Is the Manifestation of PTSD a Culture Bound Syndrome?

 

Is the Manifestation of PTSD a Culture Bound Syndrome?

Danielle Murri

University of Colorado, Colorado Springs

 

Trauma is an inevitable concept that individuals find themselves familiar with in one way or another during the course of their lives, but the degree to which trauma or traumatic stress shapes someone’s life depends on both biology and culture. When recovery from traumatic events is prolonged more than “normal” and the fight or flight reaction is not turned off even after some time, traumatic stress may turn into posttraumatic stress disorder (PTSD). This paper will discuss the cultural aspects of PTSD, specifically how trauma is viewed and treated in America, and examine the ways the Western world may be creating a culture bound syndrome with the way that trauma is handled.

 “Always alert, and forever safe”, this statement by Confucius, is a simple way to explain the suffering of those who have had profound effects from living through a traumatic experience. Trauma, for those affected with PTSD, does not seem as if it is in the past, only a distant memory. The trauma feels real and is repeated, again, and again causing crippling anxiety, fear, and a constant state of fight or flight. As Adam Cash (2006) states,

There is something inherently powerful about the experiences of trauma that somehow encourages us to separate ourselves from it, either through time, distance, or within the recesses of our unconsciousness. Trauma is something that happens to someone else, right? Murder and violence only happen in the bad parts of town. War happens on someone else’s land, in a far-off country, or on the safe technological distance of our television screens. We want to leave it behind. We want to forget about it. This logic makes sense in our day-to-day lives. Our everyday language reflects this desire in our responses to those wounded and stunned around us: “put it behind you”, “try to focus on the future”, “it happened in the past, and there is nothing you can do to change that (p.4).

In the Western world, it is encouraged that individuals “move on” fairly rapidly from traumatic events, however this is not always possible. For some of us, escaping trauma seems impossible with the intense memories, flashbacks, and hauntings of our own minds and bodies. PTSD is the struggle of trying to forget, trying to heal, trying to not live in a state of constant fear. PTSD is ‘a syndrome of reliving or re-experiencing their particular trauma or traumas again and again’ (Cash, 2006, p. 4). PTSD is an adverse reaction to trauma; these horrifying events have impacted an individual so much that their own brain and mind have created an illness.

PTSD is not a new concept. Officially it was introduced to medical records in 1980, but previous to the formal recognition, many individuals felt the heavy symptoms of an anxiety ridden, trauma related disorder. There have been many minor versions of a PTSD diagnosis. Cash (2006), describes these versions as, “a set of symptoms or syndromes identified more with a specific stressor, rather than as a universal syndrome or disorder resulting from a traumatic stressor of any type, given it is of sufficient intensity” (p. 7). Some of these versions were titled, ‘nerve-trauma hypothesis’, ‘trauma neuroses’, ‘shell shock’, ‘battle fatigue’, ‘Post-Vietnam Syndrome’, and ‘Stress Response Syndrome’. None of these versions summed up all of the experiences and symptoms of reactions to trauma until the description of post-traumatic stress disorder. The concept of PTSD has been long tied to those suffering ill effects of war, but with growing professional interest in the disorder, it has been realized that PTSD applies to a much larger group of stimulus or causal events, including rape, natural disasters, automobile accidents, and child sexual abuse.  PTSD can happen to anyone, regardless of age.

According to fifth edition of The Diagnostic and Statistical Manual of Mental Disorders (DSM-5), the diagnostic criteria for PTSD includes history of exposure to certain types of traumatic events and symptoms from four symptom clusters categorized as intrusion, avoidance, negative alterations in cognitions and mood, and alterations in arousal and reactivity. Additional criteria deal with the length that symptoms are present and how an individual is able to function.

The first section of the criteria is in regards to the traumatic stressor. One must have been exposed to death, threatened death, experienced actual or threatened injury, or actual or threatened sexual violence. One must have had direct exposure with one of the above, witnessed it occurring, been affected indirectly by learning a close friend or relative was exposed to trauma or a violent or accidental death, or with repeated exposure to these events: normally in a professional manner (e.g. first responders or military).

The second criteria states that the traumatic event is persistently re-experienced either with dissociative reactions like flashbacks, involuntary, recurrent, intrusive memories, traumatic nightmares, intense distress after reminders of the trauma, or physiologic reactivity after being exposed to trauma related stimuli.

The third criterion requires avoidance of trauma related situations after the event whether they are trauma related thoughts or emotions, or external reminders like situations, activities, items, people, or particular places.

The fourth criteria category requires negative changes in mood or cognition as a result of a traumatic event. This may mean inability to recall certain aspects of the event (not due to drugs, alcohol, or brain injury), negative beliefs of oneself or the world, distorted blame of others or self for causing the event or persisting consequences, negative trauma related emotions, diminished interest in activities previously enjoyed, feeling isolated, or consistent inability to experience positive emotions.

The last significant criteria category refers to alterations in arousal and reactivity. These alterations must have begun after the traumatic event or have worsened significantly. Alterations may be aggressiveness or irritability, recklessness or self-destructive behaviors, hyper vigilance, exaggerated startle response, problems concentrating, or changes in sleep patterns. The final criterion are involved in monitoring how long symptoms persist, as they must be present for longer than one month for an official diagnosis; and how impaired an individual is due to symptoms, whether socially, academically, or in their occupation. (American Psychiatric Association, 2013).

