Salinan Terjemahan Stress, Coping, and Development, An Integrative Perspective by Carolyn M. Aldwin PHD, PHD Emmy E. Werner [PDF]

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STRES, MENGATASI, DANPENGEMBANGAN,



Stres Mengatasi, dan Pembanguna n Sebuah Integrative Perspektif EDISI KEDUA



CAROLYN M. Aldwin Kata Pengantar oleh Emmy E. Werner



THE GUILFORD PRESS New York London



© 2007 Guilford Tekan A Divisi Guilford Publications, Inc. 72 Spring Street, New York, NY 10012 www.guilford.com Semua hak dilindungi undang-undang Tidak ada bagian dari buku ini yang boleh direproduksi, diterjemahkan, disimpan dalam sistem pengambilan, atau ditransmisikan, dalam bentuk apa pun atau dengan cara apa pun, elektronik, mekanis, fotokopi, mikrofilm, rekaman, atau lainnya, tanpa izin tertulis dari Penerbit. Dicetak di Amerika Serikat Buku ini dicetak di atas kertas bebas asam. Digit terakhir adalah nomor cetak: 987654321



Library of Congress Katalogisasi Data Publikasi Aldwin, Carolyn M. Stress, coping, and development : an integrative perspektif / Carolyn M. Aldwin ; kata pengantar oleh Emmy E. Werner. - edisi ke-2. P. cm. Termasuk referensi bibliografi dan indeks. ISBN-13: 978-1-57230-840-4 ISBN-10: 1-57230-840-0 (kain : kertas alk.) 1. Stres (Psikologi) 2. Penyesuaian (Psikologi) 3. Stres (Psikologi)— Riset. 4. Penyesuaian (Psikologi)—Penelitian. 5. Psikologi perkembangan. 6. Pikiran dan tubuh. I. Judul. BF575.S75A42 2007 155,9'042-DC22 2006101615



Tentang Penulis



Carolyn M. Aldwin, PhD, adalah Profesor dan Ketua Departemen Pembangunan Manusia dan Ilmu Keluarga di Oregon State University, Corvallis. Dia menerima gelar doktor dari University of California, San Francisco, pada tahun 1982 dan merupakan sarjana pasca doktoral Institut Kesehatan Mental Nasional dalam Pembangunan Manusia, Tuntutan Lingkungan, dan Kesehatan. Dr. Aldwin menerima penghargaan PERTAMA dari National Institute on Aging untuk studinya tentang faktor psikososial yang mempengaruhi kesehatan pada penuaan dini dalam karirnya; dia telah menerbitkan lebih dari 70 artikel dan bab di bidang ini dan baru-baru ini menjadi co-editor Handbook of Health Psychology and Aging untuk The Guilford Press. Dr. Aldwin adalah rekan dari Divisi 20 (Perkembangan Dewasa dan Penuaan) dan 38 (Psikologi Kesehatan) dari



American Psychological Association, serta dari Gerontological Society of America.



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v



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Tia edisi kedua dari New Oxford American Dictionary (2005)



mendefinisikan stres sebagai “keadaan ketegangan mental atau emosional atau ketegangan yang dihasilkan dari keadaan buruk atau sangat menuntut,” mengatasi sebagai “kemampuan untuk menangani secara efektif dengan sesuatu yang sulit, ” dan perkembangan sebagai “keadaan pertumbuhan atau kemajuan tertentu.” Para pembaca dariedisi kedua Stress, Coping, and Development mungkin, kadang-kadang, mengalami ketegangan mental dalam menangani isi buku ini secara efektif. Tetapi mereka akan mendapat imbalan yang besar atas usaha mereka! Perspektif integratif Carolyn Aldwin terikat untuk memajukan pemahaman mereka tentang tubuh penelitian stres yang telah menghasilkan ribuan publikasi ilmiah dan ratusan skala penanggulangan baru sejak edisi pertama bukunya diterbitkan pada tahun 1994.



Saya kagum pada ruang lingkup disiplin ilmu yang Aldwin gunakan untuk perusahaan ini. Mulai dari antropologi hingga sosiologi dan mengembangkan psikologi mental; dari imunologi dan neuroendokrinologi hingga filsafat dan perbandingan agama. Masing-masing perspektif yang disajikan (dari mekanisme perbaikan seluler hingga "penanganan penuh perhatian") memperluas batas penelitian stres dan koping. Aldwin melakukan pekerjaan yang luar biasa dalam membantu kita menavigasi melalui labirin masalah konseptual dan pengukuran yang dihadapi siapa pun yang cukup berani untuk melakukan penelitian di bidang ini—memang, sekitar dua pertiga dari bukunya membahas topiktopik ini. Ia juga memperkenalkan pembaca pada isu-isu statistik dalam menghadapi penelitian yang cukup kompleks. Diskusi meyakinkan Aldwin tentang isu-isu metodologis menunjuk pada paradoks tertentu: Model statistik dalam penelitian koping menjadi vii vii Kata Pengantar



lebih canggih, tetapi pengukuran sebenarnya dari stres dan strategi koping masih cukup kasar dan sangat bergantung pada kuesioner laporan diri yang tampaknya berlipat ganda pada tingkat yang mengkhawatirkan—dari sekitar 70 “skala penanggulangan” pada tahun 1994 menjadi lebih dari 200 pada tahun 2006. Aldwin berpendapat secara persuasif bahwa penelitian tentang stres dan penanggulangan perlu mengambil perspektif transaksional dan longitudinal, dengan fokus pada kehidupan masyarakat dari waktu ke waktu dan pada konteks sosial dan budaya di mana mereka dibesarkan. Namun dalam penelitian yang diulas di sepertiga terakhir bukunya— tentang topik-topik seperti koping dan kesehatan, perubahan perkembangan dalam stres dan koping, dan stres sebagai dorongan untuk perkembangan psikososial—dia hanya mengutip beberapa studi longitudinal yang berfokus pada “ mengatasi stres traumatis" dan "mengatasi transformasional." Di bidang terkait, telah terjadi ledakan penelitian virtual tentang fenomena resiliensi, proses yang mengarah pada adaptasi positif meskipun menghadapi kesulitan hidup yang signifikan. Sekarang ada lebih dari selusin studi longitudinal skala besar tentang fenomena ini di Amerika Utara, Eropa, Australia, dan Selandia Baru yang meluas dari masa kanak-kanak hingga dewasa. Temuan mereka dapat menguntungkan dihubungkan dengan hasil penelitian kontemporer tentang stres dan mengatasi. Saya telah menghabiskan sebagian besar kehidupan profesional saya mengamati dan mendokumentasikan kapasitas luar biasa manusia untuk mengatasi rintangan besar. Kadang-kadang saya merasa terbantu untuk membaca ulangfavorit saya Grook, atau pepatah, yang ditulis oleh fisikawan dan penyair Denmark Peit Hein di hari-hari tergelap Perang Dunia II, waktu yang memberi banyak generasi saya kesempatan untuk mengatasi stres traumatis. Ini berkaitan dengan kebijaksanaan, salah satu konsep kunci dalam teori adaptasi yang disajikan Aldwin di bab terakhir bukunya.



Jalan menuju kebijaksanaan? Yah, itu jelas dan sederhana untuk diungkapkan: Err dan err dan err lagi, Tapi semakin sedikit.



Saya percaya bahwa buku Aldwin akan menjadi panduan yang bermanfaat bagi mahasiswa pascasarjana dan profesional berpengalaman dalam ilmu perilaku yang bersedia melintasi garis disiplin untuk menemukan jalan itu. EMMY E. WERNER,PHD University of California, Davis Kata Pengantar



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Saya



n edisi pertama buku ini, yang diterbitkan pada tahun 1994, saya mencatat ledakan penelitian stres dan proses koping. Sekarang, lebih dari satu dekade kemudian, ada tambahan 186.000 artikel tentang stres dan 37.000 artikel tentang mengatasi dalam literatur! Jelas ada kebutuhan untuk pembaruan, karena ada kemajuan substansial dalam pengetahuan yang telah dikumpulkan oleh para peneliti stres dan koping dalam 12 tahun terakhir. Mengingat banyaknya literatur, bagaimanapun, tidak mungkin untuk meninjau setiap artikel. Jadi, saya terpaksa selektif, mengandalkan banyak ulasan yang sangat baik dari bidang-bidang tertentu serta pada artikel-artikel yang mani di lapangan. Saya telah mencoba untuk menjadi selengkap mungkin dan membuat diri saya belajar banyak. Untuk edisi ini, saya telah memberikan pembaruan umum untuk hampir semua bagian dari setiap bab dan telah menghabiskan banyak waktu untuk apa yang saya anggap sebagai area baru yang menarik. Ini termasuk pertumbuhan yang berhubungan dengan stres (Bab 15); aspek sosial dan budaya dari koping, termasuk koping diadik (Bab 13); serta pendekatan baru untuk mengatasi, seperti pengambilan sampel



pengalaman, regulasi emosi, dan koping religius (Bab 7). Kami juga menjadi jauh lebih canggih dalam pengetahuan kami tentang fisiologi stres, dan edisi saat ini juga mencerminkan perubahan itu (Bab 4). Bab 11, bab koping dan kesehatan, mencakup bagian baru tentang koping dan fisiologi. Bab 14, yang mengulas penelitian koping perkembangan anak dan orang dewasa, juga telah sangat diperluas untuk memasukkan banyak studi koping baru dalam perkembangan anak serta penekanan baru dan sangat menjanjikan pada pengaturan diri. Ini juga ix x Kata Pengantar



mencakup bagian-bagian baru tentang dewasa muda dan paruh baya. Akhirnya, bab terakhir (16) mencakup apa yang saya harap akan menjadi paradigma menyeluruh untuk penelitian stres dan mengatasi, yang menggabungkan pendekatan pengaturan diri dari perkembangan anak dengan pendekatan pengembangan diri baru dalam perkembangan orang dewasa, memperluas diskusi sebelumnya pada kesengajaan dalam pembangunan. 12 tahun terakhir juga telah melihat kontroversi besar. Selama tahun 1980-an, ada seruan untuk meninggalkan penelitian stres, mengingat masalah definisi tertentu. Selama tahun 1990-an, ada seruan untuk meninggalkan penelitian koping karena alasan yang sama. Menurut pendapat saya, ini sama saja dengan "membuang bayi dengan air mandi" dan, menurut saya, prematur. Intinya, coping itu rumit. Hampir tiga dekade yang lalu Pearlin dan Schooler (1978) memperingatkan bahwa tidak ada "peluru ajaib" dalam mengatasi penelitian, dan penelitian telah membuktikan hal ini. Tidak ada strategi tunggal yang berhasil untuk semua orang, di setiap tempat, setiap saat. Sebaliknya, sifat dan efek dari koping sangat kontekstual dan mencerminkan motivasi individu, dinamika interpersonal, dan faktor-faktor yang mungkin spesifik situasi atau budaya. Dengan demikian, dapat dimengerti bahwa mereka yang menginginkan jawaban sederhana akan frustrasi, dan menunjuk kebingungan dalam literatur sebagai alasan untuk meninggalkan kapal. Sebaliknya, bagi saya ini tampaknya merupakan teka-teki yang sangat kaya yang menawarkan jendela indah ke dalam kompleksitas adaptasi. Mengapa strategi yang berfokus pada masalah bekerja untuk satu jenis masalah dan bukan yang lain? Untuk satu orang dan bukan orang lain? Pada satu titik dalam lintasan penyakit dan bukan yang lain? Mengapa strategi yang berfokus pada emosi, yang dimaksudkan untuk mengurangi afek negatif, sering kali dikorelasikan dengan tekanan psikologis? Apakah ada strategi yang berfokus pada emosi yang benarbenar mengurangi penderitaan? Memang benar bahwa langkah-langkah penanggulangan kita agak kasar, tetapi ada langkah-langkah yang semakin canggih yang menurut saya mungkin sangat menjanjikan. Untuk itu, saya juga telah memberikan daftar terbaru tentang upaya penanggulangan di Bab 8, termasuk yang diterbitkan dalam bahasa lain. Bab ini juga mencakup tinjauan baru atas perdebatan tentang penilaian pengambilan sampel pengalaman yang dilakukan secara retrospektif versus pengalaman. 12 tahun terakhir juga telah melihat lompatan kuantitatif dalam alat



