Toxic Stress: Linking Historical Trauma to the Contemporary Health of American Indians and Alaska Natives

Item Type text; Electronic Dissertation

Authors Begay, Tommy K., Jr.

Publisher The University of Arizona.

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TOXIC STRESS: LINKING HISTORICAL TRAUMA TO THE CONTEMPORARY HEALTH OF AMERICAN INDIANS AND ALASKA NATIVES

Tommy K. Begay, Jr.

A Dissertation Submitted to the Faculty of the

DEPARTMENT OF TEACHING, LEARNING & SOCIOCULTURAL STUDIES

In Partial Fulfillment of the Requirements For the Degree of

DOCTOR OF PHILOSOPHY

WITH A MAJOR IN LANGUAGE, READING AND CULTURE

In the Graduate College

THE UNIVERSITY OF ARIZONA

2012

THE UNIVERSITY OF ARIZONA

GRADUATE COLLEGE

As members of the Dissertation Committee, we certify that we have read the dissertation prepared by Tommy K. Begay, Jr. entitled TOXIC STRESS: LINKING HISTORICAL TRAUMA TO THE CONTEMPORARY HEALTH OF AMERICAN INDIANS AND ALASKA NATIVES and recommend that it be accepted as fulfilling the dissertation requirement for the

Degree of Doctor of Philosophy

______Date: _April 4, 2012_ Richard Ruiz, Ph.D.

______Date: _April 4, 2012_ Luis C. Moll, Ph.D.

______Date: _April 4, 2012_ T. Lee Ryan, Ph.D.

Final approval and acceptance of this dissertation is contingent upon the candidate’s submission of the final copies of the dissertation to the Graduate College.

I hereby certify that I have read this dissertation prepared under my direction and recommend that it be accepted as fulfilling the dissertation requirement.

______Date: _April 4, 2012_ Dissertation Director: Richard Ruiz, Ph.D.

STATEMENT BY AUTHOR

This dissertation has been submitted in partial fulfillment of requirements for an advanced degree at the University of Arizona and is deposited in the University Library to be made available to borrowers under rules of the Library.

Brief quotations from this dissertation are allowable without special permission, provided that accurate acknowledgment of source is made. Requests for permission for extended quotation from or reproduction of this manuscript in whole or in part may be granted by the copyright holder.

SIGNED: Tommy K. Begay, Jr.

ACKNOWLEDGEMENTS

Completing a dissertation is a culmination of mental and physical effort. It is the total sum of the collaboration of others who assisted along the way in providing financial, physical, emotional, intellectual and spiritual support.

With immense gratitude, I would like to acknowledge the contributions made by the following individuals in assisting me with the completion of my Ph.D. Program:

Dr. Richard Ruiz, my dissertation advisor, colleague and friend. Throughout the years, you have provided academic guidance and assisted me with finding financial support. Many times, you provided that “fire” of light, warmth, and intellectual challenge necessary to push me forward.

Dr. Luis Moll, for your assistance with providing a path toward an understanding of the importance of considering “culture” in processes centered upon learning and healing. Since my initial discovery of Aleksandr Romanovich Luria late one night in medical library almost two decades ago, you have guided me in my understanding of cultural- historical psychology. This has been the basis of my understanding of “development” and the practical applications of neuropsychology.

Dr. Lee Ryan, for your generosity in allowing me to sit-in on several of your neuroscience classes, which eventually became the basis for the ideas presented in this dissertation. Thank you also for offering your expertise and support on my Ph.D. committee. Since those early days, I have wrestled with a better understanding of the intricate balance of culture and biology (neurophysiology and physiology) in trying to gain a better understanding of what constitutes behavior.

LRC colleagues and dear friends: Dr. Patty Anders, Dr. Norma Gonzalez, Dr. Mary Carol Combs, and Maria Fierro, who has been like - as the Navajo people would say, Shi’ma’yazhi - an “aunt” to me. Your “good enegy,” guidance, and support have been insurmountable.

My family at the Native American Research and Training Center: Dr. Jennie Joe, for your inspiration and your commitment to serving Native American people, Dr. Rob Young, Dr. Jenny Chong, Dr. Jeanette Hassin, Lisa Clore, Pandora Hughes and Mike Rothery.

I would also like to acknowledge Dr. Maria Teresa Velez, for her encouragement and support throughout the years, and Dr. Melissa Veto, for re-kindling that internal “fire” deep down inside with support at many levels, allowing me to finish my Ph.D. Program.

DEDICATION

From a place in my heart of Hózhó - harmony, balance and beauty – I dedicate this dissertation to my family.

My children: Nizhoni C. Begay, Todd M. Begay, Kyle S. Begay, Tommy K. Begay, III, Marlana D. Laughter, and my granddaughter, Emelie A. Begay. My sister: Theresa K. Begay, and her family. My brother: Bernard B. Begay, and his family. My father: Tommy K. Begay, Sr., and my stepmother, Elsie Nakai.

No matter where I go, you are always there with me.

I would also like to dedicate this work to the memory of my mother, Bernice B. Begay, whose care and compassion for children, especially her own grandchildren, became the foundation for my interest and pursuit for understanding the powerful influence of the human spirit – that intricate interaction of human development, love, hope and spirituality.

TABLE OF CONTENTS

ABSTRACT ...... 9 CHAPTER 1 INTRODUCTION ...... 10 Research Question ...... 12 Proposition ...... 12 Significance of Study ...... 14 Definitions and Explanation of Terms ...... 15 Research Limitations ...... 15 CHAPTER 2 LITERATURE REVIEW ...... 17 CHAPTER 3 METHODOLOGY ...... 24 CHAPTER 4 HISTORICAL TRAUMA ...... 29 Defining Historical Trauma ...... 30 The Impact of Historical Trauma ...... 32 Impact on the Individual ...... 33 Impact on the Family ...... 35 Impact on the Community ...... 37 CHAPTER 5 LINKING HISTORICAL TRAUMA TO CONTEMPORARY HEALTH: A PROPOSITION ...... 40 Introduction ...... 40 Theoretical Framework ...... 42 Proposition ...... 42 CHAPTER 6 PHYLOGENY, CULTURE AND ONTOGENY ...... 47 Cultural Mediation ...... 50 Historical Development ...... 51 Phylogeny and Human Development ...... 54 Culture and Hominization ...... 56

Evolution of Language and Cognition ...... 57 Culture and Biology in Ontogeny ...... 59 Phylogenetic Contributions ...... 59 Cultural Contributions ...... 60 CHAPTER 7 THE NERVOUS SYSTEM AND THE HYPOTHALAMIC-PITUITARY- ADRENAL AXIS ...... 63 Central Nervous System ...... 63 Peripheral Nervous System ...... 64 Stress and the Sympathetic Nervous System ...... 66 The Hypothalamic-pituitary-adrenal axis and stress ...... 66 The Stress Response System ...... 67 Stressors and the HPA axis ...... 69 Mental and Emotional Interpretation ...... 69 Sleep Disorders ...... 70 Metabolic/Glycemic Dysregulation ...... 71 Inflammation ...... 71 Trauma and Toxic Stress ...... 72 Consequences of Hypothalamic-pituitary-adrenal Axis Dysregulation ...... 74 Hypercortisolism ...... 74 Hypocortisolism ...... 76 Health Conditions Related to Hypothalamic-pituitary-adrenal axis ...... 78 Increased Activity of the HPA-axis ...... 79 Decreased Activity of the HPA-axis ...... 80 CHAPTER 8 KEY CONSTITUENTS OF CHILDHOOD DEVELOPMENT ...... 82 Emotional Development ...... 82 Early Experiences and Brain Development ...... 87

Relationship Development ...... 96 CHAPTER 9 THE IMPACT OF TRAUMA ...... 103 Initial Impact of Historical Trauma ...... 103 Post-traumatic Stress Disorder ...... 103 Maternal Depression ...... 106 Making the Connection from Historical Trauma to Toxic Stress ...... 112 Types of Stress: Toxic, Tolerable and Positive ...... 112 Impact of Fear and Anxiety ...... 121 Impact of Relationships and Emotional Development ...... 127 Epigenetic Consequences ...... 129 Learned Fear ...... 133 Impacts to Society ...... 140 Academic Achievement and Executive Function ...... 140 Chronic Diseases ...... 149 Substance Abuse ...... 150 Intergenerational Transmission of Dysfunctional Behaviors ...... 154 CHAPTER 10 SUMMARY ...... 158 CHAPTER 11 RECOMMENDATIONS ...... 166 REFERENCES ...... 168

ABSTRACT

The legacy of historical trauma continues to plague Indigenous populations throughout the world. This theoretical dissertation describes how biology (neurodevelopment, neurobiology and endocrinology) and culture (inter-generationally learned behaviors) are intricately intertwined in the development of dysfunctional coping behaviors that contribute to stress-related chronic diseases (heart disease, obesity, type II diabetes mellitus, depression, neurodegenerative disorders and memory impairment) in some individuals. The primary impact of the many episodes of historically traumatic genocide has been post-traumatic stress disorder (PTSD) and the onset of dysregulation of the hypothalamic-pituitary-adrenal axis (HPA-axis). PTSD has had a profound impact on relationships and behaviors, while dysregulation of the HPA-axis is associated with pathophysiology.

It is well documented that historical trauma has caused a cultural disconnect from traditional wellness and healing practices. Despite incredible resiliency, the result of this legacy has been a genesis of intergenerational, dysfunctional, coping strategies that have become subtly engrained in a viscous cycle of self-perpetuating, self-inflicting, dysfunctional behaviors that have been carried forward into the next generation as “toxic stress” - in the form of childhood abuse, domestic violence, interpersonal violence, and substance abuse. With time, the association to the initial traumatic assault erodes, leaving behind, collectively, a fragmented society that, in many places, has become the basis for a “cultural crisis”.

The approach presented in this dissertation is founded upon: 1) cultural acquisition theories that describe how existing cultural constructs and traditions are internalized by children and repeated throughout a life-time into the next generation; and 2) understanding the interaction of the autonomic nervous system (specifically, the HPA- axis and its activation by stress) and the neocortex , the basis for higher psychological processes associated with learning and cultural acquisition.

This dissertation offers an explanation for the continued impact of historically traumatic events on the contemporary health and wellness of American Indian and Alaska Native people. It is hoped that this approach leads to specific intervention and prevention measures that are culturally relevant in addressing pathophysiology, cognitive-behavioral issues and the collective cultural changes that have ensued as a result of historical trauma.

CHAPTER 1

INTRODUCTION

For generations, American Indian and Alaska Native (AIAN) people have experienced a series of traumatic, genocidal assaults that have left detrimental consequences on communities, families and individuals. Scholarship exploring historical trauma draws from the work of Maria Yellow Hose Brave Heart and her colleagues at the Takini

Network (Brave Heart, 1999a, 1999b, 2000; Brave Heart & DeBruyn, 1998). This preliminary work has made significant contributions in understanding the impact of the many genocidal acts inflicted upon AIAN communities. However, many of the concepts involved still require further clarification and development.

Historical trauma theory describes a collective complex trauma inflicted on a group of people who share a specific group identity or affiliation – ethnicity, nationality and religious affiliation. It is the legacy of numerous traumatic events that an AIAN community experiences over generations and encompasses the psychological and social responses to these events (Brave Heart, 1999a, 1999b, 2000; Brave Heart & DeBruyn,

1998). These historical events have been destructive at a physical and emotional level and are generally experienced by many people in AIAN communities (Brave Heart, 1999a,

1999b, 2000; Brave Heart & DeBruyn, 1998). It is often described as the cumulative

11 emotional and psychological wounding occurring over a lifespan and across generations, emanating from massive group trauma experiences. Historical unresolved grief is the grief that accompanies trauma, and is often associated with self-destructive behavior, suicidal thoughts and gestures, depression, anxiety, low self-esteem, anger, and difficulty recognizing and expressing emotions (Brave Heart, 1995, 1998, 1999, 2000).

An extensive literature documents these assaults, which have included community massacres, genocidal policies, pandemics from the introduction of new diseases, forced relocation, forced removal of children through Indian boarding school policies and the prohibition of spiritual and cultural practices (Stannard, 1992; Thornton, 1987). Together these events amount to a history of ethnic and cultural genocide (Smith, 2003). In addition, contemporary AIAN communities suffer from some of the highest rates of lifetime traumatic events, including interpersonal violence (Greenfield & Smith, 1999), child abuse and neglect (T.A. Cross, Earle, & Simmons, 2000), poor health (Walters,

Simoni, & Evans-Campbell, 2002), and an ongoing barrage of negative stereotypes that undermine AIAN society, identity and self-esteem.

General trauma literature (van der Kolk, McFarlane and Weisaeth, 1996) and Jewish

Holocaust literature (Yehuda, 1999; Fogelman, 1998, 1991) support the theoretical constructs underpinning the concept of historical trauma, specifically the

12 intergenerational transfer. More work is necessary specific to AINA populations and precise to the development of a culturally based trauma theory and interventions (Manson et al, 1996; Robin, Chester, and Goldman, 1996). In addition, more work is necessary for a plausible theory to describe the continued transfer of trauma across generations in order to develop prevention and intervention strategies that will be effective with this population.

Research Question

The purpose for this theoretical dissertation is to present a conceptual framework that provides insight into how historically traumatic events (e.g., acts of genocide) which happened long ago, spanning decades and generations, continues to have an impact on the contemporary health and wellness of some Native American and Alaska Native individuals.

Proposition

As a result of the many episodes of community massacres, genocidal policies, forced relocation, forced removal and abuses with in Indian boarding schools, and the prohibition of spiritual and cultural practices, generations of AIAN people continue to

13 carry forth the legacy of historical trauma. In more contemporary times, these historical traumatic events have transcended into a cycle of intergenerational, self-perpetuating, self-inflicting, dysfunctional behaviors that threaten the health and wellness of a society at an individual, familial, community and cultural level.

To explain this phenomenon, I hypothesize the following:

1. The impact of historical trauma manifests as the intergenerational expression of

toxic stress .

2. It is the impact of toxic stress that continues to move through generations,

affecting neurophysiology (as symptoms of posttraumatic stress disorder and the

dysfunctional regulation of the hypothalamic-pituitary-adrenal axis),

neurodevelopment and associated biological systems necessary for homeostasis

(e.g., the endocrine system).

3. For survival, the impact of stress on the nervous system (especially the autonomic

nervous system) and associated psychological responses are coupled to “higher

psychological processes,” cultural mediation and learning.

4. Because of the psychological and emotional impact of trauma, coping strategies

are sought to “mediate” the internal emotional and psychological conflict and pain

being experienced. As a result of the cultural disconnect from historically-derived

and culturally-appropriated traditional ways of wellness and healing, other foreign

modes, methods and substances are utilized. These new ways are often associated

with self-medication, physical force and the use of violence (e.g., what was

learned from the boarding school experience and implicated on to the family

structure).

5. Eventually, these coping strategies become subtly infused into daily, practical

routines becoming the basis for handling stress and conflict. For some, creating a

vicious re-cycling of stress (intra- and inter-personally) that has biological and

social consequences in the form of chronic diseases, substance abuse, violence

and impaired cognitive functioning.

Significance of Study

This study presents a new perspective on a formidably destructive legacy that has affected the health and wellness of American Indian and Alaska Native people for successive generations. It is a perspective that puts forth an explanation for the impact of many historically traumatic episodes on the contemporary health, wellness and culture of

AIAN people. Further scholarship is necessary to gain better insight into the contemporary issues associated with historical trauma. These findings may then be

15 applied toward the design of more specific intervention and prevention strategies that are more culturally appropriate. For far too long, an explanation for the direct process of the impact of historical trauma has remained abstract and disjointed.

Definitions and Explanation of Terms

American Indian/Alaska Native (AIAN). The official terminology set by the U.S. federal government’s Office of Management and Budget dictates that American Indian/Alaska

Native be utilized to describe the indigenous groups described in this dissertation (Robin

2002). Demographic data collected on this population is classified in such manner. When appropriate, specific Regions and Tribes are identified. However, it is common practice to also use the terms American Indian, Indian, and Native American interchangeably with

AIAN.

Research Limitations

Much of the research cited in this study relies on the work done on other racial and ethnic groups. American Indian, Alaska Native, and Native American health and social service research is quite limited. Future work in this area should be specific to this population.

Also, there is currently no support for strict biological, social or cultural determinism.

Researchers and scientists may agree on the theoretical expectations, given known factors including the general responses of environmental stimuli on physiological systems.

However, each situation is unique, offering context-specific stuations and environmental factors that affect individual, specific courses of action. The work described in this study is a culmination of what has been previously put forth in regard to the impact of historical trauma and “trauma” in general. Since the impact of trauma and stress affects human development, an extensive investigation is made into the outcomes of Adverse Childhood

Experiences.

Finally, after months of developing the conceptual framework for the processes that describe how historical trauma continues to impact the contemporary health of AIAN people, it was a challenge to superimpose this multidimensional problem into a linear process, eventually becoming words, sentences and pages on a computer screen. What is presented in this dissertation is an attempt at communicate the interaction and consequences of those interactions.

CHAPTER 2

LITERATURE REVIEW

This dissertation begins with a review of the scholarship done in the area of Historical

Trauma, the basis for a proposition put forth in this dissertation that provides for an objective, theoretical, explanation for the continuous, intergenerational impact to the contemporary health and wellness of American Indian and Alaska Natives.

Scholarship exploring historical trauma in AIAN communities draws from the seminal work of Maria Yellow Horse Brave Heart (Brave Heart, 1999a, 1999b, 2000; Brave Heart

& DeBruyn, 1998). Historical trauma is conceptualized as a collective trauma inflicted on a group of people who share a specific group identity, affiliation, ethnicity, nationality or religious association. It is the legacy of numerous traumatic assaults over generations and encompassing the psychological and social responses to these events (Brave Heart, 1999a,

1999b, 2000; Brave Heart & DeBruyn, 1998).

In order to construct the proposition that historical trauma is an antecedent to intergenerational transmission of toxic stress, the relationship between phylogeny and cultural history to shape ontogeny must be put forth. Far too often, culture has taken a subservient role to biological processes, when in essence, it is culture that is partly

18 responsible for stimulating the growth and change to biological systems. From the cultural-historical approach to Cultural Psychology, human psychological processes can be understood as the outcome of four genetic domains: phylogeny, cultural history, ontogeny and microgenesis (Vygotsky, 1977; Vygotsky & Luria, 1930/1993; Wertsch,

1985). More specifically, these processes emerge from culturally mediated, historically developed, practical activity (Leontiev, 1981; Luria, 1979; Vygotsky, 1987).

Throughout the course of development, it has been this interaction that allowed for the development of the brain (Plotkin, 2001), providing modern human beings with the capability to utilize “mind” to potentially make sense of the world around them

(Vygotsky, 1977). This process has evolved into what is referred to as higher psychological processes, a function of the neocortex of the nervous system (Plotkin,

2001). It is through this process that mediating artifacts are developed to negotiate and manipulate the physical and social environment.

Yet at the same time, it is through utilizing mediating artifacts that stimulates reciprocal relationship between neurogenesis, neurodevelopment and cultural development.

Neurogenesis is dependent upon the external stimulation of the physical, social and cultural environment. At the same time, it is the adult person that has the potential to create changes to the environment through cultural mediation, seen as tool, sign and

19 symbol use (Foley & Lahr, 2003; Lewin & Foley, 2004; Tomasello, 1999). In an abstract sense, this is the basis for technological advancement.

In regard to toxic stress and neurophysiology, the “fight or flight” defense mechanism of the autonomic nervous system physiologically prepares the body to either get ready to fight or to be ready to flee. The key component of the “stress system” is the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system (Vining &

McGinley, 1983). In environments of real or perceived threats, the stress response system becomes over-activated, resulting in the continuous pushing of the physiological stress mechanism to the point of dysfunction. The hypothalamic-pituitary-adrenal axis gets cued by sensory stimulation of environmental stress and through a cascade of events and hormones, prepares the body for action. In an environment of chronic stress, an overworked, dysfunctional stress system becomes over-stimulated and over-worked, eventually causing chronic disease (Vining & McGinley, 1983). It is analogous to running an engine until it overheats or causes some other mechanical problem.

Because of the unique capability of neurodevelopment and the plasticity of rapidly changing and growing neurons, children are more susceptible to environmental change.

Sometimes, the environments created by adults may have detrimental impacts on the development of children, especially in regard to the impact of toxic stress on

20 neurodevelopment. In order to thoroughly appreciate the impact of toxic stress, key constituents of normal childhood are addressed. The areas of development include: emotional development, early experiences and development and relationship development.

Children rapidly develop an ability to express different emotions and feelings (Saarni,

Mumme, & Campos, 1998; Thompson, Lagatta, 2006 and Thompson, 2004).

Environmental conditions also are important to childhood development. Specific experiences affect certain brain circuits during specific stages of development (Knudsen,

2004; Hess 1973). Just as in the construction of a house, certain parts of the formative structure of the brain need to happen in a sequence that supports the subsequent development. If a stage is stagnant because of neglect or adverse childhood experiences, the brain may not come together in a way that supports subsequent cognitive function.

Relationship development also lend to the childhood development of the brain (Berscheid

& Reis, 1998; Collins and Laursen, 1999; Dunn, 1993). The relationships of young children affect all aspects of their development – intellectual, social, emotional, physical, behavioral and moral.

Historical trauma has augmented the relationship between the mother and child. It is my contention that Post-traumatic Stress Disorder and subsequent maternal depression

21 indirectly changed familial patterns and have gradually been integrated into the culture

(Brave Heart, 1999a, 1998; Morisette, in Brave Heart, 1999a). This in turn, has formed the basis for the intergenerational transmission of toxic stress (NSCDC, 2007). Toxic stress causes morphological changes to the brain and behavioral changes that impact emotional development and the ability to form relationships (Loman & Gunnar, 2010).

Research shows that early exposure to circumstances that produce persistent fear and chronic anxiety can have lifelong consequences to the development of the brain. In addition, environmental influences can have an effect of the expression of genes.

The epigenome (Waddington, 1942) allows for the expression of certain genes.

Nutritional status, exposure to toxins and drugs and adverse childhood experiences may be sources of modification of the epigenome (Bernstein, Meissner, & Lander, 2007).