As seen in the description of PTSD by the DSM-5, this disorder is an illness that affects individuals socially. Gilbert Reyes (2008) states,

Perhaps more than most mental diagnoses, posttraumatic stress disorder represents a complex code of social and contextual values and expectations regarding the ways in which people are likely to be affected by their experiences and how their reactions are commonly expressed.

This complex code that Reyes speaks of, is culturally affected. In analyzing posttraumatic stress disorder, the concept of stress and stressors must be considered, which is dependent on culture. McDade (2002), explains,

Anthropology is marked by a diversity of conceptual and methodological approaches to stress research, with levels of analysis that range from global political economy to local social or ecological disruption, individual mental and physical health, and human physiology, Although the methods and goals of these approaches vary, they all share an interest in the human stress experience across cultures and the specific cultural, ecological, and historical contexts that give it meaning. Of most relevance to the analysis presented here is the work of medical and biological anthropologists who have reposted quantitative associations between exposure to nontraditional, Western ways of living – through migration or local change- and self reported symptoms of physical and emotional distress or physiological measures of stress.

The human stress experience varies and expected levels of emotion to trauma, death, or other significant stressors are heavily dependent on culture. Since PTSD is conceptualized as a disorder formed by fear and stress dysregulation, the question is then, is posttraumatic stress disorder a universal phenomenon due to high levels of trauma, or is it a culture bound syndrome?

            A culture bound disorder or syndrome is an illness that is a combination of psychiatric and somatic symptoms that is recognized within a specific culture. Finding just one definition of this concept is difficult, as anthropologists and psychologists will not agree completely. According to the American Psychiatric Association, “The term culture-bound syndrome denotes recurrent, locality-specific patterns of aberrant behavior and troubling experience that may or may not be linked to a particular DSM-IV diagnostic category. Many of these patterns are indigenously considered to be "illnesses," or at least afflictions, and most have local names. Although presentations conforming to the major DSM-IV categories can be found throughout the world, the particular symptoms, course, and social response are very often influenced by local cultural factors. In contrast, culture-bound syndromes are generally limited to specific societies or culture areas and are localized, folk, diagnostic categories that frame coherent meanings for certain repetitive, patterned, and troubling sets of experiences and observations.”

There is considerable debate as to whether PTSD should be considered a Western-linked culturally bound syndrome or if it is a universal reaction. Hinton and Lewis-Fernandez (2010) approached the DSM-5 with questions regarding the cross-cultural validity of posttraumatic stress disorder. In their study, the validity of the DSM-5 was examined when it was applied to traumatized members of culturally diverse groups. The researchers sought to answer questions like, “Does PTSD as currently defined apply equally well across cultures? Is it found with equivalent frequency? Do the symptoms that currently compose the syndrome cluster together in the same way? Or, instead, do cultural factors pattern alternate presentations of PTSD?

In the study, both biological and cultural factors were examined in regards to the development of PTSD. The main biological factor examined was that of biomarkers. A biomarker is a characteristic that is measured and evaluated objectively as an indicator of a biological state, including pathological conditions such as PTSD. Possible biomarkers for PTSD are startle responses, exaggerated physiological reactivity, and MAO-B platelet activity. Cultural factors examined were severity of trauma, as multiple studies in various countries and ethnic groups have indicated that the severity of a trauma can predict the severity of PTSD, rate of trauma, and the global presence/probability of PTSD after trauma.

            The researchers found that the DSM-5 for PTSD is valid cross-culturally. They do stipulate their findings with this statement,

The review suggests that cultural syndromes may shape symptom comorbidities and symptom profiles in important ways that should be assessed and documented to increase content validity in the assessment of trauma-related disorder. Assessing patients for somatic symptoms and cultural syndromes may also be needed to better attain content validity when PTSD is evaluated cross-culturally. A chapter on cultural aspects of psychiatric diagnoses and/or an expanded Glossary of Cultural Syndromes that describe the relationship of specific syndromes and DSM-5 disorders would help to address this issue (Hinton and Lewis-Fernandez, 2010).

Another study of the cultural aspects of PTSD proposed that the concept and definition of culture should be presented as a foundation for understanding the many influences cultural factors have on the perception, experience, clinical expression, treatment responses to trauma. Marsella (2010) calls attention to ‘healing principles’ used by the Western world as well as more traditional approaches, and emphasizes the importance of ethnocultural variables. He states, “…in spite of what appears to be common neurological processes, correlates, and consequences in the initial response to trauma exposure, ethnocultural variables exercise major influence on perceived causes, symptom manifestations, clinical parameters (i.e., onset, course, and outcome), interventions, and societal responses.”

Marsella discusses the history of PTSD, specifically among veterans, and the questions that arose with the early ‘existence’ of the anxiety bound illness. He mentions the inevitable questions that arose about the etiology, diagnosis, expression, and treatment of stress disorders, but many of these questions were ignored, because trauma and the reaction to it were assumed to be universal to all humans. In the beginning it was assumed that the human neurological response to traumatic events affected the brain’s emotional centers; specifically the hypothalamus-pituitary-adrenal axis, the amygdala, and endocrine areas. Eventually, research showed activity in the central nervous system and long-term biological consequences of severe trauma. Some of these consequences were lowered thresholds for anxiety, atrophy of the hippocampus, and atrophy of the cingulate cortex. As more research was established variations in traumatic related consequences began to arise. The idea that PTSD could be culturally variable was not widely accepted (Marsalla, 2010).

The reason culture variability was not widely accepted was because it challenged biological assumptions of psychiatric disorders and challenged ideas about the universal human experience of trauma and trauma reactions.