analisis untuk analisis data multivariat dan longitudinal. Akibatnya, saya telah memperbarui metode bab (9) dengan gambaran yang diakui agak sederhana dari teknik-teknik baru ini. Dalam edisi pertama, saya menjelaskan masalah bahwa teknik analisis kami belum mencapai kecanggihan model kami. Sekarang teknik analitis sedang mengejar, mereka sering begitu baru dan rumit—dan menggunakan “bahasa ajaib” mereka sendiri—sehingga banyak individu, terutama mereka yang belum lulus dalam 5 tahun terakhir atau lebih, tidak terbiasa dengan terminologi, kegunaannya, dan asumsinya. Dengan memberikan deskripsimatical nonmathe xiKata Pengantar



dari istilah-istilah ini, saya berharap dapat menawarkan garis hidup bagi mereka yang tenggelam di lautan LISREL, kurva pertumbuhan laten, model garis telinga hierarkis, dan semua jenis lintasan longitudinal. Saya sangat senang dengan fakta bahwa literatur tentang aspek positif dari stres, atau pertumbuhan yang berhubungan dengan stres, seperti yang sekarang disebut, telah benar-benar lepas landas (Bab 15). Seluruh bidang psikologi positif, menurut saya, merupakan perkembangan yang sangat menguntungkan, meskipun bukan tanpa kritik (lihat Lazarus, 2003). Pentingnya koping religius juga telah menjadi yang terdepan, yang mencerminkan peningkatan umum dalam religiusitas yang terlihat selama dekade terakhir, dan Bab 16 memberikan “pandangan baru” tentang mengapa koping religius seringkali efektif. Masih benar, bagaimanapun, bahwa terlalu sering bidang yang terkait erat menggunakan terminologi yang berbeda untuk merujuk pada apa yang serupa jika bukan konstruksi yang identik. Misalnya, dalam psikologi perkembangan, ada banyak studi tentang pengaturan diri (lihat Eisenberg & Zhou, 2000). Ada juga kesejajaran dalam literatur perkembangan orang dewasa antara kontrol primer dan sekunder (Schulz & Heckhausen, 1998), proses asimilatif dan akomodatif (Brandstädter, 1999), dan koping yang berfokus pada masalah dan emosi. Dalam psikologi kognitif, banyak minat telah dihasilkan oleh proses yang digunakan untuk mengkompensasi penurunan kognitif (lihat Dixon, 1996). Para peneliti di bidang itu juga berjuang dengan banyak masalah yang sama seperti yang ada dalam literatur penanggulangan, seperti, Apakah kompensasi sadar atau tidak sadar (lihat Dixon & Bäckman, 1995)? Sekali lagi, tidak mungkin bagi satu orang untuk meninjau semua bidang secara menyeluruh, tetapi saya berharap setidaknya untuk mendorong orang lain untuk memeriksa perkembangan di bidang lain ini untuk menginformasikan pekerjaan mereka sendiri, dan saya akan menyarankan bahwa bidang lain ini akan mendapat manfaat dari kekayaan stres dan mengatasi penelitian. Seperti biasa, saya berhutang budi kepada banyak orang atas kontribusi mereka pada volume ini. Saya ingin mengucapkan terima kasih kepada semua rekan saya yang cukup murah hati untuk mengirim cetak ulang dan pracetak. Tidak mungkin untuk mengutip semua studi yang sering kali luar biasa ini, tetapi saya telah melakukan yang terbaik. Mahasiswa pascasarjana saya Daria Boeninger menghabiskan banyak waktu melakukan pencarian literatur dan menemukan artikel untuk saya, dengan cara yang sangat terorganisir, yang memungkinkan revisi ini.



Mantan mahasiswa pascasarjana saya dan sekarang rekan-rekan Drs. Diane Gilmer dan Loriena Yancura telah bekerja dengan saya pada tinjauan lain tentang stres dan literatur mengatasi, dari mana saya telah meminjam secara bebas untuk pembaruan ini. Dr. Ana Paula Cupertino, mantan mahasiswa pascasarjana lain dan sekarang kolega, dengan ramah membantu saya mengatur dan melacak referensi untuk draf pertama revisi ini dan sekali lagi memberi saya tempat yang tenang untuk bekerja di Brasil, yang sangat membantu saya dalam menyelesaikan revisi ini. Dr. Crystal Park di University of Connecticut sangat murah hati dengan waktunya membaca hampir semua bab buku ini dan memberikan komentar yang sangat meyakinkan. Dr. xii Kata Pengantar



Megan McClelland di Oregon State University membaca bab perkembangan dan memiliki beberapa saran yang sangat membantu. Para mahasiswa pascasarjana di Universitas California, Davis tahun 2004 saya, kelas semester musim semi tentang Penuaan dan Adaptasi dan kelas kuartal musim dingin 2005 Universitas Negeri Oregon saya tentang Stres dan Mengatasi Sepanjang Umur juga membaca konsep bab dan memberikan umpan balik yang berguna. Sungrok Kang secara khusus membacakan buku itu dengan cermat, dan Amanda Taylor masuk dan membantu kompilasi akhir dari referensi tersebut. Sandra Frye sangat membantu dalam produksi naskah, yang saya sangat berterima kasih. Kakak-kakakku, Drs. Mary Bisson (sekarang dengan gembira menjadi mantan ketua Departemen Biologi di Universitas di Buffalo, Universitas Negeri New York) dan Lois Aldwin (seorang ahli biokimia yang mengkhususkan diri dalam pengujian sistem kekebalan), telah menjadi "senjata rahasia" saya dalam memahami biol ogi stres. Mereka berdua selalu sabar dalam menjawab pertanyaan dan menjelaskan bagianbagian yang sangat rumit. Sekali lagi editor saya, Seymour Weingarten, menunjukkan kesabaran yang luar biasa melalui banyak tenggat waktu yang terlewat dari buku ini. Saya juga harus berterima kasih kepada ribuan pria dan wanita dalam Normative Aging Study dan Davis Longitudinal Study yang telah dengan murah hati berbagi pengalaman mereka yang seringkali sangat menyakitkan dalam mengatasi stres dan trauma dalam hidup mereka. Menceritakan perjuangan mereka telah memunculkan banyak wawasan tentang proses adaptif yang disajikan dalam buku ini dan merupakan dorongan untuk penelitian saya tentang ketahanan dan pertumbuhan yang berhubungan dengan stres. Akhirnya suami dan kolega saya, Rick Levenson, selalu mendukung. Dia telah menguasai penggunaan humor sebagai strategi mengatasi dalam interaksi interpersonal, yang saya sangat berterima kasih. Dia telah mendorong saya untuk mengambil perspektif alternatif dan sering memaksa saya untuk melihat lebih dalam ke jawaban yang saya pikir pada awalnya jelas tetapi kemudian, pada pemeriksaan lebih dekat, terbukti kurang. Dan dia tidak mengeluh (banyak) pada tumpukan cetakan ulang yang sekali lagi menghiasi rumah kami dalam pelayanan revisi ini. Untuk kesabaran dan humornya, saya ingin mempersembahkan buku ini untuknya. CAROLYN M. ALDWIN DaftarDaftar



IsiIsi



BAB 1 Pendahuluan dan Tujuan Buku 1 Transaksi Pikiran-Tubuh 2 Transaksi Orang-Lingkungan 7 Organisasi Buku 9



BAB 2 Mengapa Stres Penting? 13 Minat Intrinsik 13 Relevansi Stres dengan ModelPsikososial Adaptasi15 Relevansi Stres dengan Model Biomedis Adaptasi 17 Ringkasan 22



BAB 3 Definisi Stres 23 Komponen Proses25 StresStres sebagai Keadaan Organisme 27 Stres sebagai Peristiwa Eksternal 28 Stres sebagai Transaksi antara Orang dan Lingkungan 31 Peran Emosi dan Kognisi dalam Reaksi terhadap Stres 34 Ringkasan 36



xiii xiv Daftar Isi



BAB 4 Fisiologi Stres 37 Respon Neuroendokrin terhadap Stres 37 Respon Kekebalan Terhadap Stres 46 Resistensi Seluler terhadap Stres 52 Ringkasan 53



BAB 5 Isu Desain dan Pengukuran dalam Penelitian Stres 55 Observasi Umum 55 Isu Desain dalam Penelitian Stres 57 Masalah dalam Arahan Kausal 59 Pendekatan Berbeda untuk Pengukuran Stres 62 Ukuran Mana yang Digunakan? 79



Wawancara Klinis 80 Stresor Laboratorium 81 Ringkasan 82



BAB 6 Mengapa Mengatasi Penting? 84 Minat Intrinsik 86 Akar Mitopoetik 86 Perubahan Peran Sosial 88 Relevansi Mengatasi dengan ModelPsikososial Adaptasi91 Relevansi dengan Model Biomedis Adaptasi 93 Membedakan antara Adaptasi, Mengatasi, dan Respons Emosional 95 Ringkasan 97



BAB 7 Pendekatan Teoretis untuk Mengatasi 98 Berbasis Orang Definisi Coping 100 Penentu Situasional dari Coping 113 Pendekatan Kognitif 115 Pendekatan Lebih Baru untuk Mengatasi dan Adaptasi 117 Ringkasan 125



BAB 8 Pengukuran Strategi 127 MengatasiGaya Mengatasi versus Proses Mengatasi 129 Retrospektif versus Pengambilan Sampel Pengalaman Pendekatan134 Ketidakstabilan Struktur Faktor 136 Penanganan Umum versus Khusus Strategi 139



Daftar Isi xv Skala Penilaian 141 Ringkasan 144 Lampiran 8.1. Daftar Pustaka Skala Coping 145



BAB 9 Isu Statistik dalam Penelitian Coping 161 Mekanisme Efek Coping 161 Analisis Statistik untuk Menguji Efek Mediasi dan Moderasi 166 Analisis Longitudinal Data Stres dan Mengatasi 175 Ringkasan 180



BAB 10 Mengatasi dan Kesehatan Mental 181 Kebingungan antara Penilaian dan Hasil 182 Pengubah Situasional dari Efek Mengatasi 183 Pola Mengatasi 186 Upaya Mengatasi 187



Arahan Penyebab dan Intervensi Mengatasi 189 Perbedaan Individu dalam Efektivitas Mengatasi 191 Apa Hasil yang Tepat dariMengatasi Strategi? 192 Ringkasan 193



BAB 11 Mengatasi dan Kesehatan Fisik 195 Adaptasi Terhadap Penyakit 197 Mengatasi dan Hasil Penyakit 202 Ringkasan 207



BAB 12 Mengatasi Stres Traumatis 210 Mendefinisikan Trauma 211 Gangguan Stres Pascatrauma 212 Mengatasi Trauma 220 Ringkasan 238



BAB 13 Aspekdari Mengatasi 239 Sosial BudayaAspek Sosial of Coping 239 Budaya dan Stres 245 Budaya dan Coping 257 Institusi sebagai Mekanisme Mengatasi 266 Ringkasan 270



xvi Daftar Isi



BAB 14 Studi Perkembangan Mengatasi 271 Mengatasi Masa Bayi dan Anak 272Masa Perubahan Perkembangan Stres dan Mengatasi diDewasa 292 Ringkasan 304



BAB 15 Pertumbuhan Terkait Stres dan Coping Transformasional 305 Argumen untuk Implikasi Perkembangan dari Stres 308 Stres sebagai Dorongan untuk Perkembangan Psikososial 315 Stres sebagai Dorongan untuk Perkembangan Fisiologis 332 Model Hasil Stres Positif dan Negatif 336 Ringkasan 340



BAB 16 Pengaturan Diri, Pengembangan Diri, dan Kebijaksanaan 341 Transaksionisme dan Mengatasi 342 Kehendak Bebas v ersus Deterministic Models of Adaptation 345 Mindful Coping and Wisdom 354 Ringkasan 357