Research in both animals and humans show that epigenetic changes that occur in the fetus during pregnancy can be passed on to later generations, affecting the health and welfare of children, grandchildren and their descendents (Anway, Cupp, Uzumcu, & Skinner,

2005; Champagne, 2010).

Associated with toxic stress, fear conditioning can lead to the development of anxiety disorders. This type of learning influences the processing and storage of memories

(Sanchez, Ladd, & Plotsky, 2001; Roosendaal, Barsegyan, & Lee, 2008). Emotional

22 memories are re-lived by individuals who have experienced traumatic events, subsequently activating the release of cortisol.

Ultimately, there are four major areas that are impacted by toxic stress resulting from the initial historically traumatic event: cognitive development, the potential for chronic diseases, substance abuse and the intergenerational transmission of trauma and abuse.

Executive function skills are considered the basis for working memory, inhibitory control, cognitive and mental flexibility (Diamond & Taylor, 1996; Greenberg, Riggs, Blair, 2007;

Rothbart, Posner & Kieras, 2006), which in turn, become the basis for academic achievement (Barkley, 2001 & Blair, 2002). Overstimulation of the HPA-axis as a result of toxic stress has lead to detrimental health risks, deficits in the ability to learn and substance abuse (IHS, 2003). Some of the leading causes of death among AIAN people are heart disease, cancer, unintentional injuries, type II diabetes mellitus, and stroke. This population also has a high prevalence and risk factors for mental health problems, suicide, obesity, substance abuse, teen pregnancy, liver disease and hepatitis.

There is a growing body of evidence that indicates that early traumatic experiences are associated with health problems throughout a lifespan (Shonkoff, Boyce, & McEwen,

2009). This research shows an association between adverse childhood experiences and substance abuse, intimate partner violence, anxiety, depression, suicide, ischemic heart

23 disease, smoking and obesity (Fellitti et al., 1998; Mercy & Saul, 2009; Repetti, Taylor &

Seeman, 2002). Traumatic experiences endured during childhood influence the well- being of their offspring (Yhuda & Bierer, 2008).

CHAPTER 3

METHODOLOGY

The purpose for this theoretical dissertation is to present a conceptual frame that provides some insight into how historically traumatic events continue to have an impact on the contemporary health and wellness of some Native American and Alaska Native individuals.

The literature documents traumatic assaults, which have include community massacres, genocidal policies, pandemics from the introduction of new diseases, forced relocation, forced removal of children through Indian boarding school policies and the prohibition of spiritual and cultural practices (Stannard, 1992; Thornton, 1987). Together these events amount to a history of ethnic and cultural genocide (Smith, 2003). In addition, contemporary AIAN communities suffer from some of the highest rates of lifetime traumatic events, including interpersonal violence (Greenfield & Smith, 1999), child abuse and neglect (T.A. Cross, Earle, & Simmons, 2000), poor health (Walters, Simoni,

& Evans-Campbell, 2002), and an ongoing barrage of negative stereotypes that undermine AIAN society, identity and self-esteem.

Very little has been documented to explain how historical trauma continues to affect pathophysiology at the individual, familial, community and societal levels. Of greater significance, no explanation has been offered for the intergenerational characteristics associated with historical trauma. The reason may rest with the multifaceted nature of this issue, involving physiological processes and resulting from culturally situated, specific behaviors. The outcome of these behaviors appear to be related to a breakdown of traditional culture and values, high rates of alcoholism, high rates of physical illness

(Yellow Horse-Davis, 1998).

As a student of the cultural-historical approach to Cultural Psychology, it is important to identify a general “developmental” scheme of contemporary issues facing AIAN people and their communities. To help guide this process, utilizing the literature and other sources of information, the following questions were asked: Why is this issue important?

What has been documented in the literature? What are the current outcomes? What are the epidemiological statistics for this group? What are the tentative explanations for the development of these outcomes? This information was then “sketched” onto a blank piece of paper (big piece of butcher paper, in my case) in a qausi-venn diagramatic fashion for causal analysis. I looked for gaps between what was documented and the described as “outcomes.” One immediate benefit from this approach is the identification of clear, viable research questions.

Potential explanations are put forth to explain outcomes - what I initially referred to as a

“hypothesis.” I later changed the term to “proposition” since the term “hypothesis” was more affiliated with doing some type of “experiment,” and did not apply to my inquiry.

My effort, at this point, was only to offer an objective explanation for the contemporary outcomes resulting from historical trauma. The term “proposition” seemed more appropriate for my use.

As a result of preparing a schematic diagram, and performing a general analysis, it was apparent that physiological mechanisms were being impacted intergenerationally as a result of the discontinuation of practices associated with self-identity, wellness and healing. As presented in Chapter 4 of this dissertation, spiritual and cultural practices were forcefully discontinued and prohited. It was my speculation that right around the same time of the forced removal of spiritual and cultural practices, other more foreign practices of behavior replaced the traditional ways. From my initial analysis, these areas required further analysis.

The schematic diagram identified areas for the literature review. It is difficult to identify areas of inquiry without performing this causal analysis. In the case of performing the research for this dissertation, processes associated with biological systems

(neurophysiology and physiological processes) were coupled with cultural systems and behavior (i.e., learned cultural behaviors) that, subtly and informally, were acquired by children born into families with specific traditions and cultural practices. For this dissertation, the areas of inquiry that required further analysis through an in-depth review of the literature, included: historical trauma, sociocultural theory, cultural-historical psychology, Cultural Psychology, toxic stress and associated brain neurochemistry/neurophysiology, child development theories, cognitive development theories and chronic diseases that are associated with dysregulation of stress hormones.

From the literature review, it became apparent that a cycle consisting of 1) neurophysiological responses and 2) learned “dysfunctional coping strategies” (including substance abuse, interpersonal violence, and domestic violence) were associated with the creation of “toxic stress.” This is especially significant in families with young children.

From the literature, it became apparent that toxic stress set off a cascade of involuntary, physiological responses associated with the autonomic nervous system. Over time, results in the hyper-stimulation of the body’s stress response mechanism, eventually leading to the dysregulation of the stress response system and potentially resulting in specific stress- related chronic diseases, impacting the immune system, associated with substance abuse, and deficits in cognitive development, learning and academic achievement. Health outcomes for AIAN people that survived historically traumatic events were similar to the

28 health outcomes for adults that were survivors of Adverse Childhood Experiences

(childhood abuse, sexual abuse, and neglect), which has an extensive amount of literature.

An in-depth study specific to the AIAN population is necessary to confirm the validity of the proposition presented in this dissertation. The eventual goal is to identify specific intervention and prevention strategies to stem the tide of chronic diseases, substance abuse, and low academic achievement with this population. This will require a closer analysis of the interaction between culture and biology. In regard to historical trauma and toxic stress, in the past, these two areas have been dealt with separately, and not viewed as belonging to an integrated system associated with future health and wellness.

CHAPTER 4

HISTORICAL TRAUMA

Over many decades and successive generations, American Indian and Alaska Native

(AIAN) people have experienced a series of traumatic assaults that have had enduring consequences for families and communities. An extensive literature documents these assaults, which have included community massacres, genocidal policies, pandemics from the introduction of new diseases, forced relocation, forced removal of children though

Indian boarding school policies, and prohibition of spiritual and cultural practices

(Stannard, 1992; Thornton, 1987). Together, these events amount to a history of ethnic and cultural genocide (Smith, 2003). In addition, contemporary AIAN communities suffer from some of the highest rates of lifetime traumatic events, including interpersonal violence (Greenfield & Smith, 1999), child abuse and neglect (T. A. Cross, Earle, &

Simmons, 2000), poor health (Walters, Simoni, & Evans-Campbell, 2002), and an ongoing barrage of negative stereotypes that undermine AIAN society and identity.

The ability to understand the full impacts of these traumatic events and develop appropriate and effective treatments is constrained by conceptual and empirical limitations within current models of trauma and traumatic response. Standard diagnostic categories such as posttraumatic stress disorder (PTSD) capture some of the symptoms

30 experience by AIANs (e.g., nightmares about traumatic events) but are limited in their ability to explore the additive effects of multiple traumatic events occurring over generations. Moreover, such categories offer virtually no discussion on the intergenerational transmission of trauma from person to person or within communities and give us little insight into the relationship between historical and contemporary trauma responses in AIAN communities.

Historical trauma has become increasingly important in considerations of wellness among historically oppressed communities. Research related to such trauma has been conducted with a variety of populations, including Jewish Holocaust survivors and their descendents and Japanese Americans after internment. Scholarship exploring this phenomenon in

AIAN communities draws from the seminal work of Maria Yellow Horse Brave Heart and her colleagues at the Takini Network (Brave Heart, 1999a, 1999b, 2000; Brave Heart

& DeBruyn, 1998). Such preliminary work in the field of historical trauma has made a significant contribution to the field of intergenerational traumatology, yet many of the concepts involved still require further clarification and development.

Defining Historical Trauma

Historical trauma , the term used most often by scholars of AIAN trauma, is conceptualized as a collective complex trauma inflicted on a group of people who share a specific group identity or affiliation—ethnicity, nationality, and religious affiliation. It is the legacy of numerous traumatic events a community experiences over generations and encompasses the psychological and social responses to such events (Brave Heart, 1999a,

1999b, 2000; Brave Heart & DeBruyn, 1998). It is collective in that many members of a community view the events as acute losses and experience corresponding trauma reactions. It is understood as compounding insomuch as events occurring at different time periods (often across generations) come to be seen as parts of a single traumatic trajectory.

Previous scholars have suggested that the effects of these historically traumatic events are transmitted intergenerationally as descendents continue to identify emotionally with ancestral suffering (Brave Heart, 1999a, 1999b). Thus, although the events involved may have occurred over the course of many years and generations, they continue to have clear impacts on contemporary individual and familial health, mental health, and identity.

Although there is a great deal of variation in the events associated with historical trauma, it is possible to identify three distinguishing characteristics. First, they are generally widespread among AIAN communities, and thus, at the time of the event, many people in the community experienced or were affected by the event. Second, the events generate high levels of collective distress and mourning in contemporary communities. In some

32 cases, the resulting distress has been empirically documented among contemporary populations (e.g., Brave Heart, 1999a, 1999b; Whitbeck et al., 2004), and in others the distress is visible in the narratives that communities share about the events. Third, the events are usually perpetrated by outsiders with purposeful and often destructive intent.

This third characteristic is critical to the definition of historical trauma. Indeed, as noted above, many of these events are not only human initiated and intentional but also fall under the category of genocide (e.g., physical, cultural, or ethnocide), making them particularly devastating.

The Impact of Historical Trauma

Historical trauma is best understood as having impacts at three levels—the individual, the family, and the community. Research suggests that responses at the individual level fall within the context of individual mental and physical health and may include symptoms of

PTSD and guilt, anxiety, grief, and depressive symptomology (e.g., Barocas & Barocas,

1980). Responses at the familial level have received much less research attention; however, emerging work suggests that impacts may include impaired family communication (e.g., Wardi, 1992) and stress around parenting (Brave Heart & DeBruyn,

1998). Finally, at the community level, responses may include the breakdown of traditional culture and values, the loss of traditional rites of passage, high rates of

33 alcoholism, high rates of physical illness (e.g., obesity), and internalized racism (e.g.,

Duran, Duran, Brave Heart, & Yellow Horse-Davis, 1998). Although research has not yet empirically linked such community-level responses to traumatic events, AIAN scholars and community leaders allude to these connections in their descriptions of pervasive and chronic social malfunction.

Impact on the Individual

The impact of historically traumatic events at the individual level has been well documented, and much of the research in this area has been conducted with survivors of the Jewish Holocaust and their descendents. Holocaust survivors demonstrated tremendous resiliency and coping after massive trauma, yet many also experienced a range of negative mental health symptoms. Although there is a tremendous diversity of

Holocaust experiences, early researchers were able to document and explore a range of psychological symptoms commonly seen among survivors (Felsen, 1998). These symptoms are often collectively referred to as “survivor syndrome” and include denial, agitation, anxiety, depression, intrusive thoughts, nightmares, psychic numbing, and survivor’s guilt (Barocas & Barocas, 1980; Eitinger & Strom, 1973; Neiderland, 1968,

1981).

It is important to note that for the descendants of Holocaust survivors, the negative reactions to historical trauma appear to take a different and perhaps more subtle form. For this population, rates of mental health disorder are not usually higher than those found in the general population (Felsen & Erlich, 1990; Sigal & Weinfeld, 1987; Weiss,

O’Connell, & Siiter, 1986). Moreover, although their symptoms do not meet the criteria for mental disorder, descendents are more likely to experience some symptoms of depression, higher levels of anxiety, mistrust, and guilt, difficulty handling anger, and somatization over their lifetime compared to others (Barocas & Barocas, 1980; Bar-On et al., 1998). Children of survivors may also have more difficulty expressing emotions and regulating aggression, feel guilty, have an increased tendency toward self-criticism, and be more likely to experience psychosomatic distress (Felsen, 1998). Perhaps most notably, this research also shows a pattern of stress vulnerability to future events. That is, when children of survivors experience contemporary traumatic events, they are significantly more likely than controls to develop PTSD or subthreshold PTSD symptoms (Solomon,

Kother, & Mikulincer, 1988; Yehuda, 1999).

Brave Heart and her associates (Brave Heart, 1999a, 1999b, 2000; Brave Heart &

DeBruyn, 1998) have explored the impacts of a range of historically traumatic events on mental health among the Lakota and have documented a collection of common responses, which they term “historical trauma response.” This response is similar to symptomology

35 identified among Jewish holocaust survivors and their descendents and includes: rumination over past events and lost ancestors, survivor guilt, unresolved mourning, feeling numb in response to traumatic events, anger, depression, intrusive dreams and thoughts, and fantasies about saving lost ancestors.

Impact on the Family

At the familial level, there are important but perhaps more subtle ways that historical trauma manifests itself. Research among diverse populations has shown that children and grandchildren of survivors of traumatic events have high levels of current interest in ancestral trauma (Danieli, 1998; Nagata, 1991; Whitbeck et al., 2004). In particular, scholars have suggested that among historically oppressed peoples, intergenerational trauma can become an organizing concept for family systems (Danieli, 1998; Nagata,

1991; Wardi, 1992). For example, previous research has shown that children of

Holocaust survivors may feel that they are expected to serve certain familial roles, including consoling their parents or replacing those lost in the Holocaust (Felsen, 1998).

In research with children of Jewish Holocaust survivors, Bar-On and colleagues (1998) identified two major themes that influenced interactions between children and parents.

First, many interviewees experienced a preoccupation with their parents’ trauma, which

36 influenced their willingness to talk with their parents and their behavior in general. These children of survivors strove to be “good children” by not to causing more pain in the lives of their parents and, of importance, by not to asking questions about the Holocaust for fear of triggering painful memories. Similar findings have been found among indigenous people, whereby descendents of survivors avoid bringing up their own problems or worries so as not to burden their families (Walters, Evans-Campbell, Simoni, Ronquillo,

& Bhuyan, 2006). Second, children of Holocaust survivors reported “pervasive and persistent” feelings of guilt (Bar-On et al., 1998). Some interviewees noted feeling that they were not entitled to happiness when others could not have it. Similarly, research with AIAN community leaders has illustrated that given the overwhelming nature of ancestor experiences, contemporary AIAN people may tend to trivialize their own personal problems (Walters et al., 2006).

AIAN scholars have suggested that historical trauma may also play a role in AIAN family violence. For example, high numbers of AIAN parents grew up in boarding schools or foster care and were thus deprived of traditional parental role models (T. Cross,

1986; Horejsi, Craig Heavy Runner, & Pablo, 1992). Horejsi et al. (1992) suggested that boarding school experiences may have not only interrupted the intergenerational transmission of healthy child-rearing practices but also instilled new, negative behaviors instead. Although the vast majority of AIAN parents who experienced out-of-home care

37 through boarding school or foster care are able to parent effectively, some may struggle as a result.

Impact on the Community

Community-level responses are the least studied and understood. At an intuitive level, the impact of historical trauma seems obvious. Several generations of historical assaults on

AIAN culture, social structures, and ways of life have influenced tribal communities in myriad ways, and although many AIAN communities are thriving, there continue to be assaults on tribal sovereignty and traditional practices. Other AIAN communities have been left in a weakened condition, some still without fully functioning institutions or practices that characterize healthy and self-sustaining societies. Yet historically traumatic events have only recently been seen as having potentially compounding effects on entire communities, and there is limited discussion in the literature regarding community-level impacts using a trauma framework.

Research on the effects of forced Indian boarding school attendance, for example, has looked almost exclusively on survivor mental health outcomes. More recent work has contextualized the impact of the schools as a community-wide and multifaceted intergenerational loss (Adams, 1995; Duran et al., 1998). As a result, the boarding school

38 experience was traumatic not only for the children and families involved but also for the entire community and had dire consequences over generations. As children were removed from their communities, they were also subjected to assimilationist strategies and punished for practicing cultural and spiritual ways (Adams, 1995). Consequently, boarding schools significantly contributed to the loss of language and other traditional practices. A similar phenomenon occurred in the Japanese American community through the internment camp experiences. Nagata (1991) found that the internment led to an accelerated loss of culture as survivors tended to minimize their own Japanese ancestry, feeling it was protective to acculturate and encourage their children to acculturate.

Another important consideration in terms of community-level impact for AIAN communities is the large number of historically traumatic events that involve the loss of children. In any community, the loss of many children at once has a profound implications, including emotional suffering, the loss of human capacity (e.g., future leaders), and the ability of the community to safeguard its language and culture. The loss of children in AIAN communities has occurred over generations through forced Indian boarding school attendance, federal policies supporting the trans-racial adoption of AIAN children, and historically high rates of AIAN children in living foster care. AIAN children represent the future of their communities, and when they are taken from the community the ability of community members to plan for, or envision, the future is

39 jeopardized. Although empirical evidence is still being documented, AIAN scholars have long suggested that traumatic events have also led to indigenous community-level trauma responses, including social malaise, weakened social structures, and high rates of suicide

(e.g., Duran & Duran, 1995). Similarly, elders in a Whitbeck et al. (2004) study attributed higher community rates of alcoholism and child maltreatment to historically traumatic events. Given the previously limited view of historically traumatic events, unmasking the full extent of the impact is challenging, particularly when history is often presented in fragmented pieces rather than as a continuous process and social trajectory. Viewed together, however, one might reasonably speculate that affected communities may be more susceptible to negative second-order effects.

CHAPTER 5

LINKING HISTORICAL TRAUMA TO CONTEMPORARY HEALTH:

A PROPOSITION

Introduction

This dissertation offers a "framework" to approach the impact of Historical Trauma.

Previous work in this area offered observations, descriptions and vague explanations for the patterns of behavior associated with a historical trauma and “historical unresolved grief” (Brave Heart & DeBruyn, 1998). This work has often presented data related to health and social outcomes, without providing links to an antecedent specific to processes of: 1) the intergenerational phenomenon associated with this issue, and 2) how "external" culture/environment factors impact "internal" physiology and cause disease and social/cultural distension over extended periods of time, spanning decades and generations.

This dissertation attempts to formulate an objective connection between the many historically traumatic episodes of genocide and the contemporary health, social and cultural conditions of AIAN. In order to make these connections, strong arguments need to be put forth to describe:

1) The symbiotic interaction of culture and biology in human development,

2) The relationship of the autonomic nervous system (ANS) - our primitive fight-or-

flight responses, and the higher psychological processes of the Central Nervous

System afforded through the neocortex and lending to Vygotsky's "genetic"

(developmental) learning theories, which offers a theoretical explanation for the

intergenerational phenomenon of the impact of this issue. The autonomic nervous

system is the part of the peripheral nervous system that acts as a control system

functioning largely below the level of consciousness, controlling visceral functions.

The ANS affects heart rate, digestion, respiratory rate, salivation, perspiration, pupil

diameter, micturition (urination), and sexual arousal. Whereas most of its actions are

involuntary, some, such as breathing, work in tandem with the conscious mind, and

3) How “toxic stress” impacts children, getting passed on inter-generationally as a by-

product of dysfunctional coping strategies associated with this issue. Toxic stress

refers to frequent and/or prolonged activation of the body’s stress management

system. It results from intense adverse experiences, such as childhood abuse,

maltreatment, neglect and witnessing violence. Children are unable to effectively

manage this type of stress by themselves. This can lead to permanent changes in the

development of the brain and impact other physiological systems of the body.

Theoretical Framework

This framework consists of three main areas, or theoretical underpinnings:

1) Vygotsky's meditational (tool/sign use) theories,

2) Cultural-historical psychology: human psychological processes emerge from

humanity's culturally-mediated (tools and symbols), historically developed, practical

activity (everyday activities, etc.), and

3) Neuroscience: the impact of the physical/social/cultural environment on

neurophysiology and neurodevelopment. More specifically, how the ANS interacts

with, and "guides" the higher psychological processes of the neocortex with

environmentally induced "toxic stress.”

Proposition

The proposition put forth in this theoretical dissertation is that Historical Trauma is an antecedent to the start-up of intergenerational "coping" behaviors associated with “Toxic

Stress.” The type of stress that is associated with Adverse Childhood Experiences (abuse and neglect), having the potential to permanently augment development of the brain

(NSCDC, 2007). These coping behaviors and resulting toxic stress is directly associated with:

1) Post-traumamtic Stress Disorder (PTSD), afflicting the adults primarily impacted

by the historically traumatice event, and other responses associated with the ANS,

and

2) Learned behaviors which are the basis for the intergenerational continuation of

dysfunctional coping strategies.

Besides having a psychological and physiological impact, these dysfunctional coping behaviors (often associated with acts of violence) have a primary effect on core relationships – especially the mother/child relationship. Preliminary work with the veterans of the Iraq and Afghanistan wars indicate that the symptoms of PTSD have an impact on personal relationships. Symptoms include chronic episodes of anger, frustration, fear and “dissociation” (Brown, 2008). Albeit there are cultural, historical differences in making this comparison, there is a starting point for assessing the impact of psychological stress and PTSD on survivors of historical trauma.