If ethnocultural variations in trauma and PTSD existed, this would call attention to the plasticity of the human mind and brain, especially the role of cultural factors in causing and shaping disorders and diseases. This relativity would contradict the ‘disease’ model of psychiatry... (Marsalla, 2010).

Summerfield (1999) challenged the Western assumptions about trauma and PTSD. He believed that the codified description of PTSD was wrongly being prescribed to non-Western settings, specifically after natural and man-made disasters. He, along with others challenged the normally regularly accepted concepts of the Western diagnosis of PTSD. Bracken, Giller, and Summerfield (1997) wrote:

Trauma projects which seek to objectify “suffering” as an entity apart, converting it into a technical problem to which are applied technical solutions like Western talk therapies, are discounting indigenous knowledge, capacities, and priorities. Such projects aggrandize the Western expert who defines the problem (e.g., PTSD) and brings the cure; too often it is the same problem and the same cure, whether to Cambodia, Rwanda, or elsewhere.

Resistance to the previously accepted notions that psychiatric disorders were affected by biology and not culture began to grow, and the idea that PTSD might be a culture bound disorder has grown. Suffering is clearly present in other cultures, as are emotional reactions to traumatic experiences. Marsalla previously studied prevalence rates of PTSD in other cultures in 1996 with a team of researchers. He found that prevalence rates of PTSD varied widely between cultures and that the diagnostic criteria being used at the time was not sufficiently sensitive to cultural aspects of health and could not then detect PTSD in other cultures, as it may be manifested differently. Findings from Marsalla’s studies were that some re-experiencing and arousal symptoms were more easily identified in some cultures than the avoidance and numbing systems, indicating that the experience of PTSD involves both culture bound aspects, universal aspects, and a relationship between biological and cultural influences. He also proposed that symptoms described as arousal or re-experiencing symptoms tended to have a greater biological basis with changes noted in brain function, and avoidance and numbing symptoms seem to have a significant cultural influence. Marsalla and his team concluded that “the prevalence of PTSD is highest among cultures in which avoidance and numbing are common methods of dealing with distress” (Reyes, 2008).

There are some known illnesses that resemble the Western definition of PTSD in a different cultural context. Reyes (2008) describes a disorder called Latah. Latah is seen in Malaysia and Indonesia as a condition of distress after someone is startled. A startling trigger causes a half hour display of hysterical laughter, shouted cursing, screaming, and even dancing. The outbursts are described as unpleasant for the sufferer, but the community often finds the outbursts entertaining. This cultural expression of distress is not associated with a single traumatic event causing distress like a death of a child. Reyes also describes distress disorders seen in Latin America. The concepts of Ataque de nervios and Nervios are states of vulnerability in response to a stressful life experience. Symptoms can include uncontrollable shouting, fits of crying and trembling, verbal or physical aggrestion, emotional distress, headaches, irritability, stomach disturbances, sleep disturbances, nervousness, emotional instability, and diminished concentration (Schepher Hughes 1994). Similar symptoms have been described in Greece in a disorder called nevra. Another distress disorder reported among Latinos is susto. Susto is known as soul loss due to traumatic events, which leads to symptoms of unhappiness and sickness.

The symptoms of suffering are universal and when seen in other cultures may be called a distress disorder, but many of the cultures examining the symptoms just see them as a natural reaction to trauma. In the Western world of medicine, it is categorized and stigmatized as an illness, instead of an extreme reaction to an extreme event. For this reason as well as others, I believe a diagnosis of PTSD, and the current treatment model of antidepressants and talk therapy is a culture bound syndrome. The symptoms may be universal and biologically marked, but the consideration of these symptoms as a disorder, and the treatment of a traumatized individual varies dramatically within cultures.

Since the professional interest of PTSD is has continued to rise, researchers have continued to challenge preconceived ideas of universal causes, manifestations, and treatment responses and have started to note that exposure to traumatic events might actually result in improved mental status for some trauma survivors. This phenomenon is called “post-traumatic growth” (PTG). PTG is the belief that a crisis might also be an opportunity since endurance and courage in the face of adversity and extreme stress is admirable and valued.  Additional research about PTSD, and its relationship to culture is still ongoing, so it cannot be conclusively said that PTSD is a culturally bound syndrome, however there is a question that needs to be considered. Can any psychological illness escape cultural influence? No, it cannot.

While there may be epigenetic factors contributing to the risk factors of developing PTSD, it is likely that culture has a heavier influence on how an individual reacts to a traumatic situation. It has not been conclusively verified that all cultures experience all symptoms of PTSD, indicating that it may be extremely cultural based with some biological backbone, or a culture bound syndrome. As Schepher Hughes (1994) states,

From the phenomenological oriented perspective of some medical anthropologists (concerned with the “lived-in” sense of illness), pain, disability, and other forms of human suffering are habituated bodily expressions of dynamic social relations. Sickness is more than just an unfortunate brush with nature. It is more than something that “just happens” to people. Sickness is something that humans do in uniquely original and creative ways. Illness is a form of body praxis, of bodily action.

 The idea of illness, and PTSD being a form of body praxis is important in realizing that PTSD may be a Western culturally bound syndrome. The medical anthropology perspective of a body is that it is representative of an individual (self), social, and political aspects that are not separate but rather intertwined. This anthropological body feels cultural pressures to either express or hide emotion, and in my opinion, I believe trauma related emotions are encouraged in the Western culture to be suppressed, causing psychological distress, and the criteria necessary for the arbitrary diagnosis of PTSD. PTSD is a conceptualization of a distress reaction, just like the concepts of nervios, sustos, and latah. These cultural reactions to trauma are viewed as culture-bound syndromes, just as the manifestation of PTSD in Western culture should be viewed as one.