Referensi 359 Indeks 419



STRES, COPING, DAN PENGEMBANGAN Pengenalan dan Tujuan Buku



BAB 1



Pendahuluan dan Tujuan Buku



T



homas Kuhn (1970) menunjukkan bahwa, dari waktu ke waktu , pergeseran paradigma terjadi dalam sains dan masyarakat— yaitu, asumsi mendasar tentang sifat dunia yang berubah. Naiknya teori kuman penyakit merupakan satu pergeseran paradigma, teori relativitas lain. Saya percaya kita sedang mengalami pergeseran paradigma lain— dari reduksionisme kausal ke transaksionisme. Sederhananya, dalam reduksionisme kausal, terjadinya suatu peristiwa direduksi menjadi penyebab yang mendasarinya, sedangkan dalam transaksionisme, terjadinya suatu peristiwa dipahami sebagai akibat dari pengaruh timbal balik dari sejumlah faktor. Pergeseran paradigma ini memiliki implikasi mendalam tidak hanya untuk penelitian dan praktik klinis tetapi juga untuk tatanan masyarakat dan bagaimana kita menjalankan kehidupan kita sehari-hari. Jelas masih ada ketegangan antara paradigma reduksionis lama dan paradigma transaksional baru. Ini mungkin paling jelas dalam pertumbuhan eksplosif dalam ilmu genom selama dua dekade terakhir. Di satu sisi, sejumlah besar informasi yang dihasilkan oleh Proyek Genom Manusia, yang memungkinkan kita untuk memahami lebih tepat mekanisme yang mendasari berbagai fenomena kompleks, dapat dilihat sebagai penguatan model reduksionis. Tetapi informasi yang sangat banyak juga telah memunculkan pendekatan biologi sistem yang berupaya mengintegrasikan kumpulan informasi ini dengan menggunakan matematika dan statistik (Pennisi, 2003). Dengan menggunakan teknik ini, para ahli biologi sedang menyelidiki topik-topik yang kompleks 1 2 STRES, PENANGGULANGAN, DAN PERKEMBANGAN



seperti pensinyalan sel, perkembangan anggota badan pada janin, dan bagaimana ragi beradaptasi dengan perubahan lingkungan nutrisi. Pergeseran ini terjadi di berbagai cabang ilmu pengetahuan. Hal ini paling terlihat dalam studi tentang hubungan antara pikiran dan tubuh dan antara orang dan lingkungan, tetapi disiplin ilmu lain, termasuk biologi dan fisika subatomik, juga bergeser ke paradigma transaksionis. Saya akan berpendapat dalam buku ini bahwa penelitian tentang efek psikologis dan fisik dari stres, dan bagaimana mereka dimodulasi oleh upaya mengatasi, telah berperan dalam mempengaruhi perubahan paradigma dalam ilmu psikososial dan biomedis. Fokus utama buku ini adalah menyatukan literatur dari berbagai bidang yang meneliti transaksi, baik antara pikiran dan tubuh dan antara orang dan lingkungan, dalam konteks penelitian stres, mengatasi, dan adaptasi.



TRANSAKSI PIKIRAN-BODY Selama abad ke-17 René Descartes mengusulkan isme ganda mendasar antara pikiran dan tubuh. Pikiran diadakan untuk terlibat dalam pemikiran abstrak dan bahasa, yang terpisah dan berbeda dari operasi tubuh (Eccles & Robinson, 1984). Dualisme Cartesian ini telah menjadi landasan paradigma reduksionis yang mendasari ilmu-ilmu bio kedokteran. Ini menugaskan studi tentang cara kerja fisiologis tubuh ke sains dan pertimbangan pikiran dan jiwa ke filsafat. Lebih lanjut diasumsikan bahwa, karena berbeda, pikiran dan tubuh dipengaruhi oleh faktor-faktor yang sama sekali berbeda dan bahwa komunikasi kecil terjadi di antara keduanya. Dualisme Cartesian diekspresikan dalam model penyakit penyakit, atau model biomedis dasar (Virchow, 1863). Model ini, yang lazim selama 150 tahun terakhir, menyatakan bahwa penyakit disebabkan oleh agen eksternal yang mengganggu fungsi normal tubuh, seperti agen bakteri dan virus, racun, dan berbagai jenis karsinogen. Penelitian berfokus pada mekanisme yang dengannya agen eksternal merusak kesehatan dan bagaimana kerusakan tersebut dapat diperbaiki dengan sebaik-baiknya. Model ini kemudian diperluas untuk mencakup gangguan yang disebabkan oleh agen internal, yaitu gen yang salah. Asumsi wajar yang mendasari model reduksionis adalah kausalitas searah—yaitu, a → b → c. Dalam istilah biomedis, ini berarti bahwa penyakit disebabkan oleh paparan agen a yang mengganggu fungsi biokimia sistem b yang pada gilirannya menyebabkan gejala c. Gejalagejala ini hanya dapat dikurangi dengan memulihkan fungsi sistem b, baik dengan menghilangkan agen penyebab dari tubuh (misalnya, melalui antibiotik) atau dengan mengembalikan keseimbangan biokimia. Ini sebagai Pengantar dan Tujuan Buku 3



asumsi tentang kausalitas memfokuskan penelitian pada konstitusi biokimia dasar tubuh, dan jumlah yang dipelajari telah luar biasa. Dalam istilah Kuhn (1970), paradigma ini sangat berhasil dalam memajukan pengetahuan. Tetapi asumsi apa pun menyimpan benih keterbatasannya sendiri di



dalam dirinya. Karena semakin banyak yang dipelajari tentang fisiologi dan biokimia, kompleksitas informasi itu meningkat pesat. Menjadi jelas bahwa model kausal sederhana tidak cukup untuk menggambarkan banyak fenomena (von Bertalanffy, 1969). Karena regulasi fisiologis dari sistem yang berbeda melibatkan rangkaian loop umpan balik yang sangat kompleks di antara banyak variabel, semakin banyak kondisi dan batasan ditempatkan pada model kausal sederhana. Meskipun kuman atau bakteri yang menyerang dapat menciptakan diperlukan kondisi yanguntuk penyakit tertentu, mereka mungkin tidak cukup untuk menciptakan penyakit (sebaliknya, penyakit dihasilkan dari interaksi yang sangat kompleks antara sistem inang dan agen penyakit. Misalnya, dapat dengan mudah ditunjukkan bahwa TBC terjadi ketika seseorang terinfeksi bakteri tuberkulin, yang menyebabkan peradangan dan jaringan parut pada organ, terutama paru-paru.Gejala khasnya meliputi kelelahan dan batuk darah dan dahak.Akhirnya kematian terjadi karena semakin banyak organ target yang rusak Gejala-gejala ini dapat dikurangi dengan pemberian antibiotik, nutrisi yang tepat, istirahat, dan, jika perlu, pembedahan untuk mengangkat bagian organ yang rusak. Namun, studi epidemiologi tuberkulosis dan penyakit lain menunjukkan bahwa lebih banyak orang telah terpapar. untuk atau benar-benar membawa agen bakteri atau virus daripada turun dengan penyakit, dan model penyakit harus b e diperluas untuk memasukkan konsep resistensi tuan rumah—bahwa setiap orang tidak sama-sama terpengaruh oleh agen penyerang. Investigasi resistensi inang terhadap penyakit ini dan banyak penyakit lainnya menghasilkan penemuan sistem kekebalan, sistem yang sangat kompleks di mana tubuh dapat menghancurkan agen penyerang, mengisolasi dan memecah racun, dan membantu memperbaiki kerusakan. Dalam banyak kasus, gejala penyakit sebenarnya mewakili upaya tubuh untuk mengusir agen penyerang daripada kerusakan aktif oleh agen. Dengan demikian, model kausal sederhana dari penyakit akan digantikan oleh model yang sangat kompleks yang menunjukkan interaksi di antara banyak agen. Seperti yang ditunjukkan Kuhn (1970), semakin banyak kondisi dan batasan yang ditempatkan pada sebuah model, semakin berat model itu dan semakin besar kemungkinannya untuk diganti melalui pergeseran paradigma. Tetapi pemahaman yang meningkat tentang kompleksitas interaksi yang mengarah ke keadaan penyakit ini tidak cukup untuk mempengaruhi pergeseran paradigma dari reduksionisme fisiologis ke transaksionisme pikiran-tubuh. Seseorang dapat mempelajari sistem organ apa pun dengan lebih detail dan lebih halus tanpa harus meninggalkan model 4 STRESS, COPING, AND DEVELOPMENT



don Virchow (1863). Hanya ketika seseorang mulai mempelajari interaksi lintas tingkat analisis, reduksionisme akan runtuh. Dengan kata lain, mekanisme kausal sederhana mengasumsikan sistem tertutup, menggunakan istilah von Bertalanffy (1969). Artinya, ada sejumlah variabel terbatas yang berinteraksi secara internal dan relatif kebal terhadap kekuatan luar. Misalnya, deskripsi buku teks klasik tentang sistem peredaran darah merinci komponennya, seperti jantung, vena dan arteri, kapiler dan arteriol, dan regulatornya, seperti cabang simpatik dan



parasimpatis dari sistem saraf otonom (ANS). Tetapi, ketika seseorang mulai mempelajari sistem peredaran darah dan bagaimana ia menjadi sakit secara lebih rinci, menjadi jelas bahwa sistem peredaran darah bukanlah sistem tertutup tetapi sistem terbuka — terdiri dari sejumlah besar komponen yang dipengaruhi oleh kekuatan eksternal. . Sistem peredaran darah berinteraksi tidak hanya dengan ANS tetapi juga dengan sistem saraf pusat (SSP) melalui sistem neuroendokrin dan sistem imun. Hal ini juga dipengaruhi oleh perilaku individu—apa yang dia makan, merokok, dan minum, serta apakah dan bagaimana dia berolahraga atau tidak. Pengaruh lain termasuk tingkat stres dalam kehidupan individu dan kepribadiannya, gaya kognitif, dan hubungan sosial. Jadi, alat yang disediakan oleh model medis dan reduksionisme fisiologis yang memungkinkan kita untuk memahami secara lebih rinci dan lebih rinci cara kerja tubuh juga mengungkap keterbatasan paradigma itu. Tidak ada sistem organ yang merupakan sistem yang sepenuhnya tertutup. Sebaliknya, semua tunduk pada regulasi oleh otak melalui neuroendokrin dan sistem kekebalan (Ornstein & Thompson, 1984). Ilmu psikologi meniru ilmu biomedis dalam mengekspresikan dualisme Cartesian sebagai reduksionisme fisiologis searah—yaitu, proses psikologis dapat direduksi menjadi basis neurofisiologisnya. Dalam pernyataan paling ekstrem dari sudut pandang ini, pikiran dipandang sebagai "epifenomenon" otak. Sementara banyak model yang lebih kompleks memang ada dalam teori psikiatri modern penyakit mental, kecenderungan dominan masih menganggap kausalitas mekanisme biokimia. Misalnya, jika seseorang menemukan bahwa penderita depresi yang melakukan bunuh diri memiliki kadar serotonin yang jauh lebih rendah daripada orang yang tidak bunuh diri, asumsi standarnya adalah menganggap perilaku bunuh diri itu karena ketidakseimbangan neurotransmiter dan untuk mengobati gangguan depresi dengan memulihkan keseimbangan neurotransmiter melalui obatobatan. Namun, penjelasan alternatif yang sama masuk akalnya mencakup kemungkinan bahwa ide bunuh diri menciptakan ketidakseimbangan serotonin atau bahwa ada loop umpan balik yang saling memperkuat di antara keduanya. Tentu saja, fakta bahwa kognitifperilaku ther APY sebagai baik atau lebih baik dari antidepresan dalam mengurangi depresi (Gloaguen, Cottraux, Cucherat, & Blackburn, 1998) menunjukkan bahwa de pression melibatkan interaksi kompleks antara fisiologi dan pengalaman Pendahuluan dan Tujuan dari Kitab 5



ence. Hal ini disorot oleh studi terbaru oleh Caspi dan rekan-rekannya (2003), yang menunjukkan bahwa hasil depresi dari interaksi antara bentuk-bentuk alternatif dari gen yang mengatur penyerapan serotonin dan paparan peristiwa kehidupan yang penuh tekanan. Argumen elegan bahwa pikiran tidak hanya dapat direduksi ke otak telah diusulkan oleh Eccles dan Robinson (1984), berdasarkan literatur neuropsikologi dan linguistik, dan oleh Walker (1970), berdasarkan fisika. Meskipun Popper dan Eccles (1977) mengusulkan istilah "dualisinteraksionisme" untuk menggambarkan hubungan antara pikiran dan otak, konstruksi transaksionisme mungkin lebih tepat dalam menggambarkan hubungan ini. Menurut transaksionis seperti Laz arus



(1966; Lazarus & Folkman, 1984) dan Appley dan Turnbull (1986), model dualis-interaksionis tidak lengkap karena menyiratkan bahwa dua agen saling menciptakan fenomena tetapi tetap independen dan tidak berubah. Transaksionisme, di sisi lain, mengasumsikan bahwa kedua agen tidak independen tetapi saling dipengaruhi oleh transaksi. Figure 1.1 illustrates the difference between physiological reduc tionism, interactionism, and transactionism, using emotions as the de pendent or caused phenomenon. In the top section, the arrow indicates that the brain causes the emotions. For example, serotonin is hypothe sized in older, simpler models to cause negative emotions. The middle part of the figure illustrates interactionism: that the brain and the mind (cognition) both affect emotions. Using stress terminology, one would say that the appraisal of a threat, combined with a genetic propensity to overproduce adrenaline, would result in excessive feelings of anxiety. In



BRAIN EMOTIONS Reductionist Model BRAIN MIND EMOTIONS Interactionist Model BRAIN MIND EMOTIONS Transactionist Model



FIGURE 1.1. Comparison of different causal models of emotions.