These symptoms have the potential to evolve into abusive behaviors and neglect over time. Coping behaviors become "dysfunctional" because they interfere with natural responses, like the ability to nurture, feel compassion and empathy, etc. Within generations, these coping behaviors become subtly engrained into the "practical" activities and everyday functions of a society (culturally learned processes). These familial behaviors are repeated, learned, internalized and passed on to the next generation, becoming an acceptable part of that society.

The legacy of historical trauma, specifically regarding boarding schools, has negatively impacted AIAN families. Risk factors for substance abuse, violence, mental illness, and other family problems among AIAN people may be exacerbated by trauma (Brave Heart l

999b; Robin, Chester & Goldman 1 996; Holm 1994 ). It is my contention that generations of untreated victims of historical trauma may be passing on this trauma to subsequent generations.

Having undermined the fabric of AIAN families, boarding schools have deprived these families of traditional parenting role models, impairing their capacity to parent within an indigenous healthy cultural way (Brave Heart l999a). Parental and other intergenerational boarding school experiences have interfered with parental competence, parental

emotional availability, support, and parental involvement with the schooling of their

children. It has been suggested that parents that grew up in boarding schools, especially

those most likely to have been victims of punitive or "boarding school style discipline,"

may be more likely to have experienced trauma as children and suffered from the

separation from their families for extended periods of time (Brave Heart, 1999a).

This legacy has negatively impacted parental interaction with their children and

contributes to risk factors for developing dysfunctional coping behaviors and substance

abuse problems (Brave Heart l999a, 1998; Morrissette in Brave Heart l999a). Boarding

school survivor parents lack healthy traditional role models for parenting. This places

parents at risk for parental incompetence, as far as providing their own children with an

emotionally enriched environment to foster development. Adverse childhood experiences may feed back into the cycle of emotionally unavailable parents.

The impact of intergenerational trauma is clearly illustrated in this testimony given by a

43 year-old Lakota male recovering alcoholic:

I never bonded with any parental figures in my home. At seven years old, I could

be gone for days at a time and no one would look for me . . . I've never been in a

boarding school. I wished I was [ had] because all of the abuse we've talked about

happened in my home. If it had happened by strangers, it wouldn't have been so

bad - the sexual abuse, the neglect. Then I could blame it all on another [race] . . . .

And yes, they [my parents] went to boarding school (Brave Heart 1999a).

As supported by this testimony, I believe that it is toxic stress (and its response) that gets passed on from one generation to the next. In addition to interactions associated with human "attachment", children learn and internalize familial patterns from their parents and siblings. As adults, they subtly seek to re-create that social and physical environment.

Over time, the initial source for the "coping" behavior is forgotten (i.e., the traumatic episode), leaving behind a pattern of behaviors that get infused into an intergenerational cycle.

CHAPTER 6

PHYLOGENY, CULTURE AND ONTOGENY

It is important to establish an approach to frame the study and impact of Historical

Trauma. A main reason I was personally drawn to study cultural-historical psychology in the first place has to do with identifying a theory that encompassed the cultural, historical and biological consideration for understanding the impact of Historical Trauma. This approach addresses the relationships between human mental functions and cultural, institutional, and historical situations in which the functioning occurs. Cole (1996) referred to his cultural-psychological approach to cultural psychology as a “once and future discipline”, in that:

“cultural psychology is different from specialized branches of psychology in that

it did not evolve as a subdiscipline after the founding of experimental psychology;

the idea of cultural psychology predates experimental psychology and was present

at its birth.” (1996, p. 279)

One of the implications of Cole’s formulation of cultural psychology is that it is not to be confused with, or reduced to, the subdiscipline of “cross-cultural” psychology. Instead, the origins of cultural psychology are found in Wundt’s writings. Cole’s point is that

Wundt, the figure generally considered to be the “father of psychology”, clearly saw a role for a version of cultural psychology that was on parallel with other areas of the discipline oriented toward the natural sciences (Cole, 1996).

In this chapter, I will address the relationship of phylogeny and cultural history in the development of modern man. Morphological changes to the neocortex have provided for the capacity of greater cognitive ability, which in turn, provides for the potential to develop (or modify existing) mediating artifacts (i.e., tools) as practical activity (survival) dictates. In turn, it is the use of this mediating artifact that stimulates neurogenesis, and also increases the cultural toolkit. The mediating artifact can then be shared with the group by “learning” to produce and use the mediating artifact. This interplay forms the basis for phylogeny and ontogenetic acquisition of culture. Since, from this perspective, culture is seen as the accumulation of mediating artifacts (Cole, 1996). The point here is that culture plays a significant role in the development of the brain and neurogenesis.

To begin, I take as a theoretical starting point of L.S. Vygotsky and his colleagues in that human psychological processes can be understood as the emergent outcome of four

“genetic domains” - phylogeny, cultural history, ontogeny and microgenesis (Vygotsky,

1977; Vygotsky & Luria, 1930/1993; Wertsch, 1985). The early work of cultural- historical psychologists emphasized the role of culture in development.

For the sake of this discussion, phylogeny refers to the emergence of modern man; cultural history – the emergence of mediating artifacts; ontodeny – the emergence of the individual; and microgenesis – those moment-to-moment experiences (Cole, 1996).

Emphasis will be placed on phylogeny, cultural history and ontogeny.

The expansion of cultural psychology in the direction proposed by early Russian cultural- historical psychologists is an important contemporary task. Michael Cole’s approach to cultural psychology is of particular interest because it brings cultural history into the study of human ontogeny without abandoning a commitment to an evolutionary perspective (Cole, 1996).

This perspective is founded upon the assumption that the structural uniqueness and developmental course of human psychological processes emerge from humanity’s culturally mediated, historically developing, practical activity (Leontiev, 1981; Luria,

1979; Vygotsky, 1987). Each component plays a role in how we perceive the interplay of phylogeny and cultural history for use in ontogeny.

Cultural Mediation

Human psychological processes emerged in phylogeny simultaneously with a new form of behavior in which material objects are modified as a means of regulating their interactions with both the physical world and each other. From a cultural-historical approach, these meditational devices are referred to as artifacts (tools, signs and symbols).

The basic idea of artifact (tool) mediation of human experiences is clearly expressed by

Alexander Luria (1928): “Man differs from animals in that he can make and use tools…(that) not only radically change his conditions of existence, they even react on him in that they effect a change in him and psychic condition” (p.143).

The consequence of artifact creation/use for the basic structure of behavior is “that instead of applying directly its natural function to the solution of a particular task, the child puts between that function and the task a certain auxiliary means… by the medium of which the child manages to perform the task” (Luria, 1928, p. 148, italics in original).

As environmental stressors emerge, new artifacts are designed to deal with that particular stress – what is now understood as technological advancement.

Historical Development

Vygotsky and Luria (1930/1993) included both the history of the human species and the historical change following the emergence of modern man in their approach to ontogeny.

They claim that the evolutionary, the historical, and the ontogenetic domains each has its own “turning point” in which “something new” is introduced into the process of development.

The proposed turning point in phylogeny is the appearance of tool use in apes. The turning point in modern human history is the appearance of labor and symbolic mediation.

The major turning point in ontogeny is the coming together of cultural-history and phylogeny with the acquisition of language. The products of these interactions of different “streams of history” are distinctly human - higher psychological functions. The crucial difference that distinguishes ape and human ability to use tools and human labor is the involvement of language and symbolic mediation, “tools for the mastery of behavior”, as well as nature (Cole, 1996). This combination produces a qualitatively new form of mediation, one in which tools and language unit in the artifact. At this point

“primitive man” emerges.

In one of their examples, Vygotsky and Luria (1930/1993) argue that primitive cultures natural remembering, such as that produced from “photographic” memory, is dominant.

Incidental memory concerning participation in various events, what we might call

“everyday memory”, also qualified as natural remembering, a process in which humans record the world but do not actively use their memories to transform it. This sort of

“natural” (to humans) form of everyday memory is built upon phylogenetically evolved

“elementary” psychological processes that are assumed to be universal across cultures and historical periods. Memory that is “cultural” develops through the elaboration of a

“meditational means” by which memory is accomplished and the cultural practices that incorporate the new mediators. Utilizing a calendar to keep track of the number of days in a year provides an example of what Vygotsky and Luria (1930/1993) meant by the

“cultural form of behavior”.

According to this view, culture undergoes both quantitative change in terms of the number and variety of artifacts, and qualitative change in terms of the new forms of mediated behavior potentials that they embody. As a consequence, both culture and human thinking develop. Culture, then, can be understood as the entire pool of artifacts

(including language, norms, customs, tools, values) accumulated by the social group in the course of its historical experience. From this perspective, use of an artifact as a medium becomes the process for human development. The capacity to develop within

53 this medium and to arrange for its reproduction in succeeding generations is the distinctive characteristic of modern humans. This is important in addressing how emotion

– specifically anger and fear – can be viewed as “mediators” to elicit a response, instead of using language or other meditational means.

Practical Activity

Analysis of human psychological functions must be grounded in everyday activities. A. N.

Leontiev (1981) asserted:

…human psychology is concerned with the activity of concrete individuals, which

takes place either in a collective – that is, jointly with other people – or in a

situation in which the subject deals directly with the surrounding world of objects

– for example at the potter’s wheel or a writer’s desk… With all its varied forms,

the human individual’s activity is a system in the system of social relations. It

does not exist without these relations. The specific form in which it exists is

determined by the forms and means of material and mental social interaction. (p.

11)

Two additional principles of the cultural-historical approach to cultural psychology follow: First, because phylogeny, cultural history and ontogeny are all processes that

54 occur over time and for which change is the central phenomenon to be explained, a developmental approach is required. It is for this reason that Vygotsky often invoked the idea that “to understand behavior, we must understand the history of behavior”

(Vygotsky & Luria, 1993, p. 79). Second, this perspective gives a special importance to the social origins of human thought processes. As Vygotsky (1929) suggested, all means of cultural behavior (artifacts) are social in their essence: “Social relations or relations among people genetically underlie all higher functions and their relationships” (Vygotsky,

1981, p. 163). This view of social origins arises because of the special role of adults as bearers of the cultural resources of the social group. From this perspective, the biological maturing child and the socially organized, culturally mediated, social environment “co- construct” development.

Phylogeny and Human Development

There is neurological evidence to support Geertz’s assertion of the coevolution of phylogeny and cultural history in the development of modern man. Because the human brain developed over millennia during which culture became an essential part of human life, it seems necessary to seriously consider Geertz’s assertion (1973) that

“man’s nervous system does not merely enable him to acquire culture, it

positively demands that he do so if it is going to function at all. Rather than

culture acting only to supplement, develop, and extend organically based

capacities logically and genetically prior to it, it would seem to be ingredient to

those capacities themselves. A cultureless human being would probably turn out

to be not an intrinsically talented, though unfulfilled ape, but a wholly mindless

and consequently unworkable monstrosity” (p. 68)

Contemporary anthropological evidence indicates that culture is not an “add on” to

biological human nature. Culture is a biological prerequisite to the normal functioning of

the human brain (Plotkin, 2001).

It is generally agreed upon that human beings and chimpanzee/bonobos shared a common

ancestor some 6 million years ago (Noble & Davidson, 1996). The successors to the

common ancestor that lead to H. sapiens sapiens underwent massive changes not only in the brain and in the physical morphology of the body (bipedalsim; the structure of the arms, hands, fingers, vocal tract, etc.) but also in cognitive capabilities and the accumulation of the products of the past in the form of human culture. By contrast, there is no evidence that the anatomy, body size, physical morphology, behavior, cognitive abilities and modes of life have changed markedly over the past several million years among chimpanzees and bonobos. The advent of culture has significantly contributed to the morphology of the brain and the range of cognitive abilities.

Culture and Hominization

There is a marked increase in the size of the brain in the sequence of species leading to H. sapiens sapiens . Growth appears to have been especially pronounced in the frontal and prefrontal cortical area, hippocampus and cerebellum, all heavily implicated in cognitive changes both in phylogeny and ontogeny. Of interest has been the appearance, derived from endocast moldings of the skull, of increased volume in Broca’s area that appears with Homo erectus , because of the relationship of Broca’s area to language in normally developing modern humans (Lewin & Foley, 2004).

Also widely studied are the morphological changes to other parts of the body that are associated with changes following the divergence from immediate ancestors. Such changes include bipedalism and various changes in anatomy: to the hand for fine motor control (especially the opposable thumb), pelvic region (birth and length of infancy), and the vocal apparatus necessary for rapid, fluent speech (see Lewin & Foley, 2004, for summary). Bipedelism is often considered to be the first step toward hominization. The direct advantage to bipedalism is the ability to move in an upright posture, being more efficient in the use of energy for long-distance locomotion, thus enabling bipedal creatures to get food from a relatively wider geographical area.

The hominid tool kit was slow, lasting perhaps a million years. The rate of change, the variety and the complexity of tools increased in the course of human evolution (Foley &

Lahr, 2003; Lewin & Foley, 2004). This fact has potentially important implications since the cumulative effect of cultural evolution, or the “ratchet effect” (Tomasello, 1999) is not always clearly observed. Culture as a set of shared artifacts may have been inherited by the following generations almost unchanged. When a baby is born, it inherits the culture of its parents and the presupposition for its future. Social processes give rise to individual processes through the use of mediating artifacts.

Like Plotkin (2001) quoted earlier as he was referring to the process of hominization,

Donald (2000) concludes that the brain and culture “have evolved so closely that the form of each is greatly constrained by the other” (p. 25). With the arrival of literacy, “culture actually configures the complex symbolic systems needed to support it by engineering the functional capture of the brain for epigenesist” (p.23).

Evolution of Language and Cognition

There is some disagreement as to when language became a constituent of increased cognitive and cultural complexity, some argue it was at the point of H. erectus (Bickerton,

1990; Deacon, 1997; Dunbar, 2004). Others argue that language came later, or with the

58 advent of H. sapiens sapiens, along with specialized vocal tract that could produce rapid speech (Lieberman, 1984). Whether earlier or later in hominization, symbolic language is agreed to be essential to the emergence of modern humans.

Suggestions for the important cognitive changes that may have accompanied language include increased ability to coordinate motor and special processing (Stout, Toth, Schick,

Stout, & Hutchins, 2000); Wynn, 1989), increased ability to cooperate with others over extended periods of time to produce products (Foley & Lahr, 2003), and increased ability to imitate the behavior of others (Donald, 1991, 2000; for discussion of Donald’s views, see Renfrew & Scarre, 1998).

An important conclusion, for the sake of this theoretical analysis, is that the relationships between biological, cultural, and cognitive change are reciprocal – a change to one, also changes the others. The evidence strongly supports the changes in anatomy (increased relative brain volume) is linked to a change in diet, in particular, greater intake of protein from the killing and ingestion of animals. The ability to kill and eat animals was in turned happening at the same time to anatomical changes (the ability to run long distances that evolved following the evolution of the ability to walk upright, which also freed the hands which is associated to greater dexterity of the fingers). These biological changes were both cause and result of increased sophistication of the cultural tool kit, including the

59 control of fire (Tomasello, 1999). The development of a richer diet, and the way of life associated with with it, enabled the growth of new cognitive capacities, which further enriched the cultural, which in turn supported growth of the brain. As Henry Plotkin

(2001) emphasized, human evolution and cultural evolution are two-way streets of causal interaction.

Culture and Biology in Ontogeny

Phylogenetic Contributions

Researchers have identified powerful general learning mechanisms. Even infants are able to identify sequential dependencies in the speech stream (Saffran, Aslin, & Newport,

1996) or in the mechanical movement that occurs when one object collides with another

(Baillargeon, 1994). Moreover, humans early on are conceptual learners. They are able to build concepts coherent within a larger system (Mandler, 1994), understand a set of antecedent-consequent pairs in terms of unobservable, mediating forces (Tomasello, 1999) and to “bootstrap” (i.e., create a new system of representation that is more powerful than those present, Carey, 2004). These general learning mechanisms are also products of evolution. They are heavily dependent on enlarged frontal and prefrontal cortices that have evolved through uniquely human ways of living, such as dealing with, and solving,

60 complex environmental and social problems, learning and using culturally inherited artifacts, manipulating the natural environment to their needs, and so on (Quartz &

Sejnowski, 2002).

Cultural Contributions

Ontogenetic development of the human mind requires repeated participation in culturally organized practices. The cultural history of a child’s social group provides the kinds of practices that are available as environments for development. On the other hand, developing individuals increasingly have at least limited freedom to choose the practices in which they engage and to change the features of these practices through their participation. Repeated participation enhances the cognitive, social, and physical skills needed to perform well in those practices.

Practices vary greatly both within and between social groups. In some cases, people acquire specific skills to perform competently only in a specific practice (i.e., like playing a musical instrument), whereas in other cases they acquire a rich and well-structured body of knowledge and associated skills as well. Gaining cognitive competence may require years of experience in solving problems in a domain and often takes the form of

“deliberate practice” requiring sustained concentration ((Ericsson, Krampe, & Tesch-

Romer, 1993).

We can assume that most, if not all, forms of cognitive development develop through participation in culturally organized practices. For the most part, participants in these practices are motivated to perform well because the process and product are interesting and/or significant and positively supported by the culture. Inclusion in such practices allow newcomers to participate in roles that are appropriate to their level of expertise.

This kind of sociocultural arrangement is often referred to as a “zone of proximal development” (Lave & Wenger, 1991; Vygotsky, 1978). Other people who have prior experience and shared physical, symbolic, and social tools help newcomers acquire knowledge and skills through continuous interpersonal interaction. For example, imitation plays an important role in the initial phase of learning and more mature members of the learner community, in addition to serving as role models, provide hints and suggestions for improving the skills. Practical activities require the newcomers to learn tasks and skills that promote the continued survival. Often, these skills are acquired without formal awareness. Much like the acquisition of “traditional” traits in a family – younger children effortlessly and subtly acquire the culture of the family. I believe that the acquisition of dysfunctional coping behaviors is no different. Sociocultural constraints enable us not only to be competent but also to acquire knowledge and skills in

62 a uniquely human way through participating in practices. A set of cognitive skills is a form of “culture in mind”, derived from skills using an artifact that initially exists outside of the mind (Vygotsky, 1978). It is also clear that cognitive growth in a domain is associated with the development of the corresponding values, identity and status in the community of practitioners.

In summary, changes in morphology of the brain and behavior result in changes in the cultural tool kit, that lend to changes in nutrition to support a bigger brain – that, in turn - results in further changes in morphology (growth), that in return result in changes in the cultural toolkit in the never-ending spiral of development. Each cycle (generation) lends to changes that may be regarded as technological advances in time, depending on the need to modify or invent the mediating artifact (tool). Again, the primary purpose for taking a closer look at the interaction of phylogeny, cultural history and ontogeny is two- fold: first, to show that cultural history plays a major role in ontogenetic development of the individual, lending to morphological changes to the brain and the cultural tool kit, and second, the cultural tool kit is passed on intergenerationally through those that are more experienced and who act as mentors and guides to more novice members of the group.

CHAPTER 7

THE NERVOUS SYSTEM AND THE HYPOTHALAMIC-PITUITARY-ADRENAL

AXIS

The nervous system is broken down into two major systems: the Central Nervous System and the Peripheral Nervous System (Nolte, 1993).

Central Nervous System

The Central Nervous System consists of the brain and the spinal cord. The cerebrum consists of cerebral hemispheres and the diaencephalon. The cerebrum is divided into two symmetrical cerebral hemispheres connected by the corpus collusum. The cerebrum is associated with what is referred to as higher psychological processes (a term more associated with “mind” and the neocortex): cognitive functions, emotional, sensory, and motor functions are more developed in humans than any other animal. It is what we see when we picture a human brain, the gray matter with a multitude of folds covering the cerebrum. The cerebral hemispheres consists of four lobes:

Frontal lobe – (motor cortex) motor behavior, expressive language, higher level

cognitive processes, and orientation to person, place, time, and situation

Parietal lobe – (somatosensory Cortex) involved in the processing of touch,

pressure, temperature, and pain

Occipital lobe – (visual cortex) interpretation of visual information, and the

Tempora lobel – (auditory cortex) receptive language (understanding language),

as well as memory and emotion.

Also consistsing of the CNS is the diaencephalon, specifically the thalamus and hypothalamus. The thalamus is referred to as the "central switching station" – relaying incoming sensory information (except olfactory) to the brain. The hypothalamus – controls the autonomic nervous system, and therefore maintains the body’s homeostasis, controling body temperature, metabolism, and appetite. The hypothalamus translates extreme emotions into physical responses.

Peripheral Nervous System

The Peripheral Nervous System is divided into two sub-systems (Nolte, 1993).

The Somatic Nervous System – primary function is to regulate the actions of the skeletal muscles, and the

Autonomic Nervous System – regulating involuntary activities such as heart rate, breathing, blood pressure, and digestion. Although these activities are considered involuntary, they can be altered either through specific events or through changing our perceptions about a specific experience. This system is further broken down into two complimentary systems: Sympathetic and Parasympathetic Nervous Systems.

The Sympathetic Nervous System controls what has been called the "Fight or Flight" phenomenon because of its control over the necessary bodily changes needed when we are faced with a situation where we may need to defend ourselves or escape. The

Parasympathetic Nervous System returns the body back to homeostasis after the “fight or flight” response.

These two subsystems are at work constantly shifting your body to more prepared states and more relaxed states. Every time a potentially threatening experience occurs, the sympathetic nervous system responds and the parasympathetic nervous system brings everything back to normal.

Other brain structures also of concern:

Limbic System – emotional expression, particularly the emotional component of behavior, memory, and motivation

Amygdala – attaches emotional significance to information and mediates both defensive and aggressive behavior

Hippocampus – involved more in memory, and the transfer of information from short- term to long-term memory

Stress and the Sympathetic Nervous System

The Hypothalamic-pituitary-adrenal axis and stress

As previously indicated, survivors of historical trauma have the potential to develop chronic diseases as a result of chronic, toxic stress. This chapter looks at the general mechanism of the Stress Response System.

The nervous system has evolved to provide a complex metabolic systems intended to maintain normal homeostasis. This physiologic state of balance is susceptible to various external environmental and social events, whether actual or perceived (Kirschbaum &

Hellhammer, 1989). The term “stress” has been coined to describe a “state of threatened

homeostasis or disharmony” that must then be counteracted by an “adaptive stress

response,” a complex array of physiologic and behavioral responses intended to re-

establish homeostasis (Kirschbaum & Hellhammer, 1994).