There are significant differences in the ways in which trauma is viewed and handled cross culturally ,especially in regard to the expectations of reactions and emotions following trauma which can contribute to the severity of expression as well as which symptoms are expressed. I believe that the cultural pressures in America to not slow down and experience things, but rather hide pain and discomfort, as well as admit that suffering is part of the human experience, has contributed significantly to the formation of PTSD as a culture bound illness. As research on PTSD and treatment types continues to progress, I hope the current views on trauma and ‘normal’ reactions to trauma adapt. Traumatic experiences reap traumatic outcomes and emotions. These emotions and outcomes do not need to be stigmatized, diagnosed as an illness, and medicated, but rather accepted as unpleasant suffering due to unpleasant events, and an unfortunate part of the human experience.

References

American Psychiatric Association. (2013) Diagnostic and statistical manual of mental disorders, (5th ed.). Washington, DC.

Cash, A. (2006). Concise Guides to Mental Health: Posttraumatic Stress Disorder. Hoboken,, NJ: John Wiley & Sons.

Gedo, J. (2005). Psychoanalysis as Biological Science: A Comprehensive Theory. Baltimore: Johns Hopkins University Press.

Gielen, U., Fish, J., & Draguns, J. (Eds.). (2004). Handbook of Culture, Therapy, and Healing. Mahwah, NJ: Lawrence Erlbaum Associates.

Hinton, D., & Lewis-Fernández, R. (2010). The cross-cultural validity of posttraumatic stress disorder: Implications for DSM-5. Depression and Anxiety, 783-801.

 Marsella, A. (2010). Ethnocultural Aspects of PTSD: An Overview of Concepts, Issues, and Treatments.       Traumatology, 17-26. 

McDade, T. (2002). Status Incongruity in Samoan Youth: A Biocultural Analysis of Culture Change, Stress, and Immune Function. Medical Anthropology Quarterly, 16(2), 123-150.

Plomin, R., & McClearn, G. (Eds.). (1993). Nature, Nurture, & Psychology. Washington, DC: American Psychological Association.

Reyes, G. (2008). The encyclopedia of psychological trauma. Hoboken, NJ: Wiley.

Scheper-Hughes, N. (1994). Embodied Knowledge: Thinking with the Body in Critical Medical Anthropology. In R. Borofsy (Ed.), In Assessing Cultural Anthropology (pp. 229-242). Columbus, Ohio: McGraw-Hill.

Small, M. (2006). The Culture of Our Discontent: Beyond the Medical Model of Mental Illness. Washington, D.C.: Joseph Henry Press.

 

 

Cognitive Evolution -ANTH and PSYCH Final Paper

 

Rethinking Autism: Cognitive Implications of Autism Spectrum Disorder

Danielle Murri

University of Colorado, Colorado Springs

 

Author Note

Danielle Murri, Anthropology Department, University of Colorado, Colorado Springs.

Correspondence regarding this article should be addressed to Danielle Murri, Anthropology Department, University of Colorado, Colorado Springs, 1420 Austin Bluffs Parkway, Colorado Springs, CO. E-mail: daniellemurri@gmail.com

 

Abstract

This paper focuses on how brain development disorders such as autism are defined, diagnosed, and analyzed as far as the development and potential causes  of ASD (specifically classic autism). Differing cognitive perspectives such as lacking theory of mind, dysfunctional mirror neuron systems, and the intense world syndrome are also examined and challenged.

Keywords: Autism Spectrum Disorders (ASD), Theory of Mind (ToM), Mirror Neuron System (MNS), Intense World Syndrome

Autism Spectrum Disorders are a complex grouping of disorders in brain development. These disorders are diagnosed and categorized by difficulties communicating both verbally and nonverbally, troubles with social interaction, and repetitive behaviors. There are different levels of severity indicating levels of functionality; this is often described as the autism spectrum. Under recent changes with The Diagnostic and Statistical Manual of Mental Disorders, version 5 (DSM-5), classic autistic disorder, Asperger syndrome, childhood disintegrative disorder, pervasive developmental disorder not otherwise specified (PDD-NOS), and social pragmatic communication disorder are all now grouped under one diagnostic umbrella of Autism Spectrum Disorder (ASD).

Diagnostic criteria for ASD focus on persistent difficulties in the social use of communication and social interaction which can be identified by deficits in using communication in a social context, for instance, trouble with introductions or sharing information, impairments in being able to change conversations based on the context of a situation, difficulties following basic conversation rules like rephrasing when information is misunderstood, difficulties understanding non explicit language (e.g., idioms, humor, metaphors, making inferences), taking turns listening and speaking, and using or understanding both verbal and nonverbal signals to maintain a proper conversation flow.  Deficits in nonverbal communication used for social interaction like poor body language and eye contact are also examined.

Psychologists and psychiatrists will also use criteria evaluating functional limitations that exist as a result of ineffective communication, lack of social participation or difficulties in creating, maintaining, and understanding relationships such as in academic achievement and occupational performance. Limitations may also exist due to other symptoms exhibited by those affected with ASD like repetitive patterns of behavior, interests, or activities which may include repetitive motor movements, use of objects, or speech, insistence on routines and rituals, highly restricted interests that are abnormal in focus and intensity, and hyper or hypo reactivity to sensory aspects of the environment. A key factor in the diagnosis of ASD is that symptoms must be present in the early developmental period (under three years of age), although these symptoms may have been masked by learned coping mechanisms or strategies or may not become evident until social demands coax them out. The symptoms of ASD must be considered severe enough to cause significant impairment in social or occupational areas of life (American Psychiatric Association, 2013).