6 STRESS, COPING, AND DEVELOPMENT



transactionism, the dependent variable (in this case, emotions) in turn influences both the brain and the mind. Thus, through the medium of emotions, the brain and the mind mutually affect one another. From a transactionist viewpoint, the mind is no longer reducible simply to the workings of the brain, nor, as a colleague of mine once whimsically put it, is the brain a mere epiphenomenon of the mind. Rather, the state of mind influences the workings of the body, while the state of the body influences cognitive and emotional processes. Both can be changed as a result of the transaction. For example, continuing anxi ety may affect both physiological functioning and appraisal processes. Psychiatric understanding of depression is gradually shifting from a simple neurochemical imbalance model to one that is refocusing on the structure of the brain. One of the most exciting areas of research in volves the interrelationships among stress, hippocampal size and func tioning, and depression. Traumatic or chronic stress may result in high levels of stress hormones such as cortisol, which differentially damage the hippocampus (Sapolsky, 1999). In turn, hippocampal size has been



correlated with depression (Do, Payne, Levy, MacFall, & Steffens, 2002). Current thinking is that some antidepressants work not by changing biochemical imbalance but by stimulating the growth of new neurons in the hippocampus (Manji et al., 2003). The role of coping in this system has yet to be investigated, but clearly that is an important link in this system. Sperry (1993) suggested that this cognitive revolution in psychology has formed the basis for the current paradigm shift in the sciences in gen eral. The seemingly simple addition of bidirectional arrows has enor mous implications, not only for the manner in which science is con ducted but also for much of everyday life. The body is no longer a mechanical device that sometimes requires repair. The emphasis has been slowly shifting to a disease prevention model, especially given the preva lence of chronic disease among a rapidly aging population. People are now much more aware of the impact of psychological stress on their bodies and may try to reduce that influence through myriad methods. In California, claims for stress-related disability or workmen's compensa tion have increased dramatically during the past two decades. On the other side of the equation, millions of Americans now avidly pursue physical fitness as a way of helping to manage their psychological states. In short, the fabric of our lives has changed tremendously as a direct re sult of this paradigm shift. A transactionist paradigm has greater implications also for the study of adaptation, implications that have not yet been fully under stood within psychology. In any scientific endeavor it is extremely im portant to examine one's assumptions, understand their implications for Introduction and Purpose of the Book 7



how the world is thought to function, and formalize hypotheses. Studies of stress and coping form a laboratory, as it were, for examining the role of transactional processes in adaptation. Thus, an additional purpose of this book is to explore the implications of a transactionist paradigm for stress, coping, and development. Two assumptions of transactionism are particularly relevant to stress and coping research. First, variables mutually influence each other, both within and across levels. If the mind and brain do transact, then, being regulated by the brain, organ systems are subject to influence by the mind and, in turn, anything that affects the mind (eg, society and culture). Thus, seemingly distinct levels of analysis—sociocultural, psy chological, and biological—are all linked. Further, how a culture or soci ety is structured has implications for an individual's physiological well being, not only through the direct allocation of resources (Pearlin, 1989) but also through influencing characteristic psychological states and stress levels (Colby, 1987). Second, transactionist models of necessity imply developmental pro cesses in that the focus of any transaction is change. Thus, a parallel par adigm shift in developmental sciences involves dynamic systems theory— positing that there are mutually influential changes over time (eg, Ford & Lerner, 1992). Most stress theorists focus on the immediate situation and try to show, for example, how appraisal affects coping, which in turn affects both the outcome and appraisal processes. However, a



transactionist model implies a strong possibility that both the mind and the body are altered as a result of their transaction. Theorists such as Schonpflug (1985) and Hobfoll (2002) have implied this in their eco nomic models of stress and coping as resource depletion–conservation. However, there is no reason to assume that a stress transaction has exclusively negative outcomes but rather may have positive ones as well, as is implied by Meichenbaum's (Meichenbaum & Cameron, 1983) stress inoculation theory and Dienstbier's (1989) construct of stress induced “toughness.” Aldwin and Stokols (1988) have presented various approaches to modeling change, whether positive or negative, short term or long-term, that can result from stressful interactions. Indeed, the whole area of “posttraumatic growth” is one of the most exciting new areas in psychology (see Tedeschi & Calhoun, 2004).



PERSON–ENVIRONMENT TRANSACTIONS Thus, transactionism has broad implications for the study of stress and coping in that it can link both environmental (eg, sociocultural) and de velopmental perspectives to biomedical findings. Figure 1.2 presents the 8 STRESS, COPING, AND DEVELOPMENT



view of coping as seen from the reductionist, interactionist, and trans actionist perspectives. The top part of Figure 1.2 represents the reduc tionist, or stimulus-response (SR), model of coping behavior. In this model, coping behaviors are viewed as simple responses to stressful envi ronmental stimuli. The middle part of Figure 1.2 represents the interac tionist model. Coping is hypothesized to be a function of personal and environmental characteristics. For example, the use of coping strategies is influenced by personality characteristics, such as emotionality (Bolger, 1990), as well as by the type of stressor or environmental demand (Mattlin, Wethington, & Kessler, 1990). The standard transactionist point of view (see, eg, Lazarus & Folkman, 1984) examines transactions only within the context of a sin gle stressful episode. In this model, personal and environmental variables influence appraisal, which determines the type of coping response. Coping outcomes, in turn, influence the appraisal process. Yet, inspec tion of the bottom part of Figure 1.2 suggests that coping outcomes not only influence appraisal processes within the stress context but also may have effects on both the person and the environment. For example, how a person copes with a particular stressful situation may add to his or her coping repertoire or may alter a person's outlook on the controllability or uncontrollability of the environment (eg, locus of control or explan atory style). Further, how an individual copes with a problem may alter the environment, affecting not only whether a particular problem is solved but also whether and how the problem arises for other individu als. Legal action to resolve racial or sex discrimination cases, for exam ple, may provide the means for other individuals to cope with similar



STRESS COPING



Reductionist Model STRESS PERSONALITY COPING Interactionist Model STRESS PERSONALITY COPING Transactionist Model



FIGURE 1.2. Comparison of different causal models of coping.



Introduction and Purpose of the Book 9



problems. Thus, the implications of a transactionist viewpoint extend beyond the individual stressful context to wider developmental or social situations. In stress and coping research, the environment has been viewed pri marily in interactionist terms, that is, as a stimulus or source of stress, or less frequently as a source of resources for coping with stress (eg, social support). However, a transactionist view suggests that the environment has a much more extensive role than simply its function as a stimulus or a resource. For examples, physical and social environments play a role in shaping not only the choice of coping strategies (de Ridder, 1997; Me chanic, 1978; Thoits, 1986) but also the impact of that strategy (Zautra & Manne, 1992). Further, in most theories, coping is assumed to have some effect on the problem, but studies generally focus only on its effect on the individual's well-being. From a transactionist point of view, more attention needs to be paid to the effect of coping on the environment, whether its effect on the immediate problem or on others in the situation (DeLongis, Bolger, Kessler, & Wethington, 1989). If, as Mechanic (1978) so radically suggested, coping strategies are primarily a function of cul tural patterns and institutions, then how an individual copes not only has an effect on the immediate problem but also adds to the cultural rep ertoire of coping strategies (Aldwin, 1985).



ORGANIZATION OF THE BOOK This book explores the themes presented in this introduction from the perspective of the paradigm shift in the psychological and biomedical sciences. However, any paradigm shift is accompanied by much dissen sion and argument as various opposing factions argue for the status quo or for different directions of change. This dissension is obvious in the area of stress and coping. Rather than attempt to promote any one par ticular school or theory of stress and coping, we will take an “elephant in the dark” stance. That is, no one school or theory is complete and correct— the differing approaches all have strengths and limitations, and in some



circumstances the approaches are not so much in conflict but are actually addressing quite disparate parts of the “elephant.” By exam ining the historical context and conceptual assumptions underlying dif ferent approaches, we will attempt to clarify the nature of some of the debates in the field and to show precisely where the conflict lies and how the differing approaches might be integrated, where possible. It is also true that research methods have lagged far behind the the oretical conceptualization, especially in psychology. Thus, key method ological issues of relevance to both the conduct of research and its inter 10 STRESS, COPING, AND DEVELOPMENT



pretation will also be considered. Again, rather than advocate any particular technique, we will discuss the strengths and weaknesses of the various ways in which stress and coping are measured and which tech niques may be useful for differing research questions and contexts. As with any scientific discipline, the field of psychology has gone down many blind alleys, in part because psychologists have made simpli fied assumptions for the sake of constructing theoretical models, but also in part because they have allowed their research—and to a certain extent their clinical work—to become divorced from the realities of ev eryday life. In many ways, this divorce has been useful—the best of psy chological research has often shown that “conventional wisdom” is markedly and decidedly wrong. But this divorce can also be responsible for pursuing assumptions down blind alleys, as when Watson tried to re duce thought to microscopic workings of the musculoskeletal system un derlying speech or when Hull tried to reduce memory to muscle action. Thus, putting psychology into its everyday context is important not only as a check against wrong assumptions but also is a didactic tool, a bridge for students to connect their own experiences to psychological theory. These three concerns with theory, method, and relevance influence the structure of this book. Chapter 2 discusses conceptual issues in stress research and why the construct of stress and how it is researched are important to our everyday lives. Chapter 3 discusses the different defini tions of stress and how the assumptions implicit in these definitions influence the type of research that is conducted. Our knowledge of the impact of stress on physiology has been greatly enhanced during the past decade, and this update will reflect that increased sophistication by devoting a new chapter (Chapter 4) to that topic. Chapter 5 addresses issues in stress measurement and methodology, and pays special atten tion to new techniques for assessing daily stress processes as well as eco logical momentary assessments. While the stress literature has been reviewed extensively, there have been surprisingly few exhaustive reviews of the coping literature (but see Aldwin & Yancura, 2004; Folkman & Moskowitz, 2004); the subse quent chapters attempt to fill that gap. Initially paralleling the construc tion of the chapters on stress research, Chapter 6 addresses conceptual issues in coping research; Chapter 7, definitions of coping; and Chapter 8, the measurement of coping strategies. Issues in stability and change in the factor structure of coping will be reviewed. Appendix 8.1 also in cludes a partial nonannotated bibliography of coping measures that should prove useful to both researchers and students. Chapter 9 dis cusses some of



the methodological and statistical issues in understanding Introduction and Purpose of the Book 11



the effects of coping. The statistics and design section is enhanced by in cluding newer structural equation, hierarchical, and longitudinal mod els. Chapter 10 reviews the literature on coping and mental health out comes, and Chapter 11 addresses coping and physical health outcomes. Our understanding of the neuroendocrine and immune systems has ex ploded during the past decade, and, as we shall see, the coping and health outcomes literature has been struggling to keep up. Chapter 12 examines how individuals cope with trauma and includes a new section on coping with the aftermath of the 9/11 terrorist attacks. A major limitation of stress research is that it has been almost strictly a psychological endeavor. However, there is a growing recogni tion that social and cultural contexts affect stress and coping processes. Chapter 13 reviews the small but growing body of research that demon strates the interpersonal and social influences on appraisal and coping processes and that shows how work in medical anthropology might rad ically alter our view of how coping works. This book also places the study of stress and coping in a larger developmental context. In part, this is accomplished in Chapter 14 by re viewing the coping literature in special populations—children and the elderly—as well as providing theoretical overviews of changes in coping across the lifespan. Thus Chapter 15 reviews studies on stress-related growth. In our rush to document the negative aspects of stress, we may have overlooked its positive aspects—stress as an impetus for growth and development, and transformational coping as the manifestation of a lifelong quest for greater mastery and understanding. While research in this area has also greatly increased during the past 12 years, reviews of that literature are also scarce, and the revisions to this chapter will ad dress that gap. Chapter 16 provides a summary of the various themes developed in this book and how they relate to the transactionist perspective espoused in this chapter. It also examines deterministic versus nondeterministic models of adaptation. In the 13 years since this book was first published, a greater acceptance of the importance of volition in adult development and adaptation has occurred (see Brandstädter, 1999), especially in the context of positive psychology (Seligman & Csikszentmihalyi, 2000). In summary, within the field of stress and coping, this book pro vides some insights into the nature of conceptual and methodological debates in the field in order to allow researchers and students to best de cide which particular approaches and assessment techniques are most relevant for them. In addition, integrating developmental psychology, es pecially adult developmental psychology, with an understanding of the 12 STRESS, COPING, AND DEVELOPMENT



nature of adaptation provided by stress and coping studies will enhance both fields. Adding a developmental perspective to studies of adaptation may provide an impetus to reconsidering the types of outcome measures that are used; and adding an adaptation perspective to developmental psychology may provide greater insight into the role of the environment in



promoting development, in both childhood and adulthood. STRESS, COPING, AND DEVELOPMENT Why Is Stress Important?