The Stress Response System

A vast amount of research has been conducted to understand the intricate cascade of

events that occur once the brain detects a disruption in homeostasis (a stressor) and the

hormonal responses driven by these systems (Kyrou & Tsigos, 2005). The key

components of the “stress system” are the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) (Vining & McGinley, 1983). Basically, 1) when the hypothalamus is triggered by a stressor, corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) are secreted, 2) eliciting both the release of adrenocorticotropin hormone (ACTH) from the posterior pituitary and the activation of the noradrenergic neurons of the locus caeruleas/norepinepherine (LC/NE) system in the brain. The LC/NE system is primarily responsible for the immediate “fight or flight” response driven by epinephrine and norepinephrine, while 3) ACTH drives the production of cortisol from the adrenal cortex. Under normal conditions, the production of CRH and ACTH fluctuate in a predictable circadian cycle and are inhibited by high levels of blood cortisol via a negative feedback loop.

While many metabolites within the HPA axis can be monitored, cortisol is the hormone that usually gets the most attention in clinical research and practice. Cortisol, a glucocorticoid hormone, its action is to shunt cellular processes away from long-term metabolic processes toward those that function primarily on immediate survival and homeostasis. Thus, the negative feedback loop of cortisol on its own secretion is designed to limit long-term exposure of tissues to these short-term catabolic and immunosuppressive actions. Chronic and repeated stressors can lead to one or more forms of HPA axis dysregulation, altering appropriate cortisol secretion and affecting end-organ function and developing disease.

The hormone dehydroepiandrosterone (DHEA) is also produced in the adrenal cortex; and while its secretion is affected by pituitary ACTH secretion, additional regulatory activities and aging result in an almost complete loss of the diurnal rhythm in elderly individuals (Fries, & Dettenbenborn, 2009; Chida & Steptoe, 2009). DHEA, a glucocorticoid antagonist, serves not only to prevent excessive systemic inflammation, but also to protect the neurologic structures, particularly the hippocampus, from the damaging effects of cortisol (Kimonides, Khatibi et al, 1998; Cardounel, Regelson et al,

1999). Exposure to chronic stress leads to a substantial reduction in circulating levels of

DHEA and further damages the underlying metabolic processes. Suboptimal levels of

DHEA have been detected in individuals with numerous chronic disease states, mood disorders and chronic pain syndromes (like fibromyalgia) (Morgan & Rasmussen, 2009).

Stressors and the HPA axis

It has been found that chronic exposure to a stressor leads to a recurring set of physiological outcomes (hypertrophy of the adrenal gland, atrophy of the lymphatic organs, and ulcers in the stomach). Epidemiological data suggests that acute, intense episodic or chronic exposure to HPA axis stressors in humans is related to the same phenomena (Kimonides, Khatibi et al, 1998). While numerous advances in our understanding of the stress response have been published, the same stress response mechanisms elicited by virtually all stressors remains unchanged.

Mental and Emotional Interpretation

The physiochemical responses of the HPA axis are easily triggered by non-physical events. Grief, excitement, fear, anxiety, guilt, embarrassment - all can trigger the HPA axis response. Research has shown that the magnitude of the response and recovery to these stressors is based on the individual’s perception rather than the actual stressors. The four key factors that determine the magnitude of the HPA axis response to a

70 mental/emotional stressor are its 1) novelty to the individual, 2) unpredictable nature, 3) threat to their person or ego, 4) sense of loss of control (Marin & Pilgrim, 2010; McEwen

& Wingfield, 2003). Innate qualities such as age, gender (female preponderance) and hereditary predisposition, coupled with personality characteristics (i.e. introversion and low self-esteem) and prenatal and early childhood experiences, serve to further individualize and amplify each person’s unique stress response.

Sleep Disorders

During sleep, cortisol release is normally suppressed by a decrease in CRH and a rise in growth hormone (GH) secretion. Exposure to chronic stressors results in abnormal HPA axis and SNS activation and disruption of the normal diurnal pattern of GH, CRH and

ACTH release. The result is a paradoxical rise in cortisol levels in the evening hours and initial phases of sleep. A vicious cycle ensues whereby nocturnal hypercortisolism causes sleep fragmentation, raising cortisol levels even further. Insomnia and depression are frequently observed outcomes (Vgontzas, 2008).

Metabolic/Glycemic Dysregulation

Under stressful conditions, maintaining adequate levels of glucose for brain and muscle use is important. Cortisol secretion helps maintain these levels by stimulating gluconeogenesis and causing peripheral and adipose (body fat) insulin resistance. While these effects are intended to allow for short-term “fight or flight” benefits, they can lead to disastrous consequences if maintained for more than acute episodes. Individuals who regularly consume high glycemic foods and/or are insulin resistant will often induce a hypoglycemic “crash” after a meal, triggering the cortisol response. Since cortisol itself can drive insulin resistance, this is a cycle that is difficult to control. It has been suggested that individuals with central insulin resistance be evaluated for HPA axis dysfunction and learn about lifestyle modification and diets to improve glycemic control

(Dallman & la Fleur, 2004; Dallman, Pecraro, et al, 2006; Andrews & Walker, 1999).

This is critical to the healthcare to AIAN. The IHS does not have the resources nor expertise to perform this evaluation.

Inflammation

Cortisol, like its corticosteroid analogues, is a powerful anti-inflammatory agent. Any acute or chronic inflammatory condition will signal cortisol release through normal

72 inflammatory signaling and the HPA axis. Undiagnosed inflammation in the gastrointestinal tract, chronic inflammatory conditions (joints, cardiovascular) or obesity will drive HPA axis dysfunction if not corrected. Furthermore some pharmacologic agents commonly used to treat the symptoms of chronic inflammatory diseases can further exacerbate HPA axis dysfunction (Bruni & De, 2009; Granger & Hibel, 2009;

Masharani, Shiboski, et al, 2005).

Trauma and Toxic Stress

Within the past 20 years, perhaps one of the most significant advances in violence and trauma research is the accumulating evidence that there is not a “consensual pattern” of neurobiological responses to violence and trauma exposure (Cicchetti & Rogosch, 2001).

Some children exposed to violence and trauma display the expected diurnal pattern of cortisol secretion – on average, being high in the morning and lessening throughout the day (Cicchetti & Rogosch, 2001). Others manifest hypercortisolism, which reflects heightened and prolonged HPA activity presumably related to overactivation of the stress response (Gunnar &Vazquez, 2001). Still others manifest hypocortisolism, which reflects a deficiency of cortisol evidenced either by reduced adrenocortical secretion, reduced adrenocortical reactivity, or enhanced negative feedback inhibition of the HPA axis

(Heim, Ehlert, & Hellhammer, 2000). These patterns of dysregulation carry significant

73 risk for the development and maintenance of physical and psychological illness, such as immune system disorders, depression and anxiety, poor cognitive functioning, and impaired learning (Gunnar & Vazquez, 2001; McEwen, 1998; Sapolsky, 1994).

One of the most important tasks researchers face is to understand why these different patterns emerge. There are likely multiple moderating factors that help account for the divergent patterns in HPA function, including the child’s age and gender, frequency, severity and cognitive interpretation of the trauma, proximity of measurement to periods of active trauma, genetic vulnerability, and psychopathological symptoms manifested at the time of cortisol measurement. DeBellis (2001) integrated several of these potential moderators in his theory for the variation in children’s neurobiological responses to trauma. DeBellis (2001) argues that early trauma experiences prime the HPAaxis so that base adrenocortical and cortisol secretion are “set at lower 24 hour levels” (p. 548). This may occur when repetitive trauma exposure provokes frequent elevations in cortisol and, subsequently, results in the down regulation of components of the HPA axis, resulting in low, rather than high, adrenocortical secretion later in life (Gunner & Vazquez, 2001).

Although a primed system will hyper-respond on exposure to an acute stressor, basal

HPA activity is blunted. More research continues in this area.

Consequences of Hypothalamic-pituitary-adrenal Axis Dysregulation

Hypercortisolism

Although the initial stages of the stress response are intended to promote survival, chronic exposure to stressors may lead to periods of elevated cortisol levels that are not reduced appropriately by negative feedback inhibition, creating further HPA axis abnormalities (Chrousos & Gold, 1992; Epel, 2009)) Since every organ system is adversely affected, the body eventually succumbs to stress-induced physiological and behavioral impairments.

The immune system is one of the primary systems affected by hypercortisolism. The overall actions of glucocorticoids are to suppress the immune system. Impaired cytokine production and function, loss of tissues important in immune cell production (lymphoid, thymic and splenic tissue), and impaired leukocyte trafficking contribute to increased susceptibility to infection and neoplasm. Additionally, HPA axis dysfunction and prolonged cortisol elevation may actually be the cause, rather than the consequence, of development or perpetuation of autoimmune diseases (Bateman & Singh, 1989; Johnson

& Kamilaris, 1992). Corticotropin Releasing Hormone, through its effects on

75 corticosteroids and catecholamines, further suppresses systemic inflammatory reactions while directly stimulating local inflammatory tissue responses (Trigos & Chrousos, 2002).

CRH and corticosteroids also affect insulin release and glucose regulation. Cortisol increases insulin levels; and the co-elevation of these two hormones, as well as a reduction in the levels of androgens, promotes visceral fat deposition (Toussant &

Mishiels, 1995). Visceral fat has abundant glucocorticoid receptors and is very sensitive to the effects of cortisol and insulin. Fat deposition is further promoted by increased and prolonged levels of the enzyme lipoprotein lipase (Dallman, Pecoraro, et al 2003). This vicious cycle of events inevitably plays a role in the development of such diseases as insulin resistance, hyperlipidemia, cardiovascular disease and hypertension (Pou &

Massaro, 2007). In fact, stress-induced hypercortisolism and its cardiovascular effects— visceral adiposity and other adverse sequelae—increase the all-cause mortality risk of patients two to three times and decrease life expectancy by several years (Chrousos,

2000). This has laso been reported by the IHS (Bullock, 2008).

Other conditions in which hypercortisolism and prolonged activation of the HPA axis have been demonstrated include anorexia nervosa, obsessive-compulsive disorder, panic disorder, chronic alcoholism, excessive exercising, childhood sexual abuse, pregnancy and hyperthyroidism, and melancholic depression (Chrousos & Gold, 2009; Tsigos &

Chrousos, 2002). Therapeutic approaches that help uncover these causes should be considered in subjects with hypercortisolism along with those that improve HPA axis feedback, immune support and insulin sensitivity.

Hypocortisolism

Hypocortisolism describes any condition in which paradoxically low cortisol, flattened daytime production patterns and blunted cortisol release to stressors are observed.

Evidence suggests that hypocortisolism may be a common, yet underappreciated, consequence of exposure to severe acute stress and chronic intermittent stress. Studies have confirmed states of hypocortisolism in individuals chronically exposed to stressful environments, those with unpredictable schedules and in those with traumatic early life experiences (Gunmar & Vasquez, 2001; Heim, Ehlert, et al, 2000)

Given the complexity of the stress response system, understanding of the process through which hypocortisolism arises has been a daunting task. However, since the integrity of

HPA axis function and normal diurnal patterns of cortisol release are essential for maintaining internal homeostasis, much of the available research on chronic stress and disease have implicated disruptions in these aspects to be causative.

Within the context of HPA axis dysfunction, several mechanisms have been proposed to account for the evolution of low cortisol states. One model suggests that under the influence of chronic stress, the initial adaptive hypercortisolism response transforms over time into a self-preserving hypocortisolism state in order to protect the metabolic machinery, and most importantly, the brain (Fries & Hesse, 2005; Hellhammer & Wade,

1993). Other potential mechanisms of centrally induced states of hypocortisolism include down-regulation of pituitary CRF receptors in response to elevations of CRH and hypercortisolism-induced negative central nervous system feedback on further release of stimulating hormones (Hauger, Millan, et al, 1988; Hauger & Lorang, 1990; Heim, Ehlert, et al, 1998).

“Relative” states of hypocortisolism, or cortisol resistance, may also occur despite the presence of normal or even elevated cortisol levels. Low cortisol states may also result from recurrent infectious processes as the body attempts to promote a more vigorous immune response. Left unchecked, levels of pro-inflammatory cytokines increase fueling what has been termed the “sickness response.” Patients with hypocortisolism typically suffer from fatigue, impaired cognition, sleep disturbances, anorexia and depressed mood; symptoms are also seen in patients with the sickness response (Hart, 1988; Raison &

Miller, 2003). These are symptoms of depression, also associated with trauma victims.

Immune system up-regulation is a key component of the metabolic dysregulation seen in hypocortisolism. Since cortisol is profoundly influential in maintaining homeostasis within the immune system, a decrease in baseline levels or a suboptimal stress induced rise in its levels may lead to maladaptive immune system dysfunction. Cortisol selectively suppresses cellular immunity thereby preventing tissue damage from excessive inflammation (Elenkov & Chrousos, 1999).

The result is amplification of numerous inflammatory pathways and increased susceptibility to developing inflammatory diseases, including autoimmune diseases, mood disorders, chronic fatigue syndrome, chronic pain syndromes, obesity, glucose dysregulation and fibromyalgia (Rohleder, Joksimovic, et al, 2004; McEwen & Seeman,

1999; Rosmond, Dallman, et al, 1998). Furthermore, due to down-regulation of immunity, hypocortisol patients become more vulnerable to assaults by infectious and environmental pathogens such as parasites, allergens, certain bacteria and toxins

(Elenkov & Chrousos, 1999).

Health Conditions Related to Hypothalamic-pituitary-adrenal axis

The following is a brief list of health conditions related to HPA-axis dysfunction:

Increased Activity of the HPA-axis

Cushing’s syndrome

Chronic stress

Melancholic depression

Anorexia nervosa

Obsessive-compulsive disorder

Panic disorder

Excessive exercise (obligate athleticism)

Chronic, active alcoholism

Alcohol and narcotic withdrawal

Diabetes mellitus

Central obesity (metabolic syndrome)

Post-traumatic stress disorder in children

Hyperthyroidism

Pregnancy

Decreased Activity of the HPA-axis

Adrenal Insufficiency

Atypical/seasonal depression

Chronic fatigue syndrome

Fibromyalgia

Premenstrual tension syndrome

Climacteric depression

Nicotine withdrawal

Following cessation of glucocorticoid therapy

Following Cushing’s syndrome cure

Following chronic stress

Postpartum period

Adult post-traumatic stress disorder

Hyperthyroidism

Rheumatoid arthritis

Asthma, eczema

It is important to note that there is absolutely no dispute within the medical literature, which spans almost 80 years, of the effects of both acute and chronic stress on aging,

81 disease formation and early mortality. Yet, despite the extensive research that exists substantiating the effects of stressors/chronic stress on human health and disease, there has been little recognition within the “traditional” medical community of such. Patients suffering from stress-related bodily disorders are often left to self-diagnose and self-treat without the knowledge of, consent, or approval from their medical health care provider.

Much of this stems from the fact that the signs and symptoms of HPA axis dysfunction can be subtle and often fall outside the category of true “disease” (both physically and diagnostically). In addition to this, researchers have not agreed upon specific diagnostic and therapeutic end-points by which to evaluate the wide-range of HPA axis disorders.

CHAPTER 8

KEY CONSTITUENTS OF CHILDHOOD DEVELOPMENT

In order to appreciate the effects of adverse childhood experiences, it is important to review the literature on the important contributions to childhood development and the consequences of adverse environments. This is a theoretical review of the literature, it is noted that each individual child has their own unique set of circumstances, environments, genetic makeup and buffering protectors. As previously implied, historically traumatic experiences – especially associated with boarding schools – may have provided a toxic template for parenting and interacting with children.

Emotional Development

From birth, children rapidly develop their abilities to experience and express different emotions, as well as their capacity to cope with and manage a variety of feelings (Saarni,

Mumme & Campos, 1998; Thompson, Lagattuta, 2006; Thompson, 1994). The development of these capabilities occurs at the same time as a wide range of highly visible skills in mobility (motor control), thinking (cognition), and communication (language)

(Thompson, 2001).

Yet, emotional development often receives relatively less recognition as a core emerging

capacity in the early childhood years. The foundations of social competence that are

developed in the first five years are linked to emotional well-being and affect a child’s

later ability to functionally adapt in school and to form successful relationships

throughout life (Collins & Laursen, 1999; Dunn, 1993; Cassidy & Shaver, 1999).

As a person develops into adulthood, these same social skills are essential for the

formation of lasting friendships and intimate relationships, effective parenting, the ability

to hold a job and work well with others, and for becoming a contributing member of a

community (Bercheid & Reis, 1998; Reis, Collins & Bercheid, 2000). Disregarding this

critical aspect of the developing child can lead parents to underestimate its importance

and to ignore the foundation that emotions establish for later growth and development.

Therefore, it is essential that young children’s feelings get the same level of attention as

their thinking. Indeed, learning to manage emotions is more difficult for some children

than learning to count or read and may, in some cases, be an early warning sign of future psychological problems. The failure to address difficulties in this equally important domain can result in missed opportunities for interventions. Had they been initiated early, these interventions could have yielded tremendous benefits for large numbers of children and for society.

The core features of emotional development include the ability to identify and understand one’s own feelings, to accurately read and comprehend emotional states in others, to manage strong emotions and their expression in a constructive manner, to regulate one’s own behavior, to develop empathy for others, and to establish and sustain relationships

(Thompson & Lagattuta, 2006; Denham, 1998; Harris, 1989).

The potential for emotional development is actually built into the architecture of young children’s brains in response to their individual personal experiences and the influences of the environments in which they live. Indeed, emotion is a biologically based aspect of human functioning that is “wired” into multiple regions of the central nervous system that have a long history in the evolution of our species (LeDoux, 2000; Panksepp, 1998;

Panksepp, 2000; Dawson & Fischer, 1994).

These growing interconnections among brain circuits support the emergence of increasingly mature emotional behavior, particularly in the preschool years. Stated another way, as young children develop, their early emotional experiences literally become embedded in the architecture of their brains. The emotional experiences of newborns and young infants occur most commonly during periods of interaction with a caregiver (such as feeding, comforting, and holding) (Thompson, 1998; Denham, 1998; Fogel, 1993).

Infants display distress and cry when they are hungry, cold, wet, or in other ways

85 uncomfortable, and they experience positive emotions when they are fed, soothed, and held. During this early period, children are incapable of modulating the expression of overwhelming feelings, and they have limited ability to control their emotions (LeDoux,

2000). Associations between positive emotions and the availability of sensitive and responsive caregiving are strengthened during infancy in both behavior and brain architecture (Cassidy, 1994).

The emotional states of toddlers and preschoolers are much more complex (Lewis, 2000).

They depend on their emerging capacities to interpret their own personal experiences and understand what others are doing and thinking, as well as to interpret the nuances of how others respond to them (Thompson & Lagattuta, 2006; Banerjee, 1997; Wellman, Harris,

Banerjee, Sinclair, 1995). As they build on foundations that are established earlier, they mature and acquire a better understanding of a range of emotions. They also become more capable of managing their feelings, which is one of the most challenging tasks of early childhood (Thompson, 1994; Eisenberg & Morris, 2002; Buss & Goldsmith, 1998).

By the end of the preschool years, children who have acquired a strong emotional foundation have the capability to anticipate, talk about, and use their awareness of their own and others’ feelings to better manage everyday social interactions (Thompson &

Lagattuta, 2006; Denham, 1998). Their range of emotional responses have expanded

86 dramatically and now include such feelings as pride, shame, guilt, and embarrassment — all of which influence how individuals function as contributing members of a society

(Lewis, 200; Barrett, 1998). Throughout the early childhood years, children develop increasing capacities to use language to communicate how they feel and to gain help without “melting down,” as well as to inhibit the expression of emotions that are inappropriate for a particular setting (Lagattuta & Wellman, 2002).

When feelings are not well managed, thinking can be impaired. Recent scientific advances have shown how the interrelated development of emotion and cognition relies on the emergence, maturation, and interconnection of complex neural circuits in multiple areas of the brain, including the prefrontal cortex, limbic cortex, basal forebrain, amygdala, hypothalamus, and brainstem (Davidson, Lewis, Alloy, Amaral, Bush, Cohen, et al, 2002). The circuits that are involved in the regulation of emotion are highly interactive with those that are associated with “executive functions” (such as planning, judgment, and decision-making), which are intimately involved in the development of problem-solving skills during the preschool years (Posner & Rothbart, 2000). In terms of basic brain functioning, emotions support executive functions when they are well regu- lated but interfere with attention and decision-making when they are poorly controlled

(Shonkoff & Phillips, 2000; Damasio, 1999; Davis, 1992; LeDoux, 1996).

We now know that differences in early childhood temperament — ranging from being extremely outgoing and adventurous to being shy and easily upset by anything new or unusual — are grounded in one’s biological makeup (Rothbart & Bates, 1998; Rothbart,

Derryberry & Posner, 1994). These variations lead to alternative behavioral pathways for young children as they develop individual strategies to control their emotions during the preschool years and beyond. They also present diverse challenges for parents and other adults who must respond differently to different kinds of children. When it comes to finding the “best” approach for raising young children, research indicates that one size does not fit all (Teti & Candelaria, 2002).

Early Experiences and Brain Development

The foundations for brain development are established early in life through a continuous series of interactions in which environmental conditions and personal experiences have a significant impact on how genetic predispositions get expressed (Hensch, 2005; Horn,

2004; Friederici, 2006; Katz & Shatz, 1996; Singer, 1995). Because specific experiences affect specific brain circuits during specific developmental stages—referred to as sensitive periods (Knudsen, 2004; Hess, 1973) - it is vitally important to take advantage of these early opportunities in the developmental building process. That is to say, the quality of a child’s early environment and the availability of appropriate experiences at

88 the right stages of development are crucial in determining the strength or weakness of the brain’s architecture, which, in turn, determines how well he or she will be able to think and to regulate emotions.

Just as in the construction of a house, certain parts of the formative structure of the brain need to happen in a sequence and need to be adequate to support the long-term developmental blueprint. And just as a lack of the right materials can result in blueprints that change, the lack of appropriate experiences can lead to alterations in genetic plans.