According to the U.S. Centers for Disease Control and Prevention (CDC), approximately one in sixty-eight children are classified as being on the autism spectrum. Currently there is no medical cure or fetal detection for autism, although research is being done on potential biological and environmental causes and influences on autism as well as on types of therapy to improve social outcomes. Resources and increasing amounts of information are also becoming available for parents to recognize the signs of developmental disorders, in the hope for early diagnoses. While there is no known solitary reason for which autism develops, there is substantial evidence as to how autism affects an individual both biologically with genetic abnormalities and anatomical changes within the brain, and also externally in social contexts due to the abnormalities in cognition and communication.

Knowing that autism is a disorder in brain development, it is imperative that biology and genetic factors be examined in the cause for autism. Through the late 1960’s many researchers, including child psychiatrist Leo Kanner, believed that environment and ,in fact, the level of warm heartedness between parents and children was a leading factor in the cause for autism, despite innate biological roots. Within the past few decades, however, substantial research has been done, examining the major role of genes in the development of ASD.  It has been established that autism is a polygenetic disorder, and the genes responsible most likely begin malfunctioning at an early developmental stage. Finding the genes responsible for autism has been a rapidly growing area of research. Many gene variations found among people with autism are relatively rare mutations involving protein-making genes that are critical in holding synapses together.  These mutations are known as copy number variations (CNVs), which are sections of DNA sequences over a hundreds of bases that are missing or duplicated. These sections may contain dozens of genes. Smoller (2008) states,

It is now clear that these rare duplications and deletions of DNA can be a cause of autism. As the evidence has accumulated, the emerging picture is one in which genes involved in the development of the brain are deleted, disrupted, or duplicated. These include genes involved in how neurons find their place in the brain, the formation of synapses, and the balance of excitatory and inhibitory connections-all fundamental players in how brain circuits get wired up (163).

According to Lende and Downey (2012), a specific etiology for autism has yet to be agreed on, however the ways in which ASD affect the brain are greatly accepted. On a neurobiological level, evidence suggests that ASD affects the cerebellum, superior temporal sulcus, medial temporal lobe, and frontal lobe. Some researchers have even tried to document brain abnormalities in terms of size. In numerous studies, autistic children’s heads and brains are larger than average, specifically in the frontal lobe which is involved in social and linguistic behaviors (Seung, 2012, p.19). Seung (2012) believes that not only is brain size a possible indicator for the development of ASD, the rate of brain growth is abnormal in autistic children. In order for this theory to be conclusively proven, developmental abnormalities and consistent neuropathology in the womb or infancy would have to be extensively examined (p.111). Researchers also have tried many times to connect behavioral aspects of ASD with specific regions of the brain, but evidence has pointed more towards the deficits in brain connectivity and the defects in brain developing genes. Lende and Downey (2012) state, “Behavioral deficits in autism may not emerge from abnormalities in particular brain regions, but rather, from decreased connectivity between them” (293).

Given that genes being deleted, duplicated, or disrupted from DNA sequences are highly involved in the process of brain development, one can expect the effects on the brain are extensive. Genetic research has also seen that many CNVs that can cause autism are also seen causing other brain development conditions like schizophrenia. A consequence to these genetic mutations in brain wiring may be dysfunction in the circuits necessary for the formation of theory of mind (ToM).

Ramachandran(2011), explains ToM as an innate, intuitive, yet sophisticated mental faculty.  He says,

It refers to your ability to attribute intelligent mental beingness to other people: to understand that your fellow humans behave the way they do because (you assume) they have thoughts, emotions, ideas, and motivations of more or less the same kind as you yourself possess. In other words, even though you cannot actually feel what it is like to be another individual, you use your theory of mind to automatically project intentions, perceptions, and beliefs into the minds of others. In so doing you are able to infer their feelings and intentions and to predict and influence their behavior (138).

Or as Coolidge and Wynn state, “Most simply, ToM is knowing that other individuals have minds and beliefs and that these beliefs may differ from one’s own beliefs” (81). 

It has been established that people on the autism spectrum lack this feature of modern social cognition. Those affected with autism have a difficult time reading emotions of others as well as perceiving thoughts in other individuals and do not have the concept of shared attention, one of the basic components of theory of mind.  Studies have been done with brain imaging on autistic subjects to find that there is altered function in theory of mind areas (Smoller, 2008). Theory of mind and shared attention are believed to be due the mirror neuron system. “It is thought that the mirror neuron system, in both humans and non-human primates, is involved in understanding the intentions of others, including grasping objects and other goals and in imitating others…” (Coolidge & Wynn, 2009, p. 201).

            The mirror neuron system (MNS) is distributed in regions of the frontal and parietal cortex. As it is already known that the frontal brain is affected by ASD, some use this information to conclude that the mirror neuron system must not be functioning properly in those with ASD. Ramachandran (2011) explains that observations of changes in brain size do not explain the characteristic symptoms of autism. He proposes that in order to explain ASD, neural structures in the brain whose functions line up with autism symptoms need to be examined. He suggests that mirror neurons are the answer

They (mirror neurons) provided the missing physiological basis for certain high-level abilities that had long been challenging for neuroscientists to explain. We were struck by the fact that it is precisely these presumed functions of mirror neurons-such as empathy, intention reading, mimicry, pretend play, and language learning-that are dysfunctional in autism (p.140).