CHAPTER 2



Why Is Stress Important?



The construct of stress is important on a number of levels. First, stress is intrinsically interesting, as the casual perusal of any bookstore, newspaper, or television news program would indicate. Second, stress is highly relevant to psychosocial models of adaptation. As we shall see, a transactionist viewpoint subsumes many of the current models of mental illness. Third, stress is also relevant to biomedical models of adaptation and has transformed our notions of health, the maintenance of good health, and the treatment of illness.



INTRINSIC INTEREST Stressful events are of almost unparalleled importance to people. For ex ample, the evening news can be seen primarily as a means of transmit ting information about stressful events—whether or not these events di rectly affect us. Television news focuses primarily on natural disasters, accidents and tragedies, economic dislocations, conflicts between power ful individuals (generally politicians but sometimes movie stars or sports celebrities), deaths, crimes, and punishment. Positive events are reported only rarely, and then often in the context of individuals who are strug gling to overcome tremendous odds or handicaps. A large percentage of our daily conversations focus on stressful events that happen to ourselves and others: deaths, divorces, job prob lems, car accidents, problems at school or work, illnesses (major or mi nor), and everyday “hassles” in general—missed buses, car problems, 13 14 STRESS, COPING, AND DEVELOPMENT



bureaucratic inconveniences, and the copying machine breaking down



(again) at work. Certainly soap operas focus almost exclusively on the negative life events that happened to (or were provoked by) the charac ters. One can only speculate on the reasons for this interest. Perhaps watching others struggling and grieving provides a form of catharsis, a way of discharging unhappiness and anger in a safe, nonthreatening con text, as the ancient Greeks thought. Thus, it may be more comfortable to express anger over crooked politicians rather than to confront directly unethical practices in our own work contexts. Perhaps interest in stress has an evolutionary function. Many studies during the past two decades have demonstrated that heightened emo tions enhance memory, that is, we are more likely to remember emotion ally charged events (Davidson, 2003). This phenomenon appears to be regulated by the basolateral region of the amygdala as well as by other neural structures such as the hippocampus (McGaugh, 2002). By re membering sources of trauma, we may be more likely to learn from our mistakes and avoid dangerous situations in the future. Similarly, by at tending to dangers and trauma that others face, we may learn of sources of danger in the hope of avoiding them or may vicariously learn about coping strategies, successful or unsuccessful, that others have used for dealing with problems. Interestingly, some have argued that the sort of “flashback” memory seen in posttraumatic stress disorder (PTSD) quali tatively differs from ordinary, more discursive, memory of trauma (Brewin, 2003). Interest in stress can also be seen in a larger social context. Many years ago, Durkheim (1933) posited that emotional arousal in a group setting functions primarily to enhance feelings of community and group solidarity. Although usually applied to group rituals involving large crowds (such as football games), one could also argue that the arousal of emotion through news reporting of stressful events also can function to increase communitas, either directly or indirectly. For example, reports of major natural disasters also depict rescue efforts and directly invite participation by providing information on how the viewer can help (gen erally by providing money or goods to rescue agencies). At the very least, news reports of disasters provide a shared social context and topics of conversation for individuals in a community or nation. Thus, the intrinsic interest in stress may stem from psychological, biological, and/or social causes. Whatever the reason, it is clear that stress, and how people cope with it, is intrinsically interesting for large numbers of people, both in the academic and general communities. Studies of stress have also had a major impact on psychosocial models of adaptation and on biomedical models of disease. Why Is Stress Important? 15



RELEVANCE OF STRESS TO PSYCHOSOCIAL MODELS OF ADAPTATION Early models of mental illness focused primarily on internal processes as the source of psychological problems. Psychoanalysis, for example, re lated mental illness primarily to hidden or unconscious conflicts between the id, ego, and superego, stemming from early childhood fixation in



psychosexual stages. Environmental events may trigger these conflicts, but the primary problem lies within the individual. Similarly, biomedical models try to relate symptoms to neurotransmitter imbalances, which are thought to be causal mechanisms underlying psychological distress. If a depressed person exhibits lower levels of serotonin, it is thought that the lack of serotonin causes the depressive symptoms. In both types of models, the cause or source of mental illness lies solely in the individual's makeup. Sociologists and anthropologists, on the other hand, have long pointed to the major roles that society and culture play in provoking both psychological distress and the way in which it is expressed. For ex ample, Hollingshead and Redlich (1953) first pointed to the relationship between social class and mental illness: individuals in lower socioeco nomic (SES) groups were more likely to suffer from schizophrenia, but those in the upper classes were more likely to report neuroses. From this point of view, the origin of mental illness may lie not so much within the individual but within the environment, such as the social structure and the way in which strains are distributed within society (see National Ad visory Mental Health Council, 1996, for a review). The old view was that people who have marginal roles within a society, such as the poor, are more likely to exhibit signs of emotional and social disorder because of inadequate socialization to what are considered normative social roles and behavior (Howell, 1973). Of course, this has given rise to an ongo ing debate about which comes first—socioeconomic status or mental illness? The downward mobility hypothesis argues that individuals who have psychological problems tend to do badly in the economic market place and thus become members of the lower social classes, while the social causation theory argues that it is one's position within the social structure that creates the problems that give rise to mental illness. For example, some have argued that it is the economic injustice and discrimination against individuals in lower classes, who are often minor ities, that most affects mental health. A study of depression among Native Americans, who have several times the rate of depression experi enced among the general population, found that perceived discrimina tion was strongly related to depression (Whitbeck, McMorris, Hoyt, Stubben & LaFromboise, 2002). The problem was not poor socializa 16 STRESS, COPING, AND DEVELOPMENT



tion to roles in the dominant society: Individuals who engaged in tradi tional Native American practices had lower rates of depression than those who did not. Similarly, Chandler, Lalonde, Sokol, and Hallett (2003) investigated reports of high suicide rates among Native American adolescents in Canada. They found that tribes that were actively en gaged in activities to preserve and promote their traditional culture (of ten by suing the government for abrogation of rights) had dramatically lower rates of suicide than those tribes that were not resisting. Anthropologists have observed that what constitutes abnormal be havior is a result more of cultural norms than of individual psychody namics. As Margaret Mead (1928) pointed out many years ago, what constitutes acceptable behavior in one culture may be considered abnormal and a treatable illness in another. To illustrate the importance of



culture in the origin of mental illness, anthropologists also point to the existence of culture-bound illnesses, or disorders that are specific to particular cul tures, such as amok in the Philippines or “bear illness” among the Aleuts (see Kleinman, 1980; Kleiman & Seeman, 2000). (Both of these illnesses involve public displays of extreme violence in a nonetheless ritualistic manner.) Thus, culture plays an important role in both the formation and expression of mental illness. (See Chapter 13 for further discussion of this issue.) Models of stress and psychosocial adaptation can provide a link be tween these disparate viewpoints on the origin of mental illness. Stress models acknowledge the importance of environmental effects on mental health, but they also recognize that there are individual differences in vulnerability to stress. Thus, the onus for mental illness shifts from being solely the “fault” of the individual or simply a function of social roles and cultural norms to a recognition that there are multiple factors en gendering psychological distress, some of which may be beyond individ ual control. Turner (2003) argues that the past half-century of research has demonstrated overwhelming evidence that cumulative adversities or exposure to stress accounts for a great deal of the variation in the rela tionship between social class and mental illness. The construct of vulnerability to stress is very important, because it can tie together a number of different approaches to adaptation. Vulner ability to stress may be a function of either personal or social character istics. Personal vulnerabilities may stem from an individual's history, such as exposure to traumatic situations earlier in life or a biological propensity to manic depression. Thus, this construct can encompass both psychodynamic and biological approaches to mental health. How ever, vulnerabilities may also stem from one's position in the social envi ronment, such as poverty, racism, few economic opportunities, and the like (Evans, 2004; Pearlin, 1989; Turner, 2003), which may make it Why Is Stress Important? 17



more likely that certain individuals will experience stressful events. They may have particularly adverse reactions to the events and may take longer to recover. The construct of vulnerability nonetheless acknowledges that personal problems may indeed be due to one's social or physical environ ment and thus can also encompass environmental approaches to adapta tion. A corollary construct is goodness of fit (Kahana, Lovegreen, Kahana, & Kahana, 2003; Magnusson & Toerestad, 1992). The same environ ment might be stressful to some persons because it requires capacities or preferences that they do not have; yet, it might be a comfortable or stim ulating environment for individuals who possess those capacities or have those preferences. For example, one person may prefer a work environ ment with predictable, routinized tasks and might find it difficult to deal with a more unstructured environment with chaotic, unpredictable tasks. Another person may find the first environment boring and the sec ond challenging and stimulating. Thus, the construct of goodness of fit recognizes the importance of contextualism and asserts that there are very few causal absolutes in psychology. Simply put, situations alter circumstances. Environmental situations need to be evaluated by their



effects on individuals, and individual adaptation needs to be understood in the context of particular environmental constraints. Thus, a stress and coping approach to psychosocial adaptation ac knowledges the contribution of both the person and the environment and seeks to understand the particular environmental context and per sonal skills and resources that provide for optimum adaptation. Further, a transactionist viewpoint emphasizes that the person and the environ ment are not independent contributors to stress and coping but, rather, mutually affect each other for good or for ill.



RELEVANCE OF STRESS TO BIOMEDICAL MODELS OF ADAPTATION For over 2,000 years, philosophers and scientists have been debating whether the mind and body are separate or integrated entities and, if in tegrated, the nature of the relationship (see Eccles & Robinson, 1984). The study of the effects of stress on physical health has been a great im petus to systematically investigating how the mind and body interact. As discussed in Chapter 1, the biomedical model of disease, as enunciated more than a hundred years ago by Virchow (1863), specified that individuals become ill due to external agents. Any illness can poten tially be cured if the agent is known. A person gets a cold, a heart attack, or cancer because an external agent (a germ or other toxin) infects the body, producing structural and physiological changes that are solely re 18 STRESS, COPING, AND DEVELOPMENT



sponsible for all symptoms. If the agent is identified and neutralized, the body recovers. However, it is now widely recognized that this model is too simplis tic. Not everyone who is exposed to a cold virus or tuberculosis becomes ill. Rather, the state of an individual's health reflects a dynamic interac tion between environmental forces and physiological resilience. There is increasing evidence that the latter is in part affected by psychological states. The past 20 years have seen an explosion of research into the psychosocial factors that affect health, including personality, stress, cop ing, and social support (for reviews see Aldwin & Gilmer, 2004; Dickerson & Kemeny, 2004; Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002; Krantz & McCeney, 2002; Kubzansky & Kawachi, 2000). The idea that stress can affect physical health is not at all new. In folk wisdom, people have been said “to die from a broken heart” or “to work themselves into an early grave.” Similarly, people can be “scared to death,” or fright can “turn your hair gray overnight.” What is new is that we are beginning to discover the physiological pathways that medi ate between stress and health. These pathways involve interactions be tween the neuroendocrine and immune systems. The field that studies these relationships is called psychoneuroimmunology (Ader, 1981; Ader, Felten, & Cohen, 1991). Psychoneuroimmunology seeks to understand the relationships among the psyche, or mind, the neuroendocrine system, and the immune sys tems, as well as the role of these relationships in maintenance of



health or vulnerability to illness. Figure 2.1 presents what might be called a ba sic, or generic, model illustrating the principles of psychoneuroimmun ology. Stress activates negative affect, or emotions. We may feel angry, sad, or frustrated in response to a stressful episode. There are well known physiological changes that accompany such emotions. Our hearts pound, we may breathe heavily (increase in heart and respiratory



NEUROENDOCRINE CHANGE STRESS NEGATIVE HEALTH AFFECT OUTCOMES



IMMUNE SYSTEM CHANGE



FIGURE 2.1. Standard psychoneuroimmunology model of stress and health.