Moreover, although the brain retains the capacity to adapt and change throughout life, this capacity decreases with age (Keuroghlian & Knudsen, 2007; Buonomano &

Merzenich, 1998; Karmarkar & Dan, 2006). Thus, building more advanced cognitive social, and emotional skills on a weak initial foundation of brain architecture is far more difficult and less effective than getting things right from the beginning (Knudsen,

Heckman, Cameron, & Shonkoff, 2006)

The exceptionally strong influence of early experience on brain development makes the early years of life a period of both great opportunity and great vulnerability for brain development. An early, growth-promoting environment, with adequate nutrients, free of toxins, and filled with social interactions with an attentive caregiver, prepares the architecture of the developing brain to function optimally in a healthy environment (Tang,

Akers, Reeb, Romeo & McEwen, 2006; Weaver, Cervoni, Champagne, D’Alessio,

Sharma, Seckl, et al., 2004). Conversely, an adverse early environment, one that is inadequately supplied with nutrients, contains toxins, or is deprived of appropriate sensory, social, or emotional stimulation, results in faulty brain circuitry (Grossman,

Churchhill, McKinney, Kodish, Otte & Greenough, 2003; Rice & Barone, 2000; Levitt,

2003). Once established, a weak foundation can have detrimental effects on further brain development, even if a healthy environment is restored at a later age.

The considerable susceptibility of the young, developing brain to the synergistic effects of environment and experience has enormous implications for society. An abundance of scientific evidence clearly demonstrates that critical aspects of brain architecture begin to be shaped by experience before and soon after birth, and many fundamental aspects of that architecture are established well before a child enters school (Hensch, 2005; Kuhl,

2004; Matsuzawa, Tomonoga & Tanaka, 2006).

The development of the brain depends on the mutual influences of genetics, environment, and experience. Genetics supplies a basic plan for brain development, just as an architect supplies a blueprint for building a house. The genetic plan instructs the basic properties of the nerve cells and lays down the basic rules for interconnecting nerve cells within and

90 across circuits. In this manner, genes provide the initial construction plan for the brain’s architecture.

The environment in which the brain begins to develop can have a profound influence on its initial architecture. Just as the selection of the best building materials enables the realization of the full potential of an architect’s blueprint, a healthy environment beginning in the prenatal period allows the full potential of the genetic plan for the brain to be expressed. This includes an abundant supply of nutrients, an absence of toxins, and the healthy personal and social habits of the expectant mother (Tang, Akers, Reeb,

Romeo & McEwen, 2006; Weaver, Cervoni, Champagne, D’Alessio, Sharma, Seckl, et al., 2004).

Conversely, an environment lacking in critical nutrients, or containing toxins that result from unhealthy behaviors such as excessive maternal alcohol intake during pregnancy or lead ingestion in early childhood, can cause neurons to acquire abnormal properties and aberrant connections with other brain cells (Levitt, 2003). In addition, an adverse prenatal environment can actually alter the genetic plan for the brain (Sabatini, Ebert, Lewis,

Levitt, Cameron, Mirnics, 2007; Weaver, Champagne, Brown, Dymov, Sharma, Meany, et al., 2005). These effects of threatening environmental conditions can cause neural

91 circuits to change in ways that prevent them from functioning well, or at all, even in a subsequent healthy environment.

Experience refers to the interaction of a child with his or her environment. In humans, such experience begins before birth, as the fetus senses and responds to the environment of the womb (Center on the Developing Child, 2006). This early experience influences the basic development of low-level circuits that mature at this early stage. After birth, experience plays an increasingly important role in shaping developing neural circuits so that they function optimally for each individual (Knudsen, 2004; Weaver, Cervoni,

Champagne, D’Alessio Sharma, Seckl, et al., 2004; DeBello, Feldman, Knudsen, 2001).

Just as a master carpenter modifies the blueprint for a house to adapt to the needs of its setting and the people who will live in it, experience adjusts the genetic plan for the brain and shapes the architecture of its neural circuits according to the needs and distinctive environment of the individual (Horn, 2004; Majdan & Shatz, 1996). Consequently, healthy and stimulating experience results in brain architecture that operates at its full genetic potential, and persistent adversity leads to weak brain architecture with impaired capabilities.

Early environments and experiences have an exceptionally strong influence on brain development. For most neural circuits, the effects that the environment and individual

experience can exert on their development are particularly potent just as the circuit is

maturing (Knudsen, 2004). As a circuit begins to function, its chemical environment and

the electrical information that it processes can have an enormous impact on that circuit,

causing adjustments in its genetic plan and changing its architecture in fundamental ways.

After most circuits have matured, their genetic plans and architecture can still be

modified by experience, but the extent of these later modifications tends to be far more

limited.

The period of exceptional sensitivity to the effects of environment and experience is

called a sensitive period for that circuit. Because it is far more difficult to alter neural circuits substantially after their sensitive periods have ended, experiences during these sensitive periods play an exceptionally important role in shaping the capacities of the brain. Some examples of behavioral capacities that have been shown to be affected by sensitive periods of underlying circuitry include vision (Katz, & Shatz, 1996; Hubel &

Wiesel, 1977), hearing (Keuroghlian & Knudsen, 2007), language (Newport, Bavelier, &

Neville, 2001) and responses to social cues (Horn, 2004; Knudsen, Heckman, Cameron,

& Shonkoff, 2006).

The increased flexibility of the circuitry in a young, developing brain is explained primarily by three factors. First, during its initial stages of formation, the brain develops

93 far more extensive connections than it needs in order to function optimally, and connections that are not useful are pruned away over time (Katz & Shatz, 1996) Second, the molecular environment and cellular mechanisms that enable the formation of new connections and the elimination of incorrect connections are highly active in a circuit while it is maturing (Knudsen, 2004). Finally, neural circuits are far more flexible before a particular pattern of connections has been shaped and fully activated (Hensch, 2005).

Consequently, once a particular circuitry pattern becomes established, it is difficult for the effects of new and different experiences to alter that architecture (Feldman, 2000;

Zheng & Knudsen, 2001) This means that early experience has a unique advantage in shaping the developing brain circuits before they are fully mature and stabilized. Changes to nerve cells, or neurons, and establishing pathways that connect neurons is referred to as “plasticity.”

Even within a single hierarchy—such as visual, auditory, or language development— different neural circuits mature at different times. Circuits that process lower-level information mature earlier than those that process higher-level information (Burkhalter,

Bernardo, & Charles, 1993). For example, in the neural hierarchy that analyzes visual information, low-level circuits that analyze color, shape, or motion are fully mature long before the higher-level circuits that interpret complex stimuli, such as facial expressions, or identify meaningful inputs such as frequently used objects (Pascalis, de Haan, &

Nelson, 2002; Scherf, Behrmann, Humphreys, & Luna, 2007). For the developing brain, this means that the ability to perceive simple aspects of the world and to make simple emotional and social judgments develops long before the ability to make sophisticated, cognitive analyses (Kuhl, 2004 & Thompson, 2001) Stated simply, children’s ability to interpret what they see changes over time as their brain circuitry is built. As an example, it is important that experiences provided in the earliest years are appropriate for the young child’s stage of development. Reading a picture book with a toddler who is learning to speak, for example, provides an important opportunity to point to and talk about the pictures, not to focus on the written words. The ability to decode written language comes later, when the appropriate, higher-level brain circuitry will be built.

Stressful experiences during sensitive periods alter the function and architecture of specific neural circuits, as these circuits adapt their functional properties to the adversity that has been experienced (Knudsen, 2004; Keuroghlian & Knudsen, 2007; Daw, 1997).

As shown by experiments in which animals have been subjected to significant stress, when the adverse conditions last through the end of a circuit’s sensitive period, the changes in the circuit’s development become stable and tend to persist in the adult brain

(Linkenhoker, von der Ohe, & Knudsen, 2005; Antonini, Fagiolini, & Stryker, 1999).

Subsequently, although the brain’s residual capacity for plasticity can mitigate the adverse effects of the altered circuit architecture (Keuroghlian, & Knudsen, 2007) the affected neural circuits do not process information as well as they could have if the animal had been exposed to an appropriate experience during the sensitive period. The degraded information that is transmitted by the altered neural circuit can prevent high- level circuits from receiving the information they need to shape their architectures optimally, even after a rich environment has been restored later in life.

Brain plasticity continues throughout life. Neural circuits, particularly those that are specialized for learning, continue to adapt their architecture in response to experience throughout the adult years (Keuroghlian & Knudsen, 2007; Buonomano & Merzenich,

1998). Even circuits that pass through sensitive periods maintain a degree of flexibility that allows them to adapt their architecture, at least partially, to experience in adulthood

(Karmarkar & Dan, 2006; Bergan, Ro, Ro, & Knudsen, 2005). The plasticity of many of these circuits in adult animals can be enhanced significantly by intentionally drawing attention to the information that is being processed by the circuit (Keuroghlian &

Knudsen, 2007).

The residual capacity for plasticity in mature neural circuits thus allows for some recovery of brain capabilities, even in adults. In order for the brain to take full advantage

96 of this plasticity, experience needs to be tailored to activate the relevant neural circuits and the individual’s attention must be engaged in the task (Grossman, Churchhill,

McKinney, Kodish, Otte, & Greenough, 2003). The implications for later interventions in development are clear—the task will be harder, more expensive in terms of societal and individual effort, and potentially less extensive and durable.

Relationship Development

Healthy development depends on the quality and reliability of a young child’s relationships with the important people in his or her life, both within and outside the family. Even the development of a child’s brain architecture depends on the establishment of these relationships (Berscheid & Reis, 1998; Collins & Laursen, 1999;

Dunn, 1993). Growth-promoting relationships are based on the child’s continuous give- and-take (a “serve and return” interaction) with a human partner who provides what nothing else in the world can offer – experiences that are individualized to the child’s unique personality style; that build on his or her own interests, capabilities, and initiative; that shape the child’s self-awareness; and that stimulate the growth of his or her heart and mind.

Young children experience their world as an environment of relationships, and these relationships affect virtually all aspects of their development - intellectual, social, emotional, physical, behavioral, and moral. The quality and stability of a child’s human relationships in the early years lay the foundation for a wide range of later developmental outcomes that really matter – self-confidence and sound mental health, motivation to learn, achievement in school and later in life, the ability to control aggressive impulses and resolve conflicts in nonviolent ways, knowing the difference between right and wrong, having the capacity to develop and sustain casual friendships and intimate relationships, and ultimately to be a successful parent oneself.

Stated simply, relationships are the “active ingredients” of the environment’s influence on healthy human development. They incorporate the qualities that best promote competence and well-being – individualized responsiveness, mutual action-and-interaction, and an emotional connection to another human being, be it a parent, peer, grandpar- ent, aunt, uncle, neighbor, teacher, coach, or any other person who has an important impact on the child’s early development. Relationships engage children in the human community in ways that help them define who they are, what they can become, and how and why they are important to other people (Bornstein, 2002; Cassidy & Shaver, 1999;

Cochran, Larner, Riley, Gunnarsson, & Henderson, 1990; Fogel, 1993).

Nurturing and stable relationships with caring adults are essential to healthy human development beginning from birth. Early, secure attachments contribute to the growth of a broad range of competencies, including a love of learning, a comfortable sense of “self”, positive social skills, multiple successful relationships at later ages, and a sophisticated understanding of emotions, commitment, morality, and other aspects of human relationships. Stated simply, establishing successful relationships with adults and other children provides a foundation of capacities that children will use for a lifetime (Belsky

& Cassidy, 1994; Thompson, 1999; Thompson, 2000).

The “give-and-take” interaction between parent and baby – in which young children naturally reach out for interaction through babbling, facial expressions, and gestures and adults respond with the same kind of vocalizing and gesturing back at them – builds and strengthens brain development and creates a relationship in which the baby’s experiences are affirmed and new abilities are nurtured. Children who have healthy relationships with their primary caregivers are more likely to develop insights into other people’s feelings, needs, and thoughts, which form a foundation for cooperative interactions with others and an emerging conscience. Sensitive and responsive parent-child relationships also are associated with stronger cognitive skills in young children and enhanced social competence and work skills later in school, which illustrates the connection between social/emotional development and intellectual growth. The broader quality of the home

99 environment (including toys, activities, and interactions within the family setting) also is strongly related to early cognitive and language development, and achievement in school

(Shonkoff & Phillips, 2000; Bradley, Caldwell, Rock & Ramey, 1989; Bradley, Caldwell,

& Rock, 1988; Estrada, Arsenio, Hess & Holloway, 1987).

Young children also learn a great deal from each other. They learn how to share, to engage in reciprocal interactions (e.g., taking turns, giving and receiving), to take the needs and desires of others into account, and to manage their own impulses. Just being around other children, however, is not enough. The development of friendships is essential, as children learn and play more competently in the rapport created with friends rather than when they are dealing with the social challenges of interacting with casual acquaintances or unfamiliar peers (Rubin, Bukowski & Parker, 1998; Rose-Krasnor,

1997)

The warmth and support of the caregiver in a child care setting also influence the development of important capabilities in children, including greater social competence, fewer behavior problems, and enhanced thinking and reasoning skills at school age.

Young children benefit in these ways because of the secure relationships they develop in such settings, and because of the ways in which the caregivers provide cognitively stimulating activities and support for developing positive relationships with other

100 children. Current research also suggests the additional risk that a greater amount of time in out-of-home care during infancy may be associated with greater disobedience and aggression by the time children enter school (Shonkoff & Phillips, 2000; Peisner-

Feinberg, Burchinal, Clifford, Culkin, Howes, et al., 2000; Pianta, Nimetz, & Bennett,

1997’ Lamb, 1998).

Relationships are important to school adjustment. Children who develop warm, positive relationships with their kindergarten teachers are more excited about learning, more positive about coming to school, more self-confident, and achieve more in the classroom.

Relationships with peers also are important. Children who experience greater peer acceptance and friendship tend to feel more positively about the school experience and perform better in the classroom (Pianta, 1999; Birch & Ladd, 1997; Ladd, Birch, & Buhs, 1999;

Ladd, Kochenderfer, & Coleman, 1996).

Secure and stable relationships with caring adults assure that young children are adequately nourished; protected from dangerous illnesses, exposure to toxins, and hazards that can lead to preventable injuries; provided preventive health check-ups; protected from excessive stress; and afforded predictable daily routines that convey a sense of security. These influences contribute significantly to healthy brain development and depend upon the care and support provided by individuals in the community as well as in

101 the family (Shonkoff & Phillips, 2000; Gunnar, Broderson, Nachmias, Buss, & Rigatuso,

1996).

Young children are highly vulnerable emotionally to the adverse influences of parental mental health problems and family violence. One of the most extensively documented of these vulnerabilities is the negative impact of a mother’s clinical depression on her young children’s emotional development, social sensitivity, and concept of themselves, effects that have been demonstrated in both developmental research and studies of brain functioning. Young children who grow up in seriously troubled families, especially those who are vulnerable temperamentally, are prone to the development of behavioral disorders and conduct problems (Dawson, & Ashman, 2000; Dawson, Frey, Panagiotides,

Yamada, Hessl, & Osterling, 1999; Shaw, Gilliom, Ingoldsby, & Nagin, 2003; Shaw,

Owens, Giovannelli, & Winslow, 2001).

Animal studies have shown that the quality of the mother-infant relationship can influence gene expression in areas of the brain that regulate social and emotional function and can even lead to changes in brain structure. The nature of the relationship also can have long-term influences (into adulthood) on how the body copes with stress, both physically and emotionally (Champagne, Francis, Mar, & Meaney, 2003; Meaney, 2001;

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Liu, Diorio, Tannenbaum, Caldji, Francis, Freedman, Sharms, Pearson, Plotsky, &

Meaney, 1997; & Leiderman, 1981).

The quality of early parent-child relationships can be strengthened, but successful interventions are more difficult to achieve when relationships are significantly troubled or disturbed. Preventive interventions also can produce a variety of positive outcomes, depending on the extent to which the knowledge and skills of the staff and the quality of the implementation are matched to the magnitude of the challenges being addressed

(Shonkoff & Phillips, 2000; Brooks-Gunn, Berlin, & Fuligni, 2000; Campbell, Ramey,

Pungello, Sparling, & Miller-Johnson, 2002; Currie, 2000)

Unfortunately, sometimes because of traumatic experiences, and cultural conflict, the formation of peer, maternal and familial relationships do not adequately materialize in the early years of a child’s life.

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CHAPTER 9

THE IMPACT OF TRAUMA

Initial Impact of Historical Trauma

Two major factors influence the intial impact of historical trauma: post-traumatic stress disorder and maternal depression.

Post-traumatic Stress Disorder

Numerous definitions of trauma and lifetime stressors are used within the various mental health related disciplines. Regular life stressors (e.g., loss of a job), although taxing, are considered ordinary and expected experiences in a typical life. Traumatic events, on the other hand, are outside the normal range of an individual’s experience and constitute, for that individual, an exceptional mental and physical stressor (Kessler, Sonnega, Bromet,

Hughes, & Nelson, 1995). Of importance, there is considerable variability in individual responses to potentially traumatic events and exposure does not necessarily trigger symptoms of dysfunction. Symptomology may be seen in one person after a relatively minor stressor, whereas in another person exposure to a major traumatic event may trigger only mild distress (Zuckerman, 1999). Many individuals

104 also report emotional and spiritual growth after dealing with a traumatic event (Ai,

Cascio, Santengelo, & Evans-Campbell, 2005).

Dysfunctional reactions to traumatic events are often understood through the diagnostic category of PTSD. Although PTSD was developed as a way to understand negative reactions to lifetime traumatic events in an individual, it is nevertheless commonly relied on by professionals and scholars in exploring reactions to a range of lifetime and historical or intergenerational events. According to the fourth edition text revision of the

Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric

Association, 2000), those who have experienced or witnessed an event involving actual or threatened death or serious injury and have responded with feelings of fear, helplessness, or horror may develop PTSD symptoms. These symptoms include intrusion

(e.g., dreams, thoughts that remind one of the event), detachment, avoidance, and hyperarousal (e.g., difficulty sleeping, irritability) and meet the criteria for PTSD if experienced for at least 1 month. The disorder is also associated with impairment in a person’s ability to function in typical social or family situations, feelings of helplessness, survival guilt, and feelings of being under threat. Events most often associated with

PTSD include rape, combat exposure, child maltreatment, physical attack, and being threatened with a weapon (National Center for Post-Traumatic Stress Disorder, 2006).

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This list is limited, scholars of historical trauma often cite PTSD symptoms in describing the impact of genocidal assaults (Smith, 2003).

Although individual responses vary tremendously, it is widely believed that the scope and intensity of trauma reactions are related to the severity and duration of the traumatic experience. Events that involve death or injury and long lasting events are associated with significantly higher levels of related stress (American Psychiatric Association, 2000).

Higher levels of PTSD symptomology have also been linked to events that are viewed as uncontrollable or unpredictable (National Center for Post-Traumatic Stress Disorder,

2006), involve separation from family during the event (Stevens & Slone, 2007), or are human initiated (Marmar,Weiss, & Metzler, 1998). At the individual level, traumatic stressors are generally categorized as either acute or chronic. Acute stressors occur only one time and do not include instances of physical or sexual abuse. Chronic stressors include ongoing or multiple stressors and/or incidents of physical or sexual abuse

(Kahana et al., 1997). Fletcher (1996) compared responses to both types of stressors and found that chronic or abusive stressors were associated with significantly higher levels of avoidance, numbing, trying to forget, and regressive behaviors. Conversely, those experiencing acute stressors reported more intrusive memories, somatization, and hypervigilance.

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Clearly, the historical context of AIANs includes a range of events that can be classified as both acute and chronic stressors, and responses to such stressors may include PTSD symptomology. These classifications, however useful, have important limitations for understanding AIAN health and wellness. First, they were not developed to address intergenerational trauma and do not adequately speak to the possibly compounding nature of responses to multiple stressors. Second, their focus remains on the individual and does not address the familial and social impacts of trauma reactions. Exploring these other levels is particularly important in AIAN communities, in which members tend to have strong social and family affiliations. Third, such categories do not explore the ways that historical and contemporary traumas interact or how a present-day trauma might be interpreted within the context of historical events. And fourth, work examining the factors that buffer the impact of traumatic events is still limited. To address these concerns, researchers need to begin building on traditional conceptions of trauma to explore the experiences of people from communities that have endured multiple traumatic events across generations.

Maternal Depression

Serious depression in parents and caregivers can affect and influence the well-being of the children in their care. Because chronic and severe maternal depression has potentially

107 far-reaching harmful effects on families and children, its widespread occurrence can undermine the future prosperity and well-being of society as a whole. When children grow up in an environment of depression and mental illness, the development of their brains may be seriously weakened, with implications for their ability to learn as well as for their own later physical and mental health. When interventions are not available to ensure mothers’ well-being and children’s healthy development, the missed opportunities can be substantial.

Healthy development depends on the interactive influences of genes and experiences, which shape the architecture of the developing brain. The active ingredient of those experiences can be described as mutual responsiveness of young children’s interactions with adult caregivers. For example, when an infant babbles and an adult responds appropriately with attention, gestures, or speech, this builds and strengthens connections in the child’s brain that support the development of communication and social skills.

When caregivers are sensitive and responsive to a young child’s signals, they provide an environment rich in serve and return experiences, like a good game of tennis or Ping-

Pong. However, if depression interferes with the caregiver’s ability to regularly provide such experiences, these connections in the child’s brain may not form as they should. The difference between a child who grows up in a responsive environment and one who does

108

not can be the difference between the development of strong or weak brain development,

which serves as a foundation for the learning, behavior, and health that follow.

In addition, as previously discussed, relationships are important, especially the

relationship of the mother and child. It is my contention that the primary impact of

Historical Trauma has been PTSD and the subsequent depression that has followed.

Because of PTSD, mothers were incapable of caring for their children. These children did

not have adequate parental role models and the opportunity to form strong relationships

with their caregivers, siblings and peers.