Ramachandran suggests that it seems reasonable to assume that the main cause of autism is a dysfunctional MNS, since this particular hypothesis has the advantage of explaining so many symptoms that appear unrelated in terms of a solitary cause.

            Hickok (2014), refutes the “broken mirror” hypothesis, explaining that the MNS hypothesis is working on the assumption that since mirror neurons support the reading of emotions, understandings of intention, empathy, ToM, imitations, and language, and since all of these factors are impaired in ASD, autism can be traced back to deficits in the mirror neuron system. Hickok states that if mirror neurons don’t actually support any of these functions, then the whole broken mirror hypothesis is irrelevant. He also summarizes other arguments against the broken mirror hypothesis like that of cognitive neuroscientist, Antonia Hamilton. Hamilton argues that people with ASD don’t exhibit the behavioral profiles predicted by the broken mirror hypothesis. She performed experiments on autistic children in order to demonstrate action recognition ability. In a few studies with matching action pictures with pictures of hand postures, the autistic group outperformed the control group of no autistic individuals. Hamilton and psychologist Morton Ann Gernsbacher agree that these abilities should be impaired according to the broken mirror hypothesis. Gernsbacher says

[a number of studies] are unanimous in demonstrating that autistic individuals of all ages are perfectly able to understand the intentionality of their own actions and of other humans’ actions; there is neither ‘incapacity’ nor impairment in understanding of the intentions of actions (Hickok, 2014, p. 213).

Other arguments refute the broken mirror hypothesis on the grounds of imitation. There have been imitation tests performed with findings that autistic subjects were more than capable of associating perceive and executed actions and could perform unconscious mimicry. Hikock (2014) concludes his argument against broken mirrors by stating that the problem with autism research currently is that discussion is centered on ideas on what is wrong or lacking in autistic people, whether this mean that autistic people have no mirror neuron system, or lack theory of mind, or empathy, or way to process social information. All of these theories are founded on concepts of deficiency and dysfunction, when there should be more research on excess and hypersensitivity. He proposes that maybe those with ASD don’t live in a “socially numb world, but rather a socially intense world” (p.217).

The intense world syndrome is an interesting concept, rooted in animal models of autism currently, but inferences on hyper-responsivity leading to avoidance, is often noted in ASD individuals. Autistic individuals often become overwhelmed with surrounding sensory experiences and exhibit avoidance behaviors by covering their ears or eyes. Another possible indicator of this hypersensitivity is when autistic individuals seem to not read faces or emotion, they may be avoiding making eye contact, because processing facial emotion through the eyes is too intense (Hickok, 2014, p. 224 and Greenspan, 2004, p. 309).

Markram, et. al, (2007) also propose that the intense world syndrome could be a unifying hypothesis of autism where the primary neuropathology is excessive information processing and storing in local brain circuits which then causes hyper-functioning in the brain regions most commonly affected. This hyper-functioning may be responsible for the hyper-attention, hyper-memory, and hyper-perception seen in the autism spectrum. The spectrum can then be explained by how severely certain brain areas are affected and at which stages in development the brain might be evolving due to predisposing genes. Markram explains,

We propose that these super-charged microcircuits render aspects of the world painfully intense and aversive, and autism is therefore proposed as an Intense World Syndrome. We present recent molecular, cellular, synaptic, circuit, and behavioral evidence to support this new hypothesis and re-interpret the symptomology and pathology in the light of the proposed syndrome in which the world is aversively intense.

Yet another theory proposes that whatever the cause may be for autism, it is a disorder with deficits in self-understanding. Lende and Downey (2012), report that recent findings may suggest that people affected with ASD may not properly activate brain regions associated with self-reflection. Deficits in self-understanding may lead an autistic person to use cultural norms and scripts in order to develop a sense of self. They state

While these theories provide important insights into the core deficits of autism, by studying them in isolation we may lose sight of the autistic person’s experience…the present approach aims to provide a better understanding of the ways in which autistic persons orchestrate their unique set of strengths and weaknesses to provide meaning to themselves in the world (294).

After analyzing a significant amount of research for the topic on the development of ASD, I see that a major problem in developing a unifying theory of autism is the large number of variations of the disorder itself. I agree with multiple view points on the possible causation of autism and I relate specifically to quote above, and combine it with Hikock’s thoughts that maybe the subject of autism and even all brain development disorders should not be looked at as what is wrong or lacking, but what is different and for what reasons. I think that the diagnosis and stigma surrounding autism and the entire category of autistic spectrum disorders need to be rethought. I believe that people with ASD (especially those that are high functioning on the spectrum), given the right environment, can become more socially cognitive and can excel in certain settings. I believe there have been many assumptions made in the broken mirror hypothesis, and am wary about the idea of autistic individuals completely lacking theory of mind , since studies cannot conclusively say it is lacking due to the tasks generally used. These tasks cannot reliably establish autistic individuals from non autistic individuals. However, if the task lists were amended to provide more reliable information about a lacking theory of mind, then I would more readily accept this hypothesis. I also hope that more research will be done on the intense world theory, as it would be an interesting concept in determining causation for the development of autism, and the cognitive implications of autism as a form of cognitive evolution would be quite interesting.

 

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders. 5th ed. Arlington, VA: American Psychiatric Association.

Coolidge, F., & Wynn, T. (2009). The Rise of Homo sapiens: The Evolution of Modern Thinking. The Atrium: Wiley-Blackwell. 

Greenspan, S., & Shanker, S. (2004). The First Idea: How Symbols, Language, and Intelligence Evolved from Our Early Primate Ancestors to Modern Humans. Cambridge, Massachusetts: Da Capo Press.