Why Is Stress Important? 19



rates), we may turn beet red or deathly pale (changes in peripheral vasodilation), or we may feel “butterflies” in the stomach (decrease in parasympathetic system activation). A century ago, both William James (1890) and Walter Cannon (1915) recognized the link between emotions and the neuroendocrine system, although they differed somewhat in their beliefs about causal directionality between the mind and the body (see Chapter 4). Thus, Figure 2.1 shows all relationships as bidirectional. Figure 2.1 also shows stress and emotion affecting the immune sys tem. In 1964 Solomon and Moos coined the term “psychoneuroimmun ology,” but it was not until the early 1980s that Ader and Cohen (1982) made a remarkable discovery. Using classical conditioning techniques on laboratory mice, they paired a noise with injections of a drug that sup pressed the immune system's functioning. After a few trials, they then injected saline instead of the drug. The immune function still became suppressed when the mice heard the noise. Ader had demonstrated a stimulus–response association between the perception of a noise and im mune system responses. In other words, the immune system was capable not only of learning but also of responding to a psychological stimulus. After that initial discovery, hundreds of studies have demonstrated intimate links between the mind, the brain, and the immune system (for reviews, see Gruenewald & Kemeny, 2007; Kiecolt-Glaser et al., 2002; Rabin, 1999). For example, there are receptor sites for neurotransmitters and catecholamines on immune cells such as T lymphocytes (Smith, 1991). This suggests that the immune system is hard-wired, so to speak, to respond to the mind and that this is not an accident but something that evolved for a reason. Further, there is also clear evidence that the immune system can alter neurological function, as when it triggers fevers (Dantzer, 2004). From Cannon's (1915) point of view, it makes perfect evolutionary



sense that the neuroendocrine system would respond in the manner that it does to strong emotion and stress. The “fight–flight” response, ex treme activation, is highly adaptive in that it allows an organism to re spond more vigorously in stressful situations, to fight harder or to run faster. We've all experienced this: “I was so scared! I've never run so fast in all my life!” Stress may also increase beta endorphin levels, which may block the experience of pain and allow people to function even while badly injured. However, why is it adaptive for the immune system also to respond to stress and emotions? Are we meant to become ill if we get upset? This is a conundrum only if the effects of stress are understood solely in the context of immune system suppression. Stress also activates the immune system, at least initially (Kiecolt-Glaser et al., 1992; Monjan, 1981). Such activation is highly adaptive in that it may temporarily pre 20 STRESS, COPING, AND DEVELOPMENT



vent a person from becoming ill at a time that calls for increased perfor mance. (I have often observed that students are more likely to get colds after final examinations than immediately before or during them!) If one is injured, an activated immune system can help to prevent infection and can also assist in repairs. Thus, immune system activation may be an in tegral response to adaptive challenges. However, even relatively mild stressors such as examinations may suppress immune function (Marucha, Kiecolt-Glaser, & Favagehi, 1998), and chronic stressors (Cohen et al., 1998; Glaser, Kiecolt-Glaser, Malar key, & Sheridan, 1998) or traumatic situations (Solomon, Segerstrom, Grohr, Kemeny, & Fahey, 1997) can suppress immune function for sub stantial periods of time, even years, especially if one develops symptoms of PTSD, such as intrusive thoughts (Ironson et al., 1997). Thus, in order to respond optimally to challenges and threats, there must be a synchronized activation of the mind and the neuroendocrine and immune systems. It is widely assumed that emotions are the “glue,” as it were, that ties the whole system together. In other words, emotions, both positive and negative, may mediate the relationship between stress and physiological outcomes. As shown in Figure 2.1, stress is assumed to activate the emotions, which affect the neuroendocrine system, which in turn affects the im mune system. Together, these influence the overall state of our health. However, these models may be simplistic. Work by Baum and his colleagues (Baum, Fleming, & Singer, 1983) on the Three Mile Island disaster has shown that the occurrence of stress can affect both neuroen docrine and immune system function independent of its emotional im pact. Cohen, Tyrell, and Smith (1993) also found that the influence of stress on susceptibility to a cold virus did not appear to be mediated through negative affect. Similarly, Yancura, Aldwin, Levenson, and Spiro (1996) also found that the effects of coping on the metabolic syn drome were not mediated through affect. Either individuals are not accurately reporting their emotions, perhaps due to repression, or there exist other pathways between stress and the neuroendocrine and im mune systems. Both personality (Segerstrom, 2000) and social support (Uchino, Cacioppo, & Kiecolt-Glaser, 1996) may also play a role. Figure 2.2 depicts alternative



pathways that may be interesting to investigate. One of the most interesting areas in biology today is the discovery of cellular-based mechanisms to reduce the effects of stress. Heat shock proteins (hsps) are complex systems that can mitigate the effects of stress at the cellular level in a number of different ways, including defusing free radicals or reactive oxygenating species (ROS), refolding proteins that have sustained structural damage, assisting DNA repair mechanisms, or encouraging highly damaged cells to undergo apoptosis (Sartori & Why Is Stress Important? 21 NEUROENDOCRINE CHANGE STRESS NEGATIVE HEALTH AFFECT OUTCOMES



IMMUNE SYSTEM CHANGE CELLULAR CHANGE



FIGURE 2.2. Modified psychoneuroimmunology model of stress and health.



Scherrer, 2003). They may also be involved in the regulation of immune function (Pockley, 2003). However, as of this writing, only one article has examined psychosocial factors and hsps (Lewthwaite, Owen, Coates, Henderson, & Steptoe, 2002). In summary, the study of stress is highly relevant to understanding biomedical adaptation. It is revealing how intimately the mind, the neuroendocrine system, and the immune system are related, which sug gests that a more holistic or multifactorial approach to understanding physical well-being is needed. It also provides support for the old Roman saying Mens sana, mens corpora, or “A healthy mind, a healthy body.” The most common complaint about the stress field is that the con struct of stress is very amorphous. As we shall see in Chapter 3, re searchers use different definitions of stress, depending upon their field of work and assumption system. Some, such as Kasl (1983), have gone so far as to suggest that the construct is so vague and so amorphous that it should be discarded. Alternatively, it can be argued that the various definitions of stress exist precisely because it is a very important construct with ramifications across a variety of endeavors. Different fields and philosophical tradi tions have come up with their own approaches to defining stress. Stress is a multifaceted and overdetermined phenomenon with ties to anthro pology and sociology; developmental, personality, social, clinical, com munity, and environmental psychology; and physiology and medicine. Although



this may create a certain amount of vagueness as the definition crosses disciplinary boundaries, it also provides an unparalleled oppor tunity for integrating different disciplines. 22 STRESS, COPING, AND DEVELOPMENTSUMMARY



While it is unlikely that a psychosocial Einstein will discover the “unify ing field theory” of the behavioral and social sciences, the construct of stress does provide a common ground that can integrate scientific ap proaches in a variety of fields. Thus, the construct of stress provides a framework in which the interplay between environmental, psychologi cal, and physical factors can be seen. It thereby represents a bridge link ing many different areas of scientific and clinical endeavors, providing a broader and more comprehensive understanding of human adaptation within a transactionist framework. As such, it may be one of the most important constructs in the clinical and social sciences today. STRESS, COPING, AND DEVELOPMENT Defin itions of Stress



CHAPTER 3



Definitions of Stress



The term “stress” is in such common usage that, at first glance, its meaning seems straightforward and in little need of definition, except perhaps for some minor clarifications here and there. After all, we all know what stresses us, what it feels like to be stressed—or “stressed out,” in common parlance. Indeed, the Oxford English Dictionary as sures us that the term has been in use since at least the 18th century. The problem is, of course, that the term has been in such common usage that it has taken on a variety of meanings. For example, it is both a noun and a verb. As a noun, “stress” can refer to external events or to an internal state. Similarly, the verb “stress” can be active, as in “to stress,” or pas sive, as in “to be stressed.” If the term “stress” is understood to refer to external events, what types of events does it refer to? Should only negative events, such as be



ing unemployed, be considered stressful, or can positive events, such as being promoted, also result in stress? Are only major events stressful, or can minor incidents also be troubling? Is stress to be understood as only those events that have negative consequences, or can stressful events sometimes have positive consequences? If the term refers to internal states, do we mean psychological states, as in emotional distress, or physiological ones? Note that some researchers use the term “stressor” to refer to exter nal events and use the term “strain” to refer to internal stressful states (Pearlin & Schooler, 1978). From a transactionist viewpoint, however, 23 24 STRESS, COPING, AND DEVELOPMENT



this distinction between external and internal states is hard to justify, given the importance of cognitive appraisal processes in the perception of stress. Further, many disciplines have studied one aspect or another of stress—ranging from the biological sciences such as physiology, bio chemistry, and neurophysiology; through the psychological sciences, such as psychoanalysis, personality, learning theory, developmental psy chology, and social ecology; to the social sciences, such as anthropology, sociology, and military history. Not surprisingly, the referents to the term “stress” vary across the fields, adding to the confusion. Studies of stress have included such diverse topics as men who are in combat; mice that are rotating slowly on a drum; commuters who are languishing in traffic jams; pigs that are being shipped to market; students who are taking exams; people who are working on bomb squads; workers on assembly lines; the effect of drought on trees; massive dislocations of whole popula tions; dan seterusnya. It is not surprising that some have called for abandon ing the term altogether, reasoning that, by seeming to apply to almost everything, “stress” really is too amorphous a term and really does not apply to anything (Kasl, 1983). For a number of reasons, this criticism of the term “stress” may be tantamount to throwing the baby out with the bath water. First, most researchers are quite precise about what they mean by “stress” in specific studies. Physiologists conducting studies on animal models of stress are almost always interested in the particulars of stress as a physiological state, focusing on the minutiae of neuroendocrine and immunological reactions. With notable exceptions, psychologists and sociologists generally concentrate on the definition of an external oc currence and on the individual's emotional reaction to it. Second, the fact that studies of stress are conducted at different levels of analysis should be cause for hope rather than despair. As mentioned in the pre ceding chapter, stress can be a common point for discussion across a number of disciplines, hopefully providing a pathway to integrate these disciplines. Indeed, the field of psychoneuroimmunology attempts to do just that. Although it is widely used, the term “stress” is not applied in a vague or ill-defined way. Nor is it a reified construct, an idea created by academics with little concrete reference to the real world. Rather, stress refers to that quality of experience, produced through a person–



environment transaction, that, through either overarousal or underar ousal, results in psychological or physiological distress. As we shall see, this overarching definition of stress incorporates most of the ele ments that researchers have used for identifying and studying the ef fects of this phenomenon. Definitions of Stress 25 COMPONENTS OF THE STRESS PROCESS



In order to sort through some of the initial confusion surrounding the use of the term “stress,” Mason (1975) identified three definitions of stress, or three ways in which the term “stress” has been used. Stress can refer to (1) an internal state of the organism (sometimes referred to as “strain”); (2) an external event (or “stressor”); or (3) an experience that arises from a transaction between a person and the environment. Table 3.1 presents the various components of the stress process, based loosely on Mason's categorization. Note that the table should by read only as a set of sequential columns; sympathetic activation can attend trauma or chronic role strain; a hassle may be short-term or chronic, and so forth. The table is meant primarily as a heuristic device to indicate the enor mous complexity of the stress process. As indicated in Table 3.1, stress as an internal state of the organism can refer to physiological, emotional, and cellular reactions. Studies of physiological reactions to stress focus on the peripheral and central ner TABLE 3.1. Components of the Stress Process Strain Stressor Transactions Physiological reactions