Chronic depression can manifest itself in two types of problematic parenting patterns that

disrupt the “serve and return” interaction between and child and caregiver that is essential

for healthy brain development: hostile or intrusive, and disengaged or withdrawn

(Lovejoy, Graczyk, O’Hare, & Neuman, 2000). When parents are hostile and/or intrusive, it is as if the parent is “serving” the ball in ways that make it difficult for the child to

“return.” Conversely, if a parent is withdrawn or disengaged, the child may serve the ball, but the parent doesn’t return it. In both cases, depressed mothers are less likely to respond to their infants’ cues (i.e., vocalizations and actions) or to engage with their infants and young children in positive, harmonious interactions (Field, Pickens, Prodromidis,

Malphurs, Kox, & Bendell, 2000; Gladstone, & Beardslee, 2002).

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When caregivers are hostile or withdrawn for prolonged periods of time, the game of serve and return falls apart, and the architecture of the developing brain may be affected adversely. Such patterns are particularly worrisome because, once negative parent-child interactions are established, they may persist even after a mother’s depression has improved and may make the child more likely to have negative interactions with other important adults, as well (Seifer, Dickstein, Sameroff, Magee, & Hayden, 2001; Tronick,

& Reck, 2009). When infants and young children interact with a hostile, irritable caregiver, this creates feelings of fear and anxiety in the child, which may result in the increased production of cortisol, a potentially harmful stress hormone (Dawson &

Ashman, 2000). Such a recurring physiological reaction can affect brain development, interfere with young children’s ability to learn, and increase the risk of emotional disorders (Dawson, Frey, Panagiotides, Osterling, & Hessl, 1997).

Children who experience maternal depression early in life may experience lasting effects on their brain architecture and persistent disruptions of their stress response systems.

These patterns are more pervasive when the mother is both depressed and withdrawn from her infant (Diego, Field, Jones, & Hernandez-Reif, 2006) and when deep depression occurs during the child’s second and third year, the time at which the brain systems that generate the depression-associated pattern of the brain is developing rapidly (Dawson &

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Ashman, 2000). Living with a depressed mother may also shape the development of a

child’s stress biology (Ronsaville, Municchi, Laney, Cizza, Meyer, & Haim, 2006).

Indeed, there is increasing evidence that effects on stress response systems are one mech-

anism linking maternal depression to the child’s own risk of developing depression and

other emotional disorders (Gump, Reihman, Stewart, Lonky, Darvill, Granger, &

Matthews, 2009; Halligan, Herbert, Goodyer, & Murray, 2007). When mothers are de-

pressed, both early in a child’s life and later, their children tend to produce higher and

more fluctuating levels of stress chemicals like cortisol (Essex, Klein, Cho, & Kalin,

2002; Halligan, Herbert, Goodyer, & Murray, 2004). Chronic maternal depression over

many years of a child’s life also predicts cardiovascular patterns suggestive of emergent

hypertension in childhood and abnormal stress chemical patterns in response to

laboratory testing (Gump, Reihman, Stewart, Lonky, Darvill, Granger, & Matthews,

2009).

Maternal depression may begin to affect brain development in the fetus before birth.

Depressed women produce higher levels of stress chemicals during pregnancy, which reduce fetal growth and are associated with an increased risk for premature labor (Diego,

Field, Hernandez-Reif, Schandberg, Kuhn, & Gonzalez-Quintero, 2009). Depressive symptoms in an expectant mother also have been shown to be associated with altered

111 immune functioning in her baby after birth (Mattes, McCarthy, Gong, van Eckelen,

Dunstan, & Foster, 2009). It has been found that the most pervasive neurobiological effect of maternal gestational stress is dysregulation of the offspring’s HPA axis, which results in elevated baseline cortisol levels and exaggerated cortisol responses to stress. A longitudinal study found that the intensity of the mother’s anxiety during gestation was positively correlated with the elevation of the child’s awakening cortisol levels at age 10 years (O’Conner, Heron, Golding, et al, 2002).

Elevated basal cortisol and cortisol hyper-responsiveness constitute a vulnerability to anxiety disorders, personality disorders, and addictive disorders (Huizink, Mulder, &

Buitelaar, 2004). In addition, recent research has found that prenatal depression can be linked to the silencing of a gene that controls the over-production of stress chemicals

(Oberlander, Weinberg, Papsdorf, Grunau, Misri, & Devlin, 2008). Thus, by the time of birth, the infant of a seriously depressed mother may have sustained effects on his or her stress response and immune systems that make the child even more vulnerable than average to irritable, intrusive, or withdrawn maternal care.

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Making the Connection from Historical Trauma to Toxic Stress

Types of Stress: Toxic, Tolerable and Positive

The following are descriptions for three types of stress that the National Scientific

Council on the Developing Child has identified based on available research (NSCDC,

2007):

Toxic stress refers to strong, frequent or prolonged activation of the body’s stress

management system. Stressful events that are chronic, uncontrollable, and/or

experienced without the child having access to support from caring adults tend to

provoke these types of toxic stress responses. Studies indicate that such stress re-

sponses can have an adverse impact on brain architecture. In the extreme, such as

in cases of severe, chronic abuse, toxic stress may result in the development of a

smaller brain. Less extreme exposure to toxic stress can change the stress system

so that it responds at lower thresholds to events that might not be stressful to oth-

ers, thereby increasing the risk of stress-related physical and mental illness.

Tolerable stress refers to stress responses that could affect brain architecture but

generally occur for briefer periods that allow time for the brain to recover and

113 thereby reverse potentially harmful effects. In addition to their relative brevity, one of the critical ingredients that make stressful events tolerable rather than toxic is the presence of supportive adults who create safe environments that help children learn to cope with and recover from major adverse experiences, such as the death or serious illness of a loved one, a frightening accident, or parental separation or divorce. In some circumstances, tolerable stress can even have positive effects. Nevertheless, it also can become toxic stress in the absence of supportive relationships.

Positive stress refers to moderate, short-lived stress responses, such as brief increases in heart rate or mild changes in the body’s stress hormone levels. This kind of stress is a normal part of life, and learning to adjust to it is an essential feature of healthy development. Adverse events that provoke positive stress responses tend to be those that a child can learn to control and manage well with the support of caring adults, and which occur against the backdrop of generally safe, warm, and positive relationships. The challenge of meeting new people, dealing with frustration, entering a new child care setting, getting an immunization, and overcoming a fear of animals all can be positive stressors if a child has the support needed to develop a sense of mastery. This is an important part of the normal developmental process.

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Scientific knowledge in this area comes from research on animals as well as humans.

These extensive bodies of work have generated common principles of developmental biology that support valid generalizations across species and reasonable hypotheses about humans based on consistent findings from animal studies. The ability to control exposure to negative life experiences in animals makes it additionally possible to conduct studies of the impacts of more graded forms of stress on the brain than could be done in human research. The capacity to deal with stress is controlled by a set of highly inter-related brain circuits and hormonal systems that are specifically designed to deal adaptively with environmental challenges. When an individual feels threatened, stress hormones are produced that convert the physical or emotional stress into chemical signals that are sent throughout the body as well as to the brain.

The neural circuits for dealing with stress are particularly malleable (or “plastic”) during the fetal and early childhood periods. Early experiences shape how readily they are activated and how well they can be contained and turned off. Toxic stress during this early period can affect developing brain circuits and hormonal systems in a way that leads to poorly controlled stress-responsive systems that will be overly reactive or slow to shut down when faced with threats throughout the lifespan (Loman, & Gunnar, 2010).

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Well-functioning brain systems that respond to stress are essential to preserve life.

However, like the immune system, which defends the body against threatening infections but can cause autoimmune disease when it turns against the body’s own cells, a poorly controlled response to stress can be damaging to health and well-being if activated too often or for too long (McEwen, 2008).

Frequent or sustained activation of brain systems that respond to stress can lead to heightened vulnerability to a range of behavioral and physiological disorders over a lifetime.

These undesirable outcomes can include a number of stress-related disorders affecting both mental (e.g., depression, anxiety disorders, alcoholism, drug abuse) and physical

(e.g., cardiovascular disease, diabetes, stroke) health (McEwen, 2008).

Stress responses include activation of a variety of hormone and neurochemical systems throughout the body. Two hormonal systems have received extensive attention in this regard: 1) the sympathetic-adrenomedullary (SAM) system, which produces adrenaline in the central part of the adrenal gland, and 2) the HPA-axis system, which produces cortisol in the outer shell of the adrenal gland (Sapolsky, Romero, & Munck, 2000). Both chemicals are produced under normal circumstances and help prepare the body for coping with stressors.

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Adrenaline production occurs in response to many forms of acute stress. It mobilizes energy stores and alters blood flow, thereby allowing the body to effectively deal with a range of stresses. Its release is essential to survival (Sapolsky, Romero, & Munck, 2000).

Cortisol also is produced in response to many forms of stress, and likewise helps the body cope effectively with adverse situations. It also mobilizes energy stores, as well as suppresses immune responses, when it is released acutely. Longer- term effects of cortisol include regulation of gene expression in neural circuits involved in modulating stress responsiveness, emotion, and memory (Sapolsky, Romero, & Munck, 2000).

Sustained or frequent activation of the hormonal systems that respond to stress can have serious developmental consequences, some of which may last well past the time of stress exposure. For example, when children experience toxic stress, their cortisol levels remain elevated for prolonged periods of time. Both animal and human studies show that long- term elevations in cortisol levels can alter the function of a number of neural systems, and even change the architecture of regions in the brain that are essential for learning and memory (Lupien, de Leon, Santi, Convit, Tarshish, Nair, Thakur, McEwen, Hauger, &

Meaney, 1998; McEwen, & Sapolsky, 1995).

Increases in the level of cortisol in the brain actually can turn specific genes “on” or “off” at specific times and locations (De Kloet, Rots, & Cools, 1996). Examples include

117 regulation of the glucocorticoid receptor gene, which affects the long-term responsiveness of the brain to stress-induced cortisol release, and the myelin basic protein gene, which is involved in regulating the development of the “insulation” that increases the efficiency of nerve signal transmission (Gunnar & Vazquez, 2006; Weaver, Diorio,

Seckl, Szyf, & Meaney).

High, sustained levels of cortisol or corticotropin-releasing hormone (CRH), which is the brain chemical that regulates the HPAsystem, result in damage to a part of the brain called the hippocampus. This can lead to impairments in learning, memory, and the ability to regulate certain stress responses in both young and adult animals (Brunson,

Grigoriadis, Lorang, & Baram, 2002).

Significant maternal stress during pregnancy and poor maternal care during infancy both affect the developing stress system in young animals and alters genes that are involved in brain development. Pregnant females who experience exceptionally high levels of stress have offspring that are more fearful and more reactive to stress themselves. Young animals that experience inattentive maternal care have similar problems and show impaired production of brain growth factors important for brain development and repair

(Roceri, Cirulli, Pessina, Peretto, Racagni, & Riva, 2004; Roceri, Hendriks, Racagni, &

Riva, 2002). Both groups of animals also have impaired memory and learning abilities,

118 and they experience more aging-related memory and cognitive deficits in adulthood

(McEwen, 2008; Weinstock, 2001).

Positive experiences after infancy in young animals, such as being exposed to an environment rich in opportunities for exploration and social play, have been shown to compensate to some degree for the negative behavioral consequences of prenatal stress and postnatal neglect. This compensation actually involves adaptive changes in both the architecture and the chemistry of the developing brain (such as reversal of the effects of mild adversity on stress hormone output), although deprivation-induced changes in some of the regulatory components of the stress system (e.g., reduced glucocorticoids receptors in the hippocampus) are more resistant to change (Francis, Diorio, Plotsky, & Meaney,

2002).

Individual responses to early stressful experiences can vary dramatically. This variability is thought to be related to differences among animals in the expression of so-called

“vulnerability genes,” which make it more likely that early stressors will lead to subsequent problems in stress hormone regulation and behavioral difficulties. In such cases, positive early caregiving can decrease the likelihood of these adverse outcomes, demonstrating that beneficial environmental influences can moderate the impact of

119 genetic vulnerability (Barr, Newman, Lindell, Shannon, Champoux, Lesch, Suomi,

Goldman, & Higley, 2004).

The relationships children have with their caregivers play critical roles in regulating stress hormone production during the early years of life. Those who experience the benefits of secure relationships have a more controlled stress hormone reaction when they are upset or frightened. This means that they are able to explore the world, meet challenges, and be frightened at times without sustaining the adverse neurological impacts of chronically elevated levels of hormones such as cortisol that increase reactivity of selected brain systems to stress and threat. In contrast, children whose relationships are insecure or disorganized demonstrate higher stress hormone levels when they are even mildly frightened. This results in an increased incidence of elevated cortisol levels which may alter the development of brain circuits in ways that make some children less capable of coping effectively with stress as they grow up (Loman, & Gunnar, 2010).

Research has shown that the presence of a sensitive and responsive caregiver can prevent elevations in cortisol among toddlers, even in children who tend to be temperamentally fearful or anxious (Nachmias, Gunnar, Mangelsdorf, Parritz, & Buss, 1996). Thus, sensitive and responsive caregiving from a parent or a child care provider can serve as a

120 powerful buffer against stress hormone exposure, even in children who might otherwise be highly vulnerable to stress-system activation.

The quality of the early care and education that many young children receive in programs outside their homes also plays an important role in whether (and to what extent) their brains are exposed to elevated stress hormones early in life. For example, toddlers and young preschoolers show increases in cortisol as the child care day progresses, while older preschoolers and school-aged children can manage long hours in care without activating their stress system (Vermeer, & van IJzendoorn, 2006). Young children in poorer quality child care show larger elevations, however, than those in better quality care (Gunnar, Kryzer, VanRyzin, & Phillips, 2010).

Children who grow up in families facing economic hardship commonly exhibit elevated cortisol levels. These elevations are often exacerbated when mothers experience symptoms of depression (Essex, Klein, Cho, & Kalin, 2002; Lupien, King, Meaney, &

McEwen, 2000, Lupien, King, Meaney, & McEwen, 2001). Recent research also has demonstrated that a mother’s depression during her child’s early years increases the child’s cortisol reactions to adverse family conditions later in childhood (Dawson &

Ashman, 2000; Ashman, Dawson, Panagiotides, Yamada, & Wilkins, 2002; Jones, Field,

& Fox, 1997).

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Young children who are neglected or maltreated have abnormal patterns of cortisol production that can last even after the child has been moved to a safe and loving home

(Gunnar, Morrison, Chisholm, & Schuder, 2001; Bruce, Fisher, Pears, & Levine, 2009).

This is especially true for children who show symptoms of post-traumatic stress, even if their behavior is not sufficient to warrant a definitive diagnosis of post-traumatic stress disorder (Carrion, Weems, Ray, Glaser, Hessl, & Reiss, 2002; De Bellis, Baum, Birmaher,

Keshavan, Eccard, Boring, Jenkins, & Ryan, 1999).

Impact of Fear and Anxiety

Ensuring that young children have safe, secure environments in which to grow, learn, and develop healthy brains and bodies is not only good for the children themselves but also builds a strong foundation for a thriving, prosperous society. Research shows that early exposure to circumstances that produce persistent fear and chronic anxiety can have lifelong consequences by disrupting the developing architecture of the brain.

Unfortunately, many young children are exposed to such circumstances. While some of these experiences are one-time events and others may reoccur or persist over time, all of them have the potential to affect how children learn, solve problems, and relate to others.

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All children experience fears during childhood, including fear of the dark. These fears are normal aspects of development and are temporary in nature. In contrast, threatening circumstances that persistently elicit fear and anxiety predict significant risk for adverse long-term outcomes from which children do not recover easily. Physical, sexual, or emotional abuse; significant maltreatment of one parent by the other; and the persistent threat of violence in the community are examples of such threatening circumstances in a child’s environment.

Studies show that experiences like abuse and exposure to violence can cause fear and chronic anxiety in children and that these states trigger extreme, prolonged activation of the body’s stress response system. In studies with animals, this type of chronic activation of the stress system has been shown to disrupt the efficiency of brain circuitry and lead to both immediate and long-term physical and psychological problems. This is especially true when stress-system overload occurs during sensitive periods of brain development.

While much of the evidence for the effects of stress on the development of brain architecture comes from animal studies, strong similarities in the processes of brain development across species indicate that experiences of persistent fear and chronic anxiety likely exert similarly adverse impacts on the developing brain in humans. Thus, stress-system overload can significantly diminish a child’s ability to learn and engage in typical social interactions across the lifespan.

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Many medical professionals and educators are unaware of the potentially significant, long-term risks of exposure to fear-provoking circumstances in children and lack information about the prevalence of these situations in their communities. Critically, 1 in every 7 children, and nearly 1 out of every 40 infants, in the United States experience some form of maltreatment, including chronic neglect or physical, emotional, or sexual abuse (Finkelhor, Ormrod, Turner, & Hamby, 2005; USDHHS, 2009). Child maltreatment has been shown to occur most often in families that face excessive levels of stress, such as that associated with community violence, parental drug abuse, or significant social isolation (CDC, 2009). Research also tells us that nearly half of children living in poverty witness violence, or are indirectly victims of violence (Finkelhor, Ormrod,

Turner, & Hamby, 2005). Clearly, for children in these circumstances, the frequent and repetitive threats around them create the potential for heightened fear and chronic anxiety.

Behavioral neuroscience research with animals indicate that serious, fear-triggering experiences elicit physiological responses that affect the architecture of the brain as it is developing. These experiences cause changes in brain activity and have been shown to have long-term, adverse consequences for learning, behavior, and health. The timely implementation of such interventions can prevent and treat the harmful effects of exposure to extreme, fear-eliciting circumstances. In addition to these preventive

124 measures, there also are effective treatments for children experiencing high levels of anxiety or chronic fear that result from serious emotional trauma. Despite this rapidly increasing knowledge base, however, significant gaps continue to exist in how society responds to the developmental needs of children who regularly experience serious, fear- inducing events.

Some types of fear are normal aspects of development. Infants begin to experience feelings of fear and differentiate them from other emotions between 6 and 12 months of age

(Lewis, & Michalson, 1983; Nelson, & Da Haan, 1996). Over the course of the early childhood period, toddlers and preschoolers typically express fear of a wide variety of events or individuals. For example, it is not unusual for a young child to react with wariness or distress when greeted by an unfamiliar adult. Such responses are often called

“stranger anxiety” and typically first emerge at around 9 or 10 months of age. This hesitancy toward unfamiliar people generally continues throughout childhood, but diminishes over time, as children’s social worlds expand and they interact with increasing numbers of caregivers, relatives, neighbors, and other familiar adults.

Later in early childhood, it is common for children to express fear of both imagined and real circumstances. The emergence and development of imagination, for example, may lead to fear of monsters or the dark. These reactions are typical and usually peak between

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4 and 5 years of age. Generally speaking, normal preschool fears do not disrupt a child’s life, and they dissipate by age 7 or 8. That is, while children may express these fears at certain times (e.g., bedtime) or in response to certain events (e.g., being surprised by a clown at a birthday party), their overall behavior does not otherwise suggest that they are generally fearful or distressed.

Scientific research provides an explanation for why children outgrow these normative fears. Many fears are a result of the difficulty young children have in distinguishing between the real and the imaginary. As they get older, children get better at understanding what is real and what it means for something to be “make believe.” At the same time, they develop a growing sense of control and predictability over their immediate environment, so that even very young children are less frightened by events if they have some control over them. For example, a toy that scares 12-month-olds because it is loud and unpredictable will elicit less fear if the children are shown how to turn it on and off and are allowed to do so (Gunnar-von Gnecheten, 1978). As they get older, children develop the cognitive and social skills needed to better understand predictability in their environment and, therefore, gain a greater sense of control. As these developmental capacities are mastered, many of the normal fears of childhood begin to disappear. Thus, the emergence and course of typical childhood fears are different from the fears and anxiety elicited by traumatic situations such as physical or sexual abuse or

126 exposure to violence: While typical fears disappear with age, the fear and anxiety elicited by maltreatment and other threatening circumstances do not.

Early exposure to extremely fearful events affects the developing brain, particularly in those areas involved in emotions and learning. A large and growing body of research, including animal studies as well as recent neuroimaging studies of human adults, has revealed insights into the brain circuitry that underlies how we learn to be afraid (Phelps,

& LeDoux, 2005; Degado, Olsson, & Phelps, 2006) and how we come to associate a specific event or experience with negative outcomes (LeDoux, 2000; LeDoux & Phelps,

2008). Two extensively studied structures located deep in the brain—the amygdala and the hippocampus— are involved in fear conditioning (LeDoux, 2000; LeDoux & Phelps,

2008). The amygdala detects whether a stimulus, person, or event is threatening (LeDoux,

2000; LeDoux & Phelps, 2008) and the hippocampus links the fear response to the context in which the aversive stimulus or threatening event occurred (Kim, & Fanselow,

1992). Studies also show that both the amygdala and the hippocampus play an important role in how the body then responds to this threat. Elevated stress hormones such as cortisol have been shown to affect the growth and performance of the hippocampus and the activity of the amygdala in rodents and non-human primates, and early and persistent activation of the stress response system adversely affects brain architecture in these critical regions.

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Beyond its impact on these two brain structures, heightened stress has also been shown in animals to impair the development of the prefrontal cortex, the brain region that, in humans, is critical for the emergence of executive functions—a cluster of abilities such as making, following, and altering plans; controlling and focusing attention; inhibiting impulsive behaviors; and developing the ability to hold and incorporate new information in decision-making. These skills become increasingly important throughout the school years and into adulthood. Behavioral neuroscience research in animals tells us that the prefrontal cortex is highly sensitive to the detrimental effects of excessive stress exposure and that its developing architecture is vulnerable to the negative effects of chronic fear

(Arnsten, 2009).

Impact of Relationships and Emotional Development

Young children are capable of surprisingly deep and intense feelings of sadness (including depression), grief, anxiety, and anger (which can result in unmanageable aggression), in addition to the heights of joy and happiness for which they are better known (Shaw,

Owens, Giovannelli, & Winslow, 2001; Ashman, & Dawson, 2002) For some children, the preschool years mark the beginning of enduring emotional difficulties and mental-

128 health problems that may become more severe than earlier generations of parents and clinicians ever suspected.

The emotional health of young children - or the absence of it - is closely tied to the social and emotional characteristics of the environments in which they live, which include not only their parents but also the broader context of their families and communities (Dawson

& Ashman, 2000); Cummings & Davies, 1994; Reid, Patterson, & Snyder, 2002). Young children who grow up in homes that are troubled by parental mental-health problems, substance abuse, or family violence face significant threats to their own emotional development. The experience of chronic, extreme, and/or uncontrollable maltreatment has been documented as producing measurable changes in the immature brain (Glaser,

2000; De Bellis, Keshavan, Clark, Casey, Giedd, Boring, et al., 1999).

