PTSD.
Symptoms reducers for PTSD and resulting secondary diseases discussed in this study are blueberries, EMDR, and SSRIs. These target different aspects of the disorders such as antioxidants in blueberries target free radicals and prevent inflammation and restore neurotransmitter imbalances. EMDR and SSRIs target the psyche aspect of PTSD and try to eliminate harmful mental aspects and neuro imbalances. There are a few treatments available that are alternatives to the traditional medication route. There is a need for more study on PTSD, specifically on the interactions between different processes and the spontaneous overproduction of certain cytokines. PTSD is a disorder rampant in our society and although there has been studies on this disorder and there progress made toward understanding PTSD more research is needed to create a comprehensive treatment plan for PTSD and it’s secondary disorders.
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