Emotional reactions



Sympathetic activation Negative affect Parasympathetic suppression Emotional numbing Life events Rapidity of onset Threat Moderate Other neuroendocrine stimulation/ suppression Immune



Types of stress Temporal



dimensions Cognitive



appraisals Intensity



Trauma Duration Harm/Loss Weak



suppression/ enhancement Heat shock protein activation DNA repair mechanisms suppression/ enhancement Lower positive affect Hassles/ daily stressors



Aversive physical environment Chronic role strain



Concern for others Annoyed



Cumulative adversity Fluctuation Challenge Strong At a loss Controllable/ uncontrollable Benign Ambiguous



26 STRESS, COPING, AND DEVELOPMENT



vous systems as well as neuroendocrine and immune system function. During the past 10 years, there has been a growing interest in stress protective mechanisms at the cellular level. Physical stressors such as free radicals (also known as reactive oxygen species, or ROS), wreak havoc on structures within the cell because they have a free electron that dam ages the configuration of various molecules, including DNA, and



makes them malfunction. Emotional reactions to stress generally refer to negative feelings such as anxiety, anger, and sadness, although shame, guilt, or feeling bored may also be considered stress reactions (Lazarus, 1991). While the focus in stress research is usually on negative affect, some attention has been paid to positive affect, generally in the form of opponent processes — that is, positive emotional states that arise as a sort of backlash to nega tive ones, as when a parachute jumper feels elated after initial feelings of terror (Solomon, 1980; see also Chapter 12). Emotional numbing, how ever, can also occur and is common with trauma or highly stressful life events such as bereavement or being diagnosed with a terminal illness. While the common assumption is that stress has negative physiolog ical effects, it would be more accurate to perceive stress as having an ac tivating effect, which at times can be positive as well as negative, de pending upon a variety of factors. Indeed, as we will discuss later, stress, whether at the cellular or organismic level, can eventually result in greater resilience to future stressors (see Chapter 15). The second type of definition of stress refers to the external environ ment. The earliest studies of stress focused on major trauma, such as combat and natural disasters. This characterization was later expanded to include major life events such as marriage, divorce, bereavement, or being laid off or starting a new job. Other researchers have focused on noxious environmental characteristics such as noise, overcrowding, or pollution. Others prefer to focus on more common problems, such as the chronic role strain of a bad marriage or being impoverished, while some examine the hassles or daily stressors of everyday life. There are a number of temporal dimensions of stress that deserve greater study, such as its duration, its rapidity of onset, and its linkage or spread. The animal literature indicates that the physiological effects of stress may be very different, depending upon whether the stressor is short-term, chronic, or intermittent (Dienstbier, 1989), while the studies on bereavement suggest that the suddenness of death might also affect the severity of its negative effects (Parkes & Weiss, 1983). Finally, a stressor might have a limited, easily delineated, effect, or it might start a chain reaction of events that reaches across domains. This chain reaction is termed “linkage” (Pearlin, 1989). For example, loss of a job could lead to long-term economic problems, which in turn could lead to a di Definitions of Stress 27



vorce, which in turn could lead to estrangement from children, and so forth. Finally, stress can be characterized as an experience arising from transactions between a person and the environment, especially those transactions in which there is a mismatch between an individual's re sources and the perceived challenge or need. In this schema, an individ ual's cognitive appraisal of stress—the recognition of harm, loss, threat, or challenge—must be present for any emotional or physiological reactions to occur (Lazarus & Folkman, 1984). These researchers have focused on how stress is perceived, or appraised, on its perceived characteristics (eg, threat, harm, or loss), and on the severity of the problem.



Most (although not all) researchers would agree that these are the major components of the stress process. However, there are some funda mental disagreements among different schools of thought. These dis agreements generally fall into one of two categories. First, regarding stress as an organismic state, researchers often disagree about whether there are general or specific reactions to stress—that is, whether all stressors evoke one general reaction or whether different stressors evoke specific reactions. Second, researchers emphatically disagree about the nature of causal directionality across the categories—that is, they dis agree about which comes first: cognitive, emotional, or physiological re actions to stress. For example, do we first react physiologically to stress, then emotionally, or do emotional reactions drive both the physiological and cognitive processes? In addition, researchers also disagree about causal directionality between a person and the environment. Does the environment cause emotional and physiological reactions, or does an in dividual's internal state alter his or her perception of the environment and somehow evoke problems? This section will review the major debates in the field concerning the conceptualization of stress using the framework that Mason (1975) first delineated. We will attempt to provide additional insight into vari ous debates and, where possible, suggest means by which differing posi tions can be reconciled.



STRESS AS A STATE OF THE ORGANISM Think of how your body might feel just before a big exam. Your face might be flushed or very pale, your palms might be sweaty, your hands might be trembling a little, and your mouth might be dry. These are peripheral nervous system reactions. If you have “butterflies” in your stomach, your heart is pounding, and you start hyperventilating, then your autonomic nervous system is reacting. Both are mediated by the ac 28 STRESS, COPING, AND DEVELOPMENT



tions of the sympathetic and parasympathetic nervous systems, in con junction with the endocrine system—hence the term “neuroendocrine stress reactions.” Now think of how you might feel during final exams week. You might have a cold or gingivitis (a gum inflammation). Your allergies or ulcers might get worse, or you might develop a rash. These reflect im mune system disturbances, also a common reaction to stress. There has been such an incredible increase in our understanding of the physiology of stress since the first edition of this book that a new separate chapter (Chapter 4) is devoted to it. Nonetheless, it is important to understand that we are hard-wired physiologically to respond to stress and that stress responses can involve nearly every system in the body.



STRESS AS AN EXTERNAL EVENT



Historically, stress has been viewed as a noxious external stimulus im pinging upon the organism. For millennia it has been common knowl edge that people could die from stressful events or lifestyles. We say that someone was “scared to death,” “died of a broken heart,” or “worked himself into an early grave.” External sources of stress may be either physical or sociocultural.



Physical Stressors Physical stressors include both trauma, which threatens immediate bodily harm (such as speeding cars, tornadoes, or fires) and aversive en vironmental conditions, which may have subtler but nonetheless harm ful effects, such as pollutants, noise, and the like. A “sick building” is a good example of a subtle physical stressor. In buildings in which the windows are sealed, workers may be exposed to low levels of harmful chemicals such as formaldehyde (common in carpet backings and office furniture), paint residues, cleaning compounds, or fumes given off by copying machines, which may not be immediately noticeable but can re sult in headaches, irritated eyes, rashes, and increased susceptibility to viral infections. Migraine headaches can be triggered by the flickering of improperly shielded fluorescent lights, and central heating and cooling systems that decrease humidity levels may result in irritated mucous membranes that in turn lead to nosebleeds and greater susceptibility to respiratory infections. Poor ventilation can also increase the concentra tion (and, thus, virulence) of infectious agents. Further, poorly designed work stations may result in mechanical stress, leading to eye and muscle strain; typists, computer operators, supermarket checkers, and musicians Definitions of Stress 29



may be particularly susceptible to repetitive motion injuries such as car pal tunnel syndrome. An interesting study by Evans and Jacobs (1982) has suggested that physical stressors such as poor air quality may interact with social ones to result in increased symptomatology. Evans found that residents in the Los Angeles area who lived in highly polluted neighborhoods had more symptoms when they were exposed to stressful life events than did indi viduals who lived in areas with cleaner air. Some of the adverse effects of poverty may result from living in environments that subject individuals to a wide variety of noxious stressors (Evans, 2004).



Sociocultural Stressors While stressful life events such as job loss or divorce are often seen by psychologists as occurring randomly or perhaps arising from an individ ual's psychological problems, sociologists are more likely to see the source of life events as embedded in the social structure. Pearlin (1989) has argued that stress arises as a function of the distribution of social resources as well as an individual's status and roles. A lack of social re sources either increases the probability of a stressful life event or height ens its stressfulness once it occurs. For example, having little disposable income can force a student to buy an older car with high mileage. This car



may be more likely to break down (a hassle), and the student may have little money to repair it, forcing him or her to make hard choices between rent, food, and car repair (to say nothing of leisure), thereby in creasing the situation's stressfulness. Furthermore, stressful life events may be linked; in Pearlin's terms, a primary event may lead to a second ary stressor. For example, our student may lose a much-needed job (a stressful life event) due to a lack of reliable transportation. Note that secondary stressors are not necessarily less stressful than primary stress ors and may even be more distressing, depending upon the circum stances. During a lecture in Brazil, I used the student car example in a lec ture on stress and coping (Aldwin, 2002). To my surprising, the students started giggling at this example. When asked why, they replied that they found it amusing—not one of them owned a car and, instead, took pub lic transportation, walked, or biked to school, which was at the top of a very tall hill. The wealthiest had small motorbikes. Clearly, culture influ ences the types of stressors individuals may face! One of the earliest studies of stress in the external environment was conducted by Calhoun (1962), who examined the effects of crowding on rats. He allowed rats to reproduce in a severely restricted environment. Under these conditions, social pathology among rats increased, typified 30 STRESS, COPING, AND DEVELOPMENT



by various measures of aggression, including fighting and rape. More important than crowding per se was restricted access to such basic neces sities as food and water. Increased violence was most prevalent when there was only one narrow access route to the food; when multiple path ways to the same amount of food were provided, the negative effects of crowding decreased. In other words, low levels of resources (so long as they are sufficient to sustain life) are not necessarily stressful, but inequi ties in the distribution of resources are more problematic. Several de cades of subsequent research has confirmed that crowding is also stress ful to humans but that these effects are exacerbated when combined with poverty (Evans & Saegert, 2002). The structure of social roles may also introduce opportunities for stress. Pearlin (1989) identified four types of chronic role strain. Role strain can consist of overload, as in having too much to do. Interper sonal conflict within roles (arguments with a spouse, child, or coworker) may be a source of role strain, as is interrole conflict as well (eg, jug gling parenting and work roles). Role captivity (such as being unable to quit an onerous job due to financial obligations) may be particularly problematic, as is role restructuring (eg, a daughter who becomes a caretaker for her parents). There are also ambient strains, like living in poor neighborhoods, especially violent ones, and strains that may arise from informal or elective roles (arguments with friends or fellow mem bers of a social organization). Pearlin (1989) emphasized that the social and personal context is instrumental in determining the outcome of a stressor. Not all role exits or restructuring are necessarily stressful. Exits from roles that are very stressful may be very positive (eg, leaving a job that one hates or leav ing a difficult marriage). Thus, stressors cannot be evaluated without



knowledge of both the social and the personal context. Interestingly, Schrier and Evans (2003) suggested that stressors that are evolutionarily “old” might be easier to adapt to than those that are more recent. They found that children exposed to such “new” stressors show higher in creases in cortisol than those exposed to “old” stressors. Certainly these psychosocial and sociocultural stressors can over lap. Nowhere is this better exemplified than in the environments of poor children. Evans's (2004) review showed that such children are exposed to higher levels of family violence and conflict, more dangerous neigh borhoods, and higher levels of air and water pollution.



Temporal Characteristics There are a number of temporal dimensions of stress that deserve greater study—most obviously, for example, its duration. The animal literature suggests that the physiological effects of stress may be very different, de Definitions of Stress 31



pending upon whether the stressor is short-term, chronic, or intermittent (Dienstbier, 1989). This was brought home to me when I was piloting a combat exposure scale on men in the Normative Aging Study. The scale had been developed on the basis of experience in the Vietnam war, and the length-of-exposure item went up to only about 24 months. One mer chant marine veteran whom I interviewed explained that he had been at sea for over 5 years during World War II, and while he had only seen ac tion a few times, the threat of German submarines was ever present. He was not sure how to respond—the amount of actual combat exposure was only about 2 weeks, but exposure to the threat of combat lasted over 5 years. Thus, this sailor had been subject to low-level chronic stress punctuated by intermittent intense stress. Was this sailor more or less stressed than a Vietnam veteran who had served an 18-month tour of duty with moderate combat exposure? Did the intermittency allow for recuperation and restoration, as Dienstbier (1989) would hypothe size, or did the chronic, day-after-day, low-level stress of always having to be alert for U-boats lead to a state of exhaustion, as Selye (1956) might have hypothesized? Rapidity of onset is another interesting stress parameter. On the one hand, we know that the anticipatory phase of a problem is very stressful— waiting to be laid off, for example. A commonly voiced opinion is that it would be better to die quickly of a heart attack than to linger slowly with cancer. Yet, being able to anticipate a problem also means that we can prepare for it, both emotionally and practically. While experienced parachutists generally have only mild cardiovascular reactions to a jump, Epstein (1982) related the case of a professional who had fallen asleep in the plane. When he jumped, his heightened cardiovascular reactions resembled those of a novice. Epstein speculated that the nap re sulted in a lack of preparation time; because the parachutist did not en gage in his normal coping behavior, his reactions were more severe. If the onset of a problem is too gradual, however, it may interfere with normal appraisal processes. Ecologists have coined the term “slow catastrophes” to refer to problems—such as overpopulation and the



greenhouse effect—that begin very gradually but may have disastrous consequences in the long run. Thus, the temporal patterning may have profound implications for both coping behavior and the effect of a stressor.