Hickok, G. (2014). The Myth of Mirror Neurons: The Real Neuroscience of Communication and Cognition. New York, New York: W.W. Norton & Company.

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Modern Disease and the Balance of Cleanliness

Danielle Murri / ANTH 3370 / Final Paper -Hygiene Hypothesis

 Modern Disease and the Balance of Cleanliness

Can being too clean be dangerous? The hygiene hypothesis states that there may be a such thing as being too clean.  The hygiene hypothesis is the notion that as human society has evolved from small, early civilizations into the modern, developed environment, there has been considerably less individual exposure to microbes and pathogens, which may be causing a rise in autoimmune conditions, chronic inflammation, and several diseases. It proposes that childhood exposure to germs and certain infections or pathogens helps the immune system develop properly. Exposure to these stimuli teaches the body to differentiate harmless substances from the harmful ones that trigger certain diseases. In theory, exposure to certain germs will teach the immune system not to overreact and directly will prevent inflammation and autoimmune processes.  The hygiene hypothesis is an area of science recently increasing in research, as understanding the hygiene hypothesis and immune priming may help scientists come up with better ways to treat or prevent many illnesses.

In order to understand the basis to the many forms of the hygiene hypothesis and understand the importance of the research being done with the theory itself, one must understand the value of the immune system. According to the National Institute of Allergy and Infectious Diseases, a subsection of the U.S. Department of health and human services,” The immune system is a network of cells, tissues, and organs that work together to protect the body from infection. The human body provides an ideal environment for many microbes, such as viruses, bacteria, fungi, and parasites, and the immune system prevents and limits their entry and growth to maintain optimal health.“ This network of cells, tissues, and organs is precious to the human body.  “The immune system provides protection against a variety of external (infectious disease) and internal threats (cancers), but has sizeable costs associated with maintenance and activation. Furthermore there are consequences when immune processes are misdirected and contribute to allergy, asthma, and autoimmune disease” (Stinson, Bogin, & O’Rourke, 2012, pg. 334).  The way that the immune system develops is directly correlated to the way an individual’s health will be throughout their lives.

The immune system is meant to detect intruders called antigens, which are substances (usually proteins) that live on the cells of viruses, bacteria, fungi, or parasites. Antigens may also be present on toxins, drugs, and chemicals. Once these antigens have been detected, white blood cells arrive on scene. A type of white blood cell that is critical for the immune response is the lymphocyte. Type B lymphocytes turn into cells producing antibodies, which will attach to specific antigens, making an easier target for other immune response cells to attack. Type T lymphocytes attack the antigens directly and release cytokines which help control the entire immune response. Both B and T cells will multiply once they have been triggered, and will help the immune system create a “memory” so that the body can be immunized in a way from whatever antigen was introduced. For example, those who were exposed to and developed chickenpox will be immunized from it in the future due to the white blood cell immune response memory. The immune response can overreact or lack in response causing immune system disorders or allergies. Inefficient immune responses allow for the development of diseases, whereas overactive immune responses can lead to antibodies attacking the body’s own tissues or autoimmune diseases. 

The hygiene hypothesis began in the late 1980’s when scientists were observing that older siblings in families tended to have lower incidences of hay fever. These findings were believed to be consistent with a protective influence of childhood infection that may become lost in the world of modern hygiene. One of the scientists leading these investigations was epidemiologist David P. Strachan (also known as D.P. Strachan). David P. Strachan’s original formulation of the hygiene hypothesis was based on the idea that smaller families provided insufficient microbial exposure; partly because of less person-to-person spread of microbes, but also due to higher standards of home and personal cleanliness. He examined urban living situations and farming families. Strachan's and other studies led to the view that microorganisms and macro-organisms from the environment whether it be soil, animals, or feces play a critical role in immunoregulation and in preventing inappropriate immune responses to allergens and the body itself. It was due to this portion of his research that he named it the “hygiene hypothesis”. D.P Strachan proposed that there is such a thing as too much cleanliness, and that a lack of early exposure to germs and biological stimuli that used to be experienced frequently causes a weakened immune system and response, and therefore causes allergies and similar conditions like hay fever and asthma. In developing nations and previous eras, families typically were much larger than they are today with more than one or two children. When there are more children in a family, the older children tend to expose the younger ones to more germs and the children end up developing stronger immune systems as they have been exposed to stimuli early on in life.  This could be due to the fact that children are exposed to germs at school, their friends homes, and when they are physically active outdoors. They then bring these microbes home with them, creating an environment of exposure for their entire families, but especially their siblings with whom they will be around most of the time. This concept of exposure has also been used to research children who attend daycare at early ages and their development of allergies, asthma, and autoimmune conditions. According to many studies, daycare children tend to develop fewer allergies than those who grow up in a more sterile, controlled environment.