Children’s early abilities to deal with their emotions are important not only for the foundation these capacities provide for the future, but also for the children’s current social functioning with their parents, teachers, and peers. Indeed, differences in how young children understand and regulate their own emotions are closely associated with peer and teacher perceptions of their social competence, as well as with how well-liked they are in a child-care setting or preschool classroom (Denham, Blair, DeMulder,

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Levitas, Sawyer, Aurbach-Major, & Queenan, 2003; Halberstadt, Denham, & Dunnsmore,

2001).

Epigenetic Consequences

New scientific research shows that environmental influences can actually affect whether and how genes are expressed. Thus, the old ideas that genes are “set in stone” or that they alone determine development have been disproven. In fact, scientists have discovered that early experiences can determine how genes are turned on and off and even whether some are expressed at all (Meaney, 2010). Therefore, the experiences children have early in life—and the environments in which they have them - shape their developing brain and strongly affect whether they grow up to be healthy. This growing scientific evidence supports the need for society to re-examine the way it thinks about the circumstances and experiences to which young children are exposed.

The approximately 23,000 genes that children inherit from their parents form what is called the “structural genome.” The structural genome is analogous to the hardware of a computer—both determine the boundaries of what’s possible, but neither works without an operating system to tell it what to do. In the genome, that operating system is called the epigenome (Waddington, 1942). Like the software in an operating system, the

130 epigenome determines which functions the genetic “hardware” does and does not perform (Dolinoy, Weidman, & Jirtle, 2007). This system is built over time as positive experiences, such as exposure to rich learning opportunities, or negative influences, such as environmental toxins or stressful life circumstances, leave a chemical “signature” on the genes. These signatures can be temporary or permanent, and both types affect how easily the genes are switched on or off.

Nutritional status, exposure to toxins and drugs, and the experiences of interacting with varied environments can all modify an individual’s epigenome (Bernstein, Meissner, &

Lander, 2007). Research in both animals and humans show that some epigenetic changes that occur in the fetus during pregnancy can be passed on to later generations, affecting the health and welfare of children, grandchildren, and their descendents (Anway, Cupp,

Uzumcu, & Skinner, 2005; Champagne, 2010). For example, turning on genes that increase cell growth, while at the same time switching off genes that suppress cell growth, has been shown to cause cancer (Smith, Otterson, & Plass, 2007). Repetitive, highly stressful experiences can cause epigenetic changes that damage the systems that manage one’s response to adversity later in life (Bagot, van Hasselt, Champagne, Meaney,

Krugers, Joels, 2009). On the other hand, supportive environments and rich learning experiences generate positive epigenetic signatures that activate genetic potential (Curley,

2009). In this second case, the stimulation that occurs in the brain through active use of

131 learning and memory circuits can result in epigenetic changes that establish a foundation for more effective learning capacities in the future (Sweatt, 2007).

Recent research indicates that the chemical signatures imprinted on our genes during fetal and infant development can have significant influences on brain architecture that last a lifetime. In other words, the discovery of the epigenome may offer an explanation, at the molecular level, for why and how early positive and negative experiences can have lifelong impacts (McGowen, Sasaki, D’Alessio, Dymov, Labonte, Szyf, Meaney, 2009).

The physiological activity caused by positive mastery experiences can lead to epigenetic changes that control the expression of genes in brain cells that are essential for successful learning (Sweatt, 2007; Sweatt, 2009). In a parallel fashion, exposure to damaging levels of stress early in life can lead to long-lasting epigenetic changes in brain cells that direct how our bodies respond to adversity throughout the lifespan (Shonkoff, Boyce, &

McEwen, 2009). In short, early experiences cause epigenetic adaptations in the brain that influence whether, when, and how genes build the capacity for future skills to develop.

Modification of the epigenome caused by stress during fetal and child development may affect how well or poorly we respond to stress as adults and can result in increased risk of adult disease. Some of our genes provide instructions for how our bodies respond to

132 stress, and research has shown that these genes are clearly subject to epigenetic modification. For example, research in animals has shown that stressful experiences to which the pregnant mother is exposed, or to which the offspring is exposed soon after birth, can produce epigenetic changes that chemically modify the receptor in the brain that controls the stress hormone cortisol and, therefore, determines the body’s response to threat (the fight-or-flight response) (McGowen, Sasaki, D’Alessio, Dymov, labonte, Szyf,

& Meaney, 2009).

Healthy stress responses are characterized by an elevation in blood cortisol followed by a return to baseline to avoid a highly activated state for a prolonged period of time. If young children or pregnant mothers experience toxic stress—as a result of serious adversity (such as chronic neglect, abuse, or exposure to violence) in the absence of protective relationships—persistent epigenetic changes can result (Shonkoff, Boyce, &

McEwen, 2009). These modifications have been shown to cause prolonged stress responses.

Excessive stress has been correlated with changes in brain architecture and chemistry as well as animal behaviors that resemble anxiety and depression in humans (Champagne,

Curley, 2009; Champagne, Weaver, Diorio, Dymov, Szyf, & Meany, 2006; Chen, Dube,

Rice, & Baram, 2008). Human studies have found connections between highly stressful

133 experiences in children and increased risk for later mental illnesses, including generalized anxiety disorder and major depressive disorder (Bradley, Binder, Epstein, Tang, Nair,Liu,

& Ressler, 2008; Gillespie, Bradley, Mercer, Smith, Coneely, Gapen, & Ressler, 2009).

Atypical stress responses over a lifetime can also result in increased risk for physical ailments, such as asthma, hypertension, heart disease and diabetes (Swanson, Entringer,

Buss, & Wadhwa, 2009; Shonkoff, Boyce, & McEwen, 2009; Bradley, Binder, Epstein,

Tang, Nair, Liu, & Ressler, 2008).

Learned Fear

When young children experience serious fear-triggering events, they learn to associate that fear with the context and conditions that accompanied it. Very young children can actually learn to be fearful through a process called “fear conditioning,” which is strongly connected to the development of later anxiety disorders (Watson & Rayner, 1920; Pavlov,

1927; Grillon, & Morgan, 1999; Pine, 1999). In the typical circumstances of early childhood, fear responses are activated quickly and then dissipate. However, when young children are chronically exposed to perceived or real threat, fear-system activation can be prolonged. In research studies, fear conditioning involves the pairing of a neutral stimulus

(e.g., a tone or a light) that normally does not elicit a negative emotional response with an aversive stimulus (e.g., pain) that produces fear. As this conditioning evolves, it solidifies

134 the relation between the two stimuli and then generalizes the fear response to other neutral stimuli that may share similar characteristics with the aversive stimulus.

Conditioned fear is apparent when individuals come to experience and express fear within the context in which the learning occurred . For example, a child who is physically abused by an adult may become anxious in response to both the person and the place where the fear learning occurred. Over time, the fear elicited and the consequent anxiety can become generalized, and subsequent fear responses may be elicited by other people and places that bear sometimes only small resemblances to the original conditions of trauma. Consequently, for young children who perceive the world as a threatening place, a wide range of conditions can trigger anxious behaviors that then impair their ability to learn and to interact socially with others. The extent to which these problems affect physical and mental health is influenced by the frequency of the stressful exposure and/or the emotional intensity of the fear-eliciting event.

Research indicates that unlearning fear is a fundamentally different process from fear learning. The process of unlearning conditioned fear is called “extinction” and actually involves physically separate and distinct areas of the brain’s architecture from those into which fear responses are first incorporated. Generally speaking, the unlearning process involves activity in the prefrontal cortex, which decreases the fear response by regulating

135 the activity of the amygdala (Quirk, Garcia, & Gonzalez-Lima, 2006; Sotres-Bayon,

Bush, & LeDoux, 2009; Morgan, Romanski, & LeDoux, 1993; Phelps, Delgado, Nearing,

& LeDoux, 2004). Research also indicates that fears are not just passively forgotten over time, but they must be actively unlearned. Studies show that fear learning can occur relatively early in life (Sullivan, Landers, Yeaman, & Wilson, 2000; Prather, Lavenex,

Mauldin-Jourdain, Mason, Capitano, Mendoza, & Amaral, 2001; Rudy, 1993), whereas fear unlearning, is only achieved later, when certain structures in the brain have matured

(Carew, & Rudy, 1991; Kim, & Richardson, 2008). Consequently, early fear learning can have a significant impact on the physical and mental health of a young child that can take years to remediate.

This understanding of how fear unlearning occurs can be helpful in designing interventions for anxious and fearful children. For example, research has shown that unlearning negative fear responses to specific stimuli such as animals, insects, heights, or social situations can be accomplished successfully by presenting the aversive stimulus or circumstance at a low level of intensity while the fearful individual is in a safe context.

This is the therapeutic basis for cognitive behavioral therapy. Providing additional explanations for anxious behavior during these controlled exposures has proven to be particularly successful for reducing anxiety in older children with excessive fears, as their ability to understand these explanations develops. Such interventions work well with

136 specific phobias, as well as social or generalized anxiety, but are not effective in remediating the effects of abuse or neglect.

Chronic and intense fear early in life affects the development of the stress response system and influences the processing of emotional memories (Sanchez, Ladd, & Plotsky,

2001; Nemeroff, 2004). When an individual is confronted with a threat, stress systems are activated and elevate the levels of several different stress chemicals that are circulating throughout the body (McEwen, 2007; de Kloet, Karst, & Joells, 2008). An increase in one of those chemicals, cortisol, can have a dramatic impact on how memories are processed and stored (de Kloet, Karst, & Joells, 2008; Wiegert, Joels, & Krugers, 2008).

The production of cortisol and adrenalin (as well as noradrenaline in the brain) in a normal stress response leads to memory formation for events and places that generate danger. More specifically, elevated cortisol levels can strengthen the formation of memories of emotional events (Roozendaal, Barsegyan, & Lee, 2008; McGaugh, Cahill,

& Roozendaal, 2006) block the ability to unlearn fear memories (Yang, Chao, Ro, Wo, &

Lu, 2007) and enhance the formation of memories of the surrounding context in which the fearful event occurred (Brinks, de Kloet, & Oitzl, 2008). Interestingly, too much cortisol can also have the opposite effect and actually impair memory and learning in non-threatening contexts (Roozendaal, McEwen, & Chattarji, 2009). Thus, the biological response to stress is intimately involved in both fear learning and unlearning.

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These memories are relived by individuals who experienced a traumatic event when cues in the environment activate those memories. This repeated recall or retrieval of the memory makes emotional memories both more easily activated and more resistant to being forgotten (de Kloet, Karst, & Joells, 2008; Wiegert, Joels, & Krugers, 2008). The repeated recall of a traumatic event can lead to additional release of cortisol, even in the absence of the actual event. Behavioral neuroscience research with animals has shown that chronic elevation of cortisol can have a number of detrimental effects, including increased damage to brain cells in areas that support learning, thereby leading to increased impairment in subsequent memory formation (Wiegert, Joels, & Krugers, 2008;

Roozendaal, Barsegyan, & Lee, 2008).

Persistent fear can distort how a child perceives and responds to threat . Fear learning typically takes place in specific contexts and results in those fears becoming associated with the places where the learning occurred. Children may also express fear in response to situations that are similar (not identical) to those initially learned or to situations that are similar to the contexts in which the original learning occurred. These are called

“generalized” fear responses, and they are thought to underlie the expression of later anxiety disorders, including post-traumatic stress disorder (PTSD) (Grillon, & Morgan,

1999; Grillon, 2002; Davis, 2006). Thus, although all individuals display a heightened

138 fear response when faced with threatening contexts (Grillon, 2002; Lissek, Powers,

McClure, Phelps, Woldehawariat; Grillon, & Pine, 2005) individuals with anxiety disorders show this same increased fear response when faced with similar contexts that are known to be safe (Grillon, 2002; Powers, McClure, Phelps, Woldehawariat; Grillon,

& Pine, 2005; Lissek, Biggs, Rabin, Cornwell, Alvarez, Pine, & Grillon, 2008). Indeed, children who have had chronic and intense fearful experiences often lose the capacity to differentiate between threat and safety. This impairs their ability to learn and interact with others, because they frequently perceive threat in familiar social circumstances, such as on the playground or in school. These responses inhibit their ability to learn and often lead to serious anxiety disorders (Grillon, Dierker, & Merikangas, 1998; Reeb-Sutherland,

Helfinstein, Degnam, Perez-Edgar, Henderson, Lissek, Chronis-Tuscano, Grillon, Pine,

& Fox, 2009).

Young children who have been exposed to traumatic circumstances also have difficulty identifying and responding to different expressions of emotions, and, therefore, have trouble forming healthy relationships (Wismer, Ziegler, Kurian, Jacoris, & Pollack, 2005;

Zeaneh, Smyke, & Dumitrescu, 2002; Zeaneh, Smyke, & Koga, 2005; O’Conner, Rutter,

& The English and Romanian Adoptees (ERA) Study Team, 2000; O’Conner,

Bredenkamp, & Rutter, 1999). These deficits lead to general problems with social interaction, such as understanding others’ facial expressions and emotions. For example,

139 children raised in physically abusive households show heightened sensitivity (compared with non-abused children) to angry faces, which negatively affects their brain function and behavior (Pollak, Messner, Kistler, & Cohn, 2009; Pollak, & Kistler, 2002; Pollak,

Cicchetti, Hornung, & Reed, 2000; Pollak, & Tolley-Schell, 2003).

Learning to identify anger—quickly and successfully—in order to avoid being harmed is a highly adaptive and appropriate response to an abusive environment. However, an increased tendency to assume someone is angry when his or her facial expression is ambiguous can be inappropriate and maladaptive in a typical, non-threatening social setting and even dangerous in unfamiliar social settings (Pollak, 2008). This “attention bias” to threat is associated with interpreting ambiguous information in a negative fashion, and it is linked to greater vulnerability to stress and anxious behaviors as well as to a greater likelihood to respond aggressively as a form of self-defense in neutral circumstances that are erroneously viewed as threatening. Thus, the extent to which children with a heightened attention bias to threat view the world as a hostile and threatening place can be viewed as both a logical adaptation to an abusive environment and a potent risk factor for behavior problems in later childhood, adolescence, and adult life.

Early exposure to intense or persistent fear-triggering events affects children’s ability to learn. There is extensive and growing evidence that prolonged and/or excessive exposure

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to fear and states of anxiety can cause levels of stress that can impair early learning and

adversely affect later performance in school, the workplace, and the community. Multiple

studies in humans have documented problems in cognitive control and learning as a result

of toxic stress (Shonkoff, Boyce, & McEwen, 2009). These findings have been

strengthened by research evidence from non-human primates and rodents that is

expanding our understanding of the brain mechanisms underlying these difficulties.

Impacts to Society

There are four major areas that have long-term consequences associated with

intergerational Toxic Stress: cognitive development, chronic diseases, substance abuse,

and the intergenerational transmission of dysfunctional behaviors.

Academic Achievement and Executive Function

We are born with the potential to develop the ability to stay focused on daily tasks and goals - or not - depending on our experiences during infancy, throughout childhood, and into adolescence. This is a core quality of Executive Function and a key component for development, learning in school and academic achievement. Yet, adverse environments resulting from neglect, abuse, and/or exposure to violence can impair the development of

141 executive function skills as a result of the disruptive effects of toxic stress on the developing architecture of the brain. Completing most tasks requires the successful orchestration of several types of executive function skills. Among those who study these functions, three dimensions are frequently highlighted: working memory, inhibitory control, and cognitive or mental flexibility (Diamond & Taylor, 1996; Greenberg, Riggs,

Blair, 2007; Rothbart, Posner, & Kieras, 2006). These skills develop through practice and are strengthened by the experiences through which they are applied and honed. Providing the support that children need to build these skills at home, in child care and preschool programs, and in other settings they experience regularly is one of society’s most important responsibilities.

In the brain, executive function refers to a group of skills that helps us to focus on multiple streams of information at the same time, monitor errors, make decisions in light of available information, revise plans as necessary, and resist the urge to let frustration lead to hasty actions. Acquiring the early building blocks of these skills is one of the most important and challenging tasks of the early childhood years, and the opportunity to build further on these rudimentary capacities is critical to healthy development through middle childhood and adolescence. Just as we rely on our well-developed personal “air traffic control system” to make it through our complex days without stumbling, young children depend on their emerging executive function skills to help them as they learn to read and

142 write, remember the steps in performing an arithmetic problem, take part in class discussions or group projects, and enter into and sustain play with other children.

The increasingly competent executive functioning of childhood and adolescence enable children to plan and act in a way that makes them good students and friends. Children who do not have opportunities to use and strengthen these skills, fail to become proficient

- or children who lack the capacity for proficiency because of disabilities or, for that matter, adults who lose it due to brain injury or old age - have a very hard time managing the routine tasks of daily life. Studying, sustaining friendships, holding down a job, or managing a crisis pose even bigger challenges.

The process of development is sometimes portrayed as one in which children gradually manage more and more aspects of their environments and lives on their own. We would not trust two-year-olds to stop going after a ball just because it rolled into the street, get ready in the morning (brush their teeth, pick out their clothes, and get dressed) by themselves, or even clean up their toys without reminders. Adults set up the framework

(i.e., establishing routines, providing cues, breaking big tasks into smaller chunks) that helps children use the executive function skills they are developing to the best of their abilities.

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The evidence on the development and consequences of executive functioning in the earliest years of life conveys three important messages. First, executive function skills are crucial building blocks for the early development of both cognitive and social capacities.

Second, both normative differences in the nature and pace of individual developmental trajectories and the impacts of significant adversity will affect how the development of executive functioning will unfold for any given child. Third, several interventions focused on supporting the development of specific executive function skills have demonstrated at least short-term effectiveness, with evidence also emerging that they may have impacts on other aspects of learning as well.

Researchers are making major strides in identifying the key brain regions executive function skills depend on. These include circuits and systems that primarily involve the prefrontal cortex, but also include the anterior cingulate, parietal cortex, and hippocampus. The gradual acquisition of executive function skills corresponds closely to the extended development of these prefrontal brain regions from infancy through late adolescence (Diamond, 2002; Diamond, 1998; Goldman-Rakic, 1987). The formative development of these regions occurs during early childhood, as the relevant circuits emerge, mature, and forge critical interconnections. These circuits are then refined and made more efficient during adolescence and into the early adult years. It is also important to note that the brain regions and circuits associated with executive functioning have

144 extensive interconnections with deeper brain structures that control the developing child’s responses to threat and stress (Bush, Luu, & Posner, 2000; Drevets, & Raichle, 1998).

This implies that the developing executive functioning system both influences and is affected by the young child’s experience and management of threat, stress (Rueda, Posner,

& Rothbart, 2005; Blair, Zelazo, Greenberg, 2005) and strong emotions. Thus, extended exposure to threatening situations can compromise the development and deployment of executive function skills, yet well-developed capabilities in these areas can also help children (and adults) manage stress effectively.

Executive functioning is distinct from (yet foundational to) school readiness and academic success. Researchers that study executive function skills refer to them as the biological foundation for school readiness (Barkley, 2001; Blair, 2002). They argue that strong working memory, cognitive self-control, and “attention skills” provide the basis upon which children’s abilities to learn to read, write, and do math can be built. In practice, these skills process (i.e., the how ) of learning - focusing, remembering, planning—that enables children to effectively and efficiently master the content (i.e., the what ) of learning—reading, writing, computation. They enable children to acquire knowledge and to participate in the school experience as actively engaged and competent learners. Children with stronger working memory, inhibition, and these skills also have been found to make larger gains on tests of early math, language, and literacy

145 development during the preschool years than their peers with weaker executive function skills (Bierman, Nix, Greenberg, Blair, & Domitrovich, 2008; Blair, & Razza, 2007;

Espey, McDairmid, Kwik, Stalets, hamby, & Senn, 2004; Fuchs, Compton, Fuchs,

Paulsen, Bryant, Hamlett, 2005).

Children’s executive function skills provide the link between early school achievement and social and emotional development. Young children who have problems staying focused and resisting urges to respond impulsively - two core executive function skills - not only have trouble in school but also have trouble following directions generally and are at elevated risk of displaying aggressive and confrontational behavior with adults and other children (Eisenberg, Fabes, Nyman, Bernzeig, & Pinuelas, 1994; Hill, Degnan,

Calkins, & Keane, 2006). Executive functions like completing tasks, solving problems, organizing information, and making (and revising, if necessary) deliberate plans, are important facilitators of interpersonal interactions and behavior.

Environments that foster executive functioning are characterized by adult-child relationships (both within and outside the home) that guide children from complete dependence on adult support to gradual assumption of the “executive” role for themselves.

Such environments neither expect children to have more advanced skills than are reasonable for their age, nor do they treat them as if they had no executive capabilities.

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Children who routinely experience social interactions that provide these kinds of opportunities are more capable of resisting distractions, controlling their behavior and emotions towards others, complying with adult requests and rules, and engaging in goal- directed behavior by the time they get to school. Experts also hypothesize that more ordered and predictable environments foster the development of executive function skills by offering children ample experiences that involve give-and-take interactions with others (Barkley, 2001, Bodrova & Leong, 2007; Bodrova, & Leong, 2005).

Adverse environments resulting from neglect, abuse, and/or exposure to violence can impair the development of executive function skills as a result of the disruptive effects of toxic stress on the development of the brain. Chaotic (and unpredictable) environments can also lead to poor self-regulatory behaviors and impulse control (Evans, & Wachs,

2010). A number of studies have shown that exposure to highly stressful early environment is associated with deficits in the development of children’s working memory, attention, and inhibitory control skills (Lengua, Honorado, & Bush, 2007; Maughan &

Cicchetti, 2002).

Damaging fear and toxic stress are likely mechanisms that explain these effects, in part, because they affect the chemistry of brain circuits involved in the development of these

147 capacities, and they impair the specific neuronal architecture that is engaged when we try to keep information in working memory, inhibit a habitual action, or address problems in a flexible manner. All adults have had the experience of encountering a threat, being gripped by fear or anxiety, and having trouble thinking. Under such circumstances, the brain goes into high “fight-or-flight” mode, and we have to calm ourselves down before we can mobilize our executive function skills to plan and execute a well-considered response.