STRESS AS A TRANSACTION BETWEEN THE PERSON AND THE ENVIRONMENT From Lazarus's point of view (Lazarus & Folkman, 1984; Lazarus, 1991), depicting stress merely as an external event ignores individual dif 32 STRESS, COPING, AND DEVELOPMENT



ferences in the perception or appraisal of stress. What is stressful for one individual at one point in time may not be stressful for another individ ual or the same individual at another point in time. For example, losing a job may have a very different meaning or very different consequences for a teenager as opposed to a middle-aged man. If a teenager loses at job at a fast-food restaurant, chances are very likely that he or she can easily find another at a different establishment. A middle-aged factory worker or manager, however, may have a very difficult time finding other work. Thus, the same life event, job loss, may be more or less stressful depending upon its individual and social context. In this model, stress can also be seen as a combination of environ mental demands and individual resources, and cognitive processes are central. According to Lazarus, the perception of stress, or its appraisal, depends upon the extent of the environmental demand and the amount of resources that an individual has available to cope with that demand. Theoretically, the person first recognizes that there is a problem and then determines what resources are required to deal with that problem. Stress results from an imbalance between the requirements of the environmen tal situation and one's ability to cope with it. For example, a car's break ing down is somewhat stressful for most people, a more or less minor occurrence that requires either the knowledge and ability to fix the car oneself or sufficient money to hire a mechanic to fix it. But, for a home less family living in a car, its mechanical failure might well be an insur mountable problem creating extreme stress. In the Lazarus and Folkman (1984) theory, five types of appraisal are generally identified: harm, threat, loss, challenge, or benign. How ever, there are other types that may also be important, such as concern over others' problems (Aldwin, 1990). Further, the one-stressor, one appraisal, one-emotion model (Smith & Lazarus, 1993), though concep tually elegant, may not capture the complexities of everyday life. In a study that included over 1,000 interviews with older men, we found that very few individuals used only one appraisal—most used at least two (Aldwin, Sutton, Chiara, & Spiro, 1996). Further, in pilot testing, we found that these five appraisals did not fit all of the situations, and we included three additional ones. Some problems were simply annoyances, while others were concerns over other people's problems (usually those of a close friend or relative), while for some types of problems our re spondents indicated that they were simply at a loss for what to do next. Further, a



follow-up study showed that most of the men responded to problems with anger, regardless of the appraisal (Yancura, Aldwin, & Spiro, 2002). Presumably it is more culturally acceptable for men in our culture to respond to problems with anger rather than with sadness or grief. Definitions of Stress 33



The other dimension of appraisal that is important is the problem's severity, which may in part be related to what Folkman and Lazarus (1980) termed “secondary” appraisal. Perceived severity of a problem is a function of the (mis)match between environmental demands and indi vidual resources, as mentioned earlier. Sociologically inclined researchers often object to the primacy of ap praisal in this model. They point out that there are objective external cir cumstances (such as the unemployment rate) that do not depend upon an individual's perception. Further, centering stress upon cognitive ap praisal gives too much credence to rational cognitive processes and im plies that stress is solely dependent upon subjective perception without much regard to objective factors (see Hobfoll, 1989, for a review of this position). However, it is a mistake to believe that a cognitive appraisal ap proach neglects environmental considerations. On the contrary, it seeks to understand how stress is a product of both the environment and the individual. Obviously, some environmental characteristics are so over whelming as to result in a nearly universal experience of stress (as in ma jor traumas such as wars, devastating earthquakes, etc.). However, most environments are more ambiguous and more subject to individual inter pretations. Without an understanding of how this interpretation occurs, it is impossible to understand an individual's experience of and response to stress. It could be argued that the centrality of appraisal processes may ap ply more to social than to physical sources of stress. Most people will re act without thinking to an imminent source of physical danger of which they are at least minimally aware (eg, jumping out of the way of a speeding bus). Further, subtle stressors, such as being in a sick building, may have negative effects without the individual's even being aware of their source. However, it is also true that, given repeated exposure, indi viduals may learn to appraise imminent sources of physical danger very differently as they develop specific coping strategies. People drive on highways every day, where the slightest wrong move can (and often does) result in death; Boston pedestrians learn to avoid without effort seemingly homicidal Boston drivers; parachutists come to love stepping out into empty space thousands of feet above the earth. It is also likely that a person with a chronic respiratory ailment such as asthma may find even very subtle problems with sealed buildings intolerable. And, as in Calhoun's (1962) experiment with rats, the perceived access to physi cal resources may be more important than the actual level of resources, even in rats. Thus, appraisal processes may also play a role along with physical stressors. Lawton and Nahemow's (1973) construct of environmental compe 34 STRESS, COPING, AND DEVELOPMENT



tence is relevant to this argument. This theory, originally promulgated in the context of aging and person–environment models, argued that an older person's functional ability reflected an interaction between the dif ficulty of the environment and the individual's resources. Some environ ments are so difficult that very few people could be considered “compe tent” within them—for example, at 17,600 feet, the base camp at Mount Everest is an extremely strenuous environment. Others are too easy and do not contain enough stimulation or challenges (eg, most skilled nurs ing facilities, at least for the residents). However, most environments fall between these two extremes. A two-story home with one bathroom on the second floor is not a problem at all for most seniors, but for one with serious mobility problems that environment might simply be too diffi cult. Thus, one cannot determine the functional ability of a person only by assessing the individual's own capacity; rather, some knowledge of the environmental challenges and resources is critical. Similarly, one can not determine whether or not most environments are stressful unless one has some knowledge of the resources of the individuals in them. Another major criticism of the appraisal model of stress lies in its emphasis on the primacy of cognition, as opposed to emotion. Several theorists have argued that emotions are primary—that one becomes aware that a problem exists because of one's emotional reaction to an event.



THE ROLE OF EMOTIONS AND COGNITION IN REACTIONS TO STRESS James–Lange versus Cannon The James–Lange hypothesis (James, 1890; Lange & James, 1922) held that the body's emotional (visceral) reaction to stress occurred prior to and resulted in conscious responses. We run, therefore we are afraid; we fight, therefore we are angry. Cannon (1929), however, believed that neural processing was primary (with pathways originating in the thala mus). Cannon pointed out that the viscera have very slow reaction times and that the perception of and reaction to stress takes place very quickly. Therefore, neural (eg, mental) processing must occur first. Schachter and Singer (1962) attempted to test the James–Lange hypothesis by in jecting subjects with adrenaline in order to stimulate sympathetic ner vous system arousal and then by putting them in either an aversive or a congenial environment. Subjects who had been injected with adrenaline showed stronger responses to the environment—and, thus, were said to “label” their emotions in the context of the environment. However, at tempts to replicate this study have generally had little success (Marshall & Zimbardo, 1979). Definitions of Stress 35Lazarus versus Zajonc



The James–Cannon debate has its modern counterpart in a similar de bate between Lazarus (1982, 1984) and Zajonc (1984) as to whether cognitive or emotional reactions are primary in stress reactions. Lazarus argued that the cognitive processes of appraisal are central in determin ing whether a situation is potentially threatening or harmful, and thus



cognition determines both the perception of stress and the individual's emotional reaction to it. Zajonc, however, argued that simple awareness should not be equated with cognition and that emotional reaction to stress occurs before and may be at odds with cognitive reactions. The debate hinges on the definitions of emotion and cognition. Zajonc's implicit definition of cognition is similar to logical, conscious thought, whereas Lazarus's definition is closer to general awareness. It is true that one does need to become aware of a stress before one reacts to it. However, is that awareness primarily emotional or rational? In other words, do people become angry or afraid first and then impute a reason for their feelings, or do they define and recognize a situation as threaten ing and then emotionally react to it? Put in these terms, it becomes clear that the answer is: both. On some occasions, we may react first and think later; on other occasions, we may not become upset until we fully realize the threat in the situa tion. Implicit in this debate is the assumption that consciousness is uni tary and that all neurological processing is sequential: first emotions, then cognition, or vice versa. However, current work in neuropsychology makes it abundantly clear that consciousness is not unitary—there are often multiple and parallel processing systems that may be more or less independent of each other (see Carver & Scheier, 1999, for a review). In short, critiques of the centrality of appraisal in stress theory are correct when they argue that people are not rational beings who coldly analyze environmental conditions and come to logical conclusions. However, I believe that this is a caricature of the appraisal process. The awareness of a stressful condition (whether it is harm, loss, threat, or challenge) may arise in a number of ways. We may intuit a problem, as when “a little voice” tells us that something isn't quite right, that danger is imminent, and that we must stop and find out what is wrong. We may also use logical analysis to determine that the present course of action will eventually result in harm of some sort. At other times it seems as if the body can react before the mind has a chance to recognize the danger, as when a soldier “instinctively” dodges a blow before he is even fully aware that one is coming. All of these are examples of the appraisal pro cess, whether it is conscious or unconscious, rational or irrational. It seems to me a truism that a person must be aware of a problem before 36 STRESS, COPING, AND DEVELOPMENT



he or she begins to cope with it—however that awareness is defined or comes about—again, with the exception of the imperceptibility of some nonetheless noxious physical stressors. Indeed, Lazarus's later work (1991, p. 153) underscores the widely held proposition that there are indeed two modes for imputing meaning to a situation, “one conscious, deliberate, and under volitional control, the other automatic, unconscious, and uncontrollable” (emphasis in the original). Further, these two modes are understood to operate in an often simultaneous and parallel fashion and may in fact be contradictory. Ep stein (1994) termed this dichotomy “rational” versus “experiential.” This may be best illustrated with phobias. An individual may con sciously be aware that accidents in an elevator or airplane are statisti cally unlikely but nonetheless be consumed with dread. Thus, cognition and emotion



inform each other. People may use logical reasoning to calm themselves, or they may develop elaborate cognitive justifications (rationalizations) for overblown emotional reactions.



SUMMARY There is little argument about the various components of the stress pro cess (see Table 3.1). Rather, differences among stress researchers arise primarily because of the varying degrees of emphasis put on individual components and because of disagreements about the causal ordering of the components. Sometimes the debate is healthy and forces us to re think our positions with greater clarity. At other times, however, feuds arise, passing on through generations of academics, usually over the or dering of two little boxes in a labyrinthine maze of boxes depicting what are actually rather similar views of the stress process. A transactional framework is integrative, because it acknowledges the importance of all of these components. Stress is, indeed, partially a function of the environment, but it is also partially a function of the in ternal characteristics of the individual (whether psychological, hor monal, or immunological). It makes little sense to ignore one at the ex pense of the other. Rather, it is of greater importance to trace out the manner in which these transactions occur. Further, it is quite likely that, depending upon the context or the individual, differing components may assume more or less significance. The recognition of multidirectionality between the components also renders the exact causal sequencing less important. The important point is to understand clearly which compo nents of the stress process are important in a given context and to make sure that the appropriate concepts and tools are being utilized, whether in research or clinical work.



STRESS, COPING, AND DEVELOPMENT The Physiology of Stress



CHAPTER 4



The Physiology of Stress



As noted in the preceding chapter, human bodies are “hard



wired” to respond to stress. In general, when we think of stress re sponses, we think of neuroendocrine responses, such as rapid heart rates, greater alertness, and the capacity for bursts of energy. The im mune system also responds to stress and also regulates stress responses. But there are also stress response mechanisms at the cellular level that are phylogenetically very old—in other words, they are found in simple organisms such as amoebas, in plants, and in animals. Indeed, the sheer number and redundancy of physiological systems designed to cope with stress suggest that the ability to respond to stress is terribly important in adaptation