 Not only did Strachan research health and hygiene among families, he also researched the ‘hygiene revolution’ that began in the early nineteenth century when the health system began to focus more on daily hygiene, which then led to the decrease in medications and more drastic medical interventions and treatments.  The concept of personal hygiene also led to many public health changes like the sanitation of water, garbage collections, and the separation of waste areas from living areas.  Although these public health changes reduced the prevalence of life threatening diseases like cholera and typhoid fever, it also began depriving people from their “old friends”, the microbes that used to inhabit the same environments. The original formulation of this hypothesis is attributed to D.P. Strachan, but has evolved into the “old friends hypothesis” (also called the biome depletion theory) proposed by Graham Rook in 2003.  This new version of the hypothesis provides a rational link between multiple inflammatory disorders and microbial exposure. The original hypothesis only examined reduced microbial exposure in correlation with allergic diseases like asthma, hay fever, and seasonal allergies. The newer proposals apply to a much broader range of chronic inflammatory illnesses such as diabetes, depression, anxiety, and autoimmune disorders like multiple sclerosis. Evidence may also hint that contribute levels of microbe exposure trigger autism and similar disorders. Graham Rook also looks at broader implications of inflammation caused by improper immune responses. Chronic inflammation can trigger the growth of cancer cells, and therefore some forms of cancer could also be linked to his version of the hygiene hypothesis.  

The newer proposals of the hygiene hypothesis like the “old friends” theory, argue that vital exposures are to not common childhood infections or recently evolving pathogens as the original hypothesis suggested, but rather microbes that were present in hunter-gatherer times when the immune system was just beginning to evolve. These microbes evolved with the human race, and eventually people became dependent on these microbes in order for their immune systems to develop and function properly. This view of the hygiene hypothesis is also known as the Darwinian approach.

            Not much research has been made public on the newer versions of the hygiene hypothesis, however quite a bit of research has been conducted on the original version focusing on the necessity of microbe exposure at a young age.

Although it is a hard leap from mice to humans in a study, researchers at Brigham and Women’s Hospital in Boston have been comparing mice living in ‘normal’ environments with others who have been kept in germ free environments. The germ free mice were found to have high levels of special white blood cells (iNKT) in their lungs and intestines indicating levels of inflammation. These types of cells and inflammation are common in autoimmune diseases as well as asthma, (in the lungs), and ulcerative colitis (intestines).  The germ free mice proved to be much more susceptible to disease than the mice living in an environment with natural microbes present. Even when the germ free mice were introduced to a normal environment with bacteria later in their lives, they still had higher levels of inflammatory cells and diseased lungs and intestines (“Early Bacteria Exposure Important for Building Immunity, Study Says”). This evidence backs up the concept of “immune priming”, and that there must be a window at a very early age when microbes must be present in order to create a healthy, strong immune system and response.

            Numerous studies are being conducted on infants to try to determine when this “window of opportunity” is as far as the best timing to expose individuals to pathogens and microbes.  These studies also provide different avenues of microbe exposure, specifically examining the impact of household pets and siblings on infant microbiota in their gut (Azad, et. al, 2013).

            Although to date, the hygiene hypothesis is still unproven and therefore a hypothesis still, there is substantial data being gathered to look at the implications of such a concept. The hypothesis has been used to look at whether or not vaccinations are beneficial, as well as whether hyper-cleanliness at a young age may trigger life long chronic conditions or diseases. Recently, the field of medicine has been using the concept of the hygiene hypothesis to try alternative treatment measures such as probiotics, helminthic therapy, and oral capsilated microbiota transplantation (frozen fecal pills). The idea behind all of these treatment or preventative measures is to reintroduce microbiota to the body in order to heal, reverse, or prevent illnesses. They are used to trigger immune responses, and the hope is that if the immune response can be triggered appropriately, the immune systems may begin to positively adapt to the reintroduction of microbes and become strong. Although there are no health treatments for disease directly responding to changes in hygiene, many lifestyle changes can increase individual and familial exposure to microbes. There is a healthy balance as with anything, and risks associated with allowing more microbe or pathogen exposure. Some simple lifestyle changes could be to have more physical interaction with others (especially as a child), to breastfeed babies, have more natural childbirths, and encourage children to play and interact with non sterile natural outdoor environments. There is still much to be researched and tested about the hygiene hypothesis before it can become scientific fact, however, the concept has already begun to revolutionize the way that people think and react with bacteria in their environments and has also changed the focus of medicine in regards to some autoimmune and allergic conditions.

References

Azad, M., Konya, T., Maughan, H., Guttman, D., Field, C., Sears, M., ... Kozyrskyj, A. (2013, January 1). Infant gut microbiota and the hygiene hypothesis of allergic disease: Impact of household pets and siblings on microbiota composition and diversity. Retrieved December 6, 2014, from http://www.aacijournal.com/content/9/1/15

Bloomfield, S., Stanwell-Smith, R., Crevel, R., & Pickup, J. (5, September 25). Summary. Retrieved December 11, 2014, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448690/

Human Energetics. (2012). In S. Stinson, B. Bogin, & D. O'Rourke (Eds.), Human biology: An evolutionary and biocultural perspective. New York: Wiley.

Immune response: MedlinePlus Medical Encyclopedia. (2014, May 1). Retrieved December 1, 2014, from http://www.nlm.nih.gov/medlineplus/ency/article/000821.htm

Mirsky, S. (2011, April 1). Can It Be Bad to Be Too Clean?: The Hygiene Hypothesis. Retrieved December 1, 2014, from http://www.scientificamerican.com/podcast/episode/can-it-be-bad-to-be-too-clean-the-h-11-04-06/

Rook, G. (2012, April 1). A Darwinian View of the Hygiene or “Old Friends” Hypothesis. Retrieved December 2, 2014, from http://www.microbemagazine.org/index.php?option=com_content&view=article&id=4700:a-darwinian-view-of-the-hygiene-or-old-friends-hypothesis&catid=950&Itemid=1301

Welsh, J. (2012, March 22). Early Bacteria Exposure Important for Building Immunity, Study Says. Retrieved December 7, 2014, from http://www.livescience.com/36217-early-bacterial-exposure-immunity.html