In adults and children, acute stress can even cause less-efficient prefrontal cortex activity, leading to a temporary “blip” in executive functioning (Arnsten, 1998). Thus, chronic fear and anxiety associated with living in highly threatening, chaotic, or stressful environments can make it very difficult for young children to engage their executive abilities - even in situations (like school) where they may, in fact, be safe (Liston,

McEwen, & Casey, 2009; Liston, Miller, Goldwater, Radley, Rocher, Hof, Morrison, &

McEwen, 2006).

Children who experience adversity at an early age are more likely to exhibit deficits in executive functioning, suggesting that these capacities are vulnerable to disruption early in the developmental process. Among the conditions that have been studied and found to affect the development of executive function skills are early abuse and neglect (Sanchez,

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& Pollack, 2009), orphanage rearing (Bos, Fox, Zeanah, & Nelson, 2009; Colvert, Rutter,

Kreppner, Beckett, Castle, Groothues, et al., 2008), prematurity and/or perinatal complications (Curtis, Lindeke, Georgieff, & Nelson, 2002; Feldman, 2009), and prenatal alcohol exposure (Jacobson, & Jacobson, 2000). For example, children with a history of exposure to alcohol before birth have been found to display high levels of impulsivity and disorganization, along with evidence of impaired development of the prefrontal cortex

(Olson, Streissguth, Sampson, Barr, Bookstein, & Theide, 1997).

Evidence is also accumulating that childhood maltreatment disrupts the attention systems that affect how children notice, interpret, and respond to social interactions (Dodge, Pettit,

Bates, & Valente, 1995; Pollak, & Tolley-Schell, 2003). Despite subsequent adoption, maltreated children who experienced unstable foster care placements have been found to perform poorly on tests of executive functioning (Lewis, Dozier, Ackerman, &

Sepulveda-Kozakowski, 2007), as well as to display oppositional behavior towards their adoptive parents. Furthermore, larger numbers of unique foster care placements have been found to predict lower scores on a wide range of neuropsychological executive functioning tests (Korkman, Kirk, & Kemp, 1998), suggesting that frequent changes in a child’s primary caregiver may disrupt the development of these important skills. in light of this evidence, it is not surprising that children with a history of early social deprivation from being raised in an orphanage have also been found to perform significantly more

149 poorly than their non-institutionalized peers on neuropsychological tests of executive function skills (Bos, Fox, Zeanah, & Nelson, 2009; Colvert, Rutter, Kreppner, Beckett,

Castle, Groothues, et al., 2008). While all young children benefit from experiences that promote executive functioning, those who exhibit problems in self-regulation need particularly sensitive adult support. When children have experienced serious trauma or abuse, concern is always warranted. Children require stable, secure environments to grow and flourish. A stressful, chaotic family and subsequent childhood has the potential to create detrimental health and social issues later in life. It is my contention that historical trauma has the potential to be an antecedent to familial patterns that results in such childhood stress, chaos and outcomes.

Chronic Diseases

As previously discussed, the impact of toxic stress on the HPA-axis has the potential to lead to detrimental health risks, deficits in the ability to learn and substance abuse.

According to the IHS (2003), some of the leading causes of death among AIAN people are heart disease, cancer, unintentional injuries (accidents), type II diabetes mellitus, and stroke. AIAN people also have a high prevalence and risk factors for mental health problems, suicide, obesity, substance abuse, teen pregnancy, liver disease and hepatitis.

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There is a growing body of evidence that early traumatic experiences are associated with health problems throughout the lifespan (Shonkoff, Boyce, & McEwen, 2009). In fact, research shows an association between child maltreatment and a broad range of problems including substance abuse, intimate partner violence, teenage pregnancy, anxiety, depression, suicide, diabetes, ischemic heart disease, sexually transmitted diseases, smoking, and obesity (Fellitti et al., 1998; Mercy & Saul, 2009; Repetti, Taylor, &

Seeman, 2002). Some of our nation’s most serious health concerns can be linked to trauma from abuse and neglect early in life. Preventing maltreatment can be a powerful lever to move the population toward greater health and well-being.

Substance Abuse

Childhood exposure to trauma, often associated with parental substance abuse, influences perceptual and emotional experiences of childhood events, with these effects continuing into adulthood. Substance abuse is implicated in parental neglect, physical and sexual abuse and is related to emotional problems and sexual victimization of offspring among

Alaska Native females (Segal, 2003).

The traumatized individual attempts to self-medicate to reduce the emotional pain (Segal,

2003). Relatives of primary trauma survivors with PTSD manifest a higher prevalence of

151 substance use disorders as well as mood and anxiety disorders (Yehuda, 1999). Suicide attempts among children of substance abusers appear to be more prevalent (Segal, 2003).

Another possible manifestation of intergenerational trauma transfer, childhood sexual abuse reported among boarding school survivors, is a significant risk factor for substance abuse as well as depression, and/or anxiety disorders (Brave Heart & DeBruyn In press;

Brave Heart 1999a; Robin, Chester & Goldman 1996). Substance abuse and depression are both prevalent among AIAN individuals and are correlated with PTSD (Brave Heart

& DeBruyn, 1998; Brave Heart 1999b ; Robin et al 1996).

A large body of research reports strong associations between adverse childhood experiences and subsequent development of substance abuse disorders. A prospective study followed substantiated cases of child abuse and neglect (and demographically matched controls) into young adulthood, and found support for the hypothesis that childhood victimization plays a causal role in the development of alcohol abuse symptoms (Kendler, Bulik, Silberg, et al., 2000).

The trauma may continue to manifest itself among AIAN youth as alcohol use, which is more prevalent than in the general U.S. population at 96% for Indian males and 92% for females by the 12th grade for lifetime use (Oetting & Beauvais 1989). Not only is the frequency and intensity of drinking greater, and negative consequences are more

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prevalent and severe, but the age at first involvement with alcohol is younger for Indian

youths (Beauvais et al.- see Brave Heart & DeBruyn, 1998). Alcohol remains the drug of

choice, although inhalants and marijuana use are prevalent.

In general, children who have been sexually or physically abused manifest abnormal

baseline and stressor-responsive cortisol levels (either abnormally elevated or abnormally

flat). Childhood abuse may initially sensitize the stress response system, thus rendering

persons who were abused during childhood particularly vulnerable to stress and

increasing their risk for stress-related disorders. This vulnerability may result in

hypersecretion of corticotropin-releasing hormone whenever they are stressed. A lack of

feedback inhibition may also increase the discharge of central corticotropin-releasing

hormone (Fries, Ziegler, Kurian, et al., 2005).

Stress and disorders that are related to chronic stress tend to increase dendritic atrophy

(reduction in size), accelerate neuronal degeneration, and subvert neuronal regeneration

in the hippocampus and hippocampal and prefrontal cortex (Magarinos, McEwen, Flugge,

& Fuchs, 1996; Uno, Tarara, & Else, 1989; Gould, Tanapat, & McEwen, 1998). In the developing brain, elevated levels of cortisol may lead to structural deviations or deficits through accelerated loss of neurons, delays in myelination (of axons), abnormalities in developmentally appropriate synaptic pruning, and inhibition of neurogenesis (Heim,

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Plotsky, & Nemeroff, 2004). Sustained cortisol exposure truncates and impairs neurogenesis in the hippocampal and prefrontal cortex (Saplosky, Uno, Rebert, & Finch,

1990; Roy & Sapolsky, 2003). Reduced baseline and hyporesponsive cortisol levels also

can cause neuronal damage.

Together, these processes feed the downward spiral by potentiating hippocampal and

cortical atrophy. Neuronal degeneration in the hippocampus and the prefrontal cortex

diminishes the capacity of these regions to modulate or inhibit amygdalar stress or fear

pathways and the HPA axis, and also undermines hippocampal negative feedback control

over cortisol release. Evidence of neuronal loss in the anterior cingulate cortex has been

reported in children, adolescents, and nonhuman primates with histories of adverse

experiences early in life (De Bellis, Keshavan, Spencer, & Hall, 2000). In addition, adult

survivors of early abuse have been found to have changes in hippocampal structure and

function (De Bellis, Keshavan, Spencer, & Hall, 2000). Thus, these stress-induced

processes may lead to compromised executive function, impaired affect regulation, and a

greater incidence of impulsive behaviors.

Most studies of drug self-administration have reported increases in responding after

repeated or prolonged exposure to stress levels of cortisol, which enhance drug response

by selectively facilitating dopamine transmission in the “reward center” of the brain, the

154 nucleus accumbens (Martinelli & Piazza, 2002). During chronic stress, repeated increases in cortisol result in sensitization of the reward system. This sensitized state, which can persist after the end of the stress, renders the subject more responsive to pleasurable substances and behaviors that trigger release of mesolimbic dopamine and consequently more vulnerable to develop an addictive disorder. Put another way, chronic stress causes prolonged release of cortisol, which in turn, causes morphological changes to the brain’s pleasure center, rendering an individual more sensitive to psychoactive substances and addiction.

Intergenerational Transmission of Dysfunctional Behaviors

Traumatic experiences endured during childhood or as an adult, might profoundly influence the well-being of their offspring (Yehuda & Bierer, 2008). The transmission of stressor effects (within individuals and communities alike) have been explored in specific populations that endured collective trauma. Some of the research, frequently based on data from Holocaust Survivors and their families, has implicated biological (largely neuroendocrine) changes, as well as the possible influence of parenting and attachment styles, in mediating the intergenerational effects of trauma. There exists a marked diversity of experiences among Holocaust Survivors, and a wide range of psychological symptoms have been documented, including denial, agitation, anxiety, depression,

155 mistrust, intrusive thoughts, survivor’s guilt, disorganized reasoning, and difficulty expressing emotions, although these were frequently at levels below those meeting the full criteria for a clinical diagnosis (Barocas & Barocas, 1980; Bar-On et al., 1998; Felsen,

1998).

Despite numerous anecdotal accounts of similar intergenerational effects among survivors of trauma in AIAN groups, few studies empirically assessed the issue of intergenerational transmission of trauma. It is suggested that children who have experienced trauma might develop coping styles that are particularly ineffective or even counter-productive. Perhaps as a result of these ineffective coping styles, these individuals may be at increased risk of further stressor encounters (stress proliferation), increased psychological and neurochemical reactivity to stressors, and the promotion of poor mental health. These factors, alone or in combination, may result in impaired parenting and might thus increase the likelihood of early life trauma or stressors being encountered by their offspring. In this next generation, these adverse experiences might result in the recapitulation of the events outlined in the preceding generation, and so on.

I propose that cultural-historical developmental theories may offer direction for future inquiry. From a Vygotskian perspective, and subscribed to by cultural-historical theorists, the social world does have primacy over the individual. Society is the bearer of the cultural heritage without which the development of the individual mind is impossible.

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When parents and other members of the community create what Sara Harkness and

Charles Super (1986) have aptly referred to as a developmental niche for the newcomer, the nature of that niche (including the forms of social relationships it requires and affords) embody not only the adult's cultural past but presuppositions about the child's future as well. The niche is simultaneously a socio-physical location, a cultural medium, and an interpretive frame. Children in human developmental niches are both natural and cultural entities at the start of post-natal development.

Newborns are, of course, ignorant of the meanings of the artifacts they encounter and the ways in which those artifacts (including words of the language as well as diapers, mobiles, and pacifiers) are to be incorporated into action. At birth the cultural past is, literally, thrust upon them – including behaviors, values and other cultural artifacts.

This is not to say that the process of becoming socialized can be reduced to simple learning or that there is no room for active construction in it. Social processes give rise to individual processes and that both are essentially mediated by artifacts. Vygotsky explicated the first of these two claims in his general genetic law of cultural development according to which interpersonal/inter-mental processes are the precursors and necessary condition for the emergence of individual/intra-mental (psychological) processes.

According to this perspective, if a child is born into a world of interpersonal violence,

157 there is a good chance these behaviors will eventually become internalized intra-mentally and expressed later as child grows into an adult.

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CHAPTER 10

SUMMARY

The purpose for this theoretical dissertation is to present a conceptual framework for the understanding of how the many episodes of historical trauma, spanning decades and generations, continues to impact the health and wellness of the American Indians and

Alaska Native people. In developing this framework, I’ve relied upon a cultural-historical perspective, focusing on development and the fusion of biology and culture to impose changes to behavior. The focus of this analysis has been on health and the development of chronic diseases, substance abuse and cognitive development. These areas impose a challenge to the overall well-being of any society, especially, AIAN populations.

An outcome of trauma is stress , more specifically, toxic stress. Physiological processes are drastically impacted by toxic stress and the ensuing release of cortisol , a glucocorticoid stress hormone. In previous chapters, I have presented how chronic toxic stress impacts the development of children, affecting the growth of the brain, which in turn is associated with behavioral development, and the long-term ability to cope with future stressors (see Chapter 9). In addition to the scholarly work previously done on historical trauma, I believe the ramifications extend beyond what has been well documented as “grief” (historically unresolved grief, see Chapter 1). In addition to grief

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and the physiological implications of toxic stress, there is also a learned behavioral

response that has emerged as a result to this trauma. This behavioral response is guided

by an autonomic response that extends beyond conscious memories of horrific, traumatic

events. Experienced over-and-over it may become the basis for coping behaviors that

become dysfunctional when they stifle growth or lead to behaviors that result in injury to self or others (depression, frustration, rage, substance abuse, interpersonal violence, domestic violence, sexual abuse and/or childhood abuse). In Vygotskian terms, these behaviors mediate an internal conflict; and as a result, become accepted, learned and inter-generationally transferred, eventually becoming subtly infused into the culture.

Survivors of initial traumatic events suffered grave psychological symptoms, in addition to physical injuries and fatalities that occurred as a result of massacres or other genocidal acts. As documented, these psychological symptoms have been described as depression, guilt and grief (see Chapter 4). Symptoms that resemble PTSD and depressive disorders

(see Chapter 9). I believe that this is the first step toward the disruption of the parent/child relationship, especially impacting the benefits of the mother/child relationship, the cornerstone for healthy emotional development and the foundation for developing and maintaining healthy, life-long relationships (see Chapter 8).

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From an approach of cultural-historical psychology, human psychological processes emerge from the outcome of four genetic domains: phylogeny, cultural history, ontogeny, microgenesis; in addition to, humanity’s culturally mediated, historically developing, practical activity (Chapter 6). From this perspective, culture plays a significant role in neurodevelopment, neurogenesis and neurophysiology, which in turn, guides cultural development and behavior.

Cultural mediation played a significant role in neurogenesis and the emergence of modern man (see Chapter 6). As a result of the morphological changes to the brain and the subsequent increased cognitive ability, cultural mediation (tool, sign, and symbol use) has the potential to shape the external physical, social and cultural environments. At the same time, neurodevelopment and neurophysiology are dependent upon sensory stimulation (see Chapter 7) from the environment.

The more we partake in certain activities, the more likely the physiological mechanisms of neurogenesis and neurodevelopment become activated. Whether that includes an increase in synaptic activity of neurotransmitters, or the development and thickening of myelin tracts (the white matter of the brain) to improve the efficiency of the connections from one area of the brain to another, there is a neurophysiological response to the external stimuli (see Chapter 7).

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From a cultural-historical perspective, the mental activities associated with “higher psychological processes” are associated with the neocortex, that area of the brain that phylogenetically was the last part to develop, and distinguishes modern man from other hominid and primate species (see Chapter 6). These mental psychological processes form the basis for perception, emotions, memory, thinking, motivation and language, functions associated with the “mind.”

Lower psychological processes, on the other hand, refer to those elementary processes that are biologically programmed, natural behaviors that are immediate responses to external environmental stimuli. These processes are involuntary in nature. As previously mentioned (see Chapter 9), stress activates the HPA-axis (in addition to other areas of the brain), which in turn, is associated to a cascade of involuntary responses that help the body respond to whatever is causing the stress. The problem arises when this stress is overwhelming, prolonged and not buffered or relieved by the care and nurturance of caregivers. Over a long period of time, the HPA-axis may begin to cause the dysregulated release of cortisol. Too much or too little cortisol impacts other physiological systems leading to physical illness, immune system disorders, depression, anxiety, poor cognitive functioning and impaired learning (Chapter 7).

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As documented in the literature, the major impact of historical traumatic events on survivors is described as post-traumatic stress disorder and associated depression. As previously mentioned, this initial assault impacted key relationships, especially the mother-child relationship. This relationship is critical for neurodevelopment, emotional development, and the development of future relationships (see Chapter 9). These are key mechanisms for social interaction, social learning and the ability to solve future problems.

Coupled with the loss of traditional, cultural, spiritual healing practices, the impact of fear, anxiety and hopelessness is amplified.

In association to higher psychological processes, when a child is born into a particular society, any function of the cultural development appears twice: first, in the social plane, interpsychologically, then, within the child, internalized intrapsychologically. This is referred to as Vygotsky’s Genetic Law of Cultural Development (see Chapter 9). This describes, theoretically, how a child subtly acquires the culture that he or she is born into.

The balance of neurodevelopment and cultural traditions lend to the intergenerational continuation of processes and skills necessary for survival and growth. Phylogeny (the evolution of modern man) and cultural history (tool use) have contributed to ontogeny

(growth of the individual), more specifically, the development of specific parts of the brain that allow for higher psychological processes, learning and social interaction.

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Before a child is born, there are parental expectations that are based upon gender and cultural values (as an example, pink for girls and blue for boys, etc.). Because of the expanded neocortex, and assets afforded by higher psychological processes, children acquire the cultural immediately available to him or her. Because of what Michael

Tomasello refers to as the “ratchet effect” (Tomasello, 1999), cumulative cultural evolution moves forward in time (history). As a result, children born into a new generation are exposed to a continuous accumulation of mediating artifacts (tools, signs and symbols), lending to processes we refer to as “technology”, or the continuous motification of those physical, ideological, conceptual items deemed necessary for practical living and survival. From a cultural-historical perspective, the accumulation of mediating artifacts is referred to as “culture”.

As the child matures, and is stimulated by these cultural artifacts and the natural environment, neurogenesis is constantly taking place, and connections are made to various parts of the brain, depending upon the type of sensory stimulation. This is referred to as plasticity, changes to nervous tissue (neurons and whie matter tracts) in response to sensory stiumuli. As changes occur, the architecture of the brain unfolds. The more stimulation and variations of that stimulus, the greater is the potential for change and growth.

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On the other hand, neglected children do not receive adequate sensory stimulation, and the result may be underdevelopment of various parts of the brain. Like the foundation of a house, the potential is greater for future deficits if underlying structures are underdeveloped. Children in environments of toxic stress, also have potential for morphological and physiological deficits in the brain. Of equal importance, is the cultural acquisition of these behaviors and the potential for the continuation into the next generation.

Four major areas are impacted by toxic stress: 1) chronic disease development (see

Chapter 7); 2) interference with brain development, specifically the formation of the prefrontal cortex, affecting Executive Function (Chapter 9), a key component in development, learning in school and academic achievement, since it is associated with working memory and inhibitory control; 3) substance abuse, primarily through self- medication to reduce emotional pain and to compensate for deficits in cognitive functioning (see Chapter 9); and 4) the intergenerational transmission of dysfunctional behaviors, as theorized in Vygotsky’s Genetic Law of Cultural Development (previously mentioned, see Chapter 9), “any function in the child’s cultural development appears twice, in a social plane (interpsychologically), then, internalized within the child

(intrapsychologically)” (Vygotsky, 1981, see Chapter 9). Children learn to acquire the values and traditional behaviors in their home culture; internalize this, and as adults, past

165 this on to their own children. This is the basic unit for the intergeneration transmission of culturally-acquired behaviors. My contention is that children acquire these culturally- learned, dysfunctional coping behaviors, and pass them on to the next generation as they become adults and have their own families, continuing the devastating legacy associated with historical trauma.

As previously mentioned in Chapter 1, there is currently no support for strict biological, social or cultural determinism. Just because a person endures certain experiences, does not guarantee a specific outcome. There are genetic, biological and social factors that influence outcomes. Each situation is unique, offering context-specific stuations and environmental factors that affect individual, specific course of action. The work described in this study is a culmination of what has been previously put forth in regard to historical trauma and the impact of trauma, in general. Since the impact of trauma and stress has devasting consequences on human development, and historical trauma is associated with this trauma, an extensive investigation is made into the outcomes of

Adverse Childhood Experiences.

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CHAPTER 11

RECOMMENDATIONS

There is a need to increase our understanding of how current life stressors and traumatic events are experienced within the context of historical trauma. More scholarship and research exploring the relationship between historical and current traumas will lead to more holistic and refined models of impacts. Work in this area should also involve examining the ways that secondary stressors such as high rates of drug use in a community are modified when interpreted within a context of historical trauma.

Given what we know about the impacts of cumulative trauma over time, scholars of trauma must be committed to developing effective treatments for current and historical trauma that target not only individuals but also families and communities. Although there is a significant amount of literature on the treatment of posttraumatic stress at the individual level, such treatment models need to be modified to account for historical trauma. As previously reported, research on Toxic Stress, adverse childhood experiences and the boarding school experience should be done specific to AIAN individuals, families and communities. The results of this scholarly inquiry should go toward developing culturally appropriate intervention and prevention strategies that address the biological and cultural consequences of early childhood development. A number of tribes

167 have already embarked on community-level healing processes by reinstating traditional social practices and structures. The development of tribal courts and health clinics and tribe-managed social service providers might also be seen as a pathway to restore the social unit to functioning health.

Finally, and perhaps most important, future scholarship must directly investigate resilience and healing around the continuum of trauma in AIAN communities. Although much of the literature on historical and cumulative trauma has focused on negative outcomes, there is a small but growing literature exploring the strengths and resiliencies that result from survival and adaptation. After enduring generations of oppression and threats to family and community systems, many victims of trauma, abuse and their children shared a worldview focused on the family and the need for close community ties

(Cross, 1998). In this dissertation, it has been argued that in indigenous communities, a history of historical trauma has severed community ties and underscored the importance of retaining culture and tradition. As a result, self-identity, self-esteem, and hope have been over-shadowed by the impact of dysfunctional coping behaviors that have emerged from intergenerational patterns of violence, substance abuse and impaired cognitive development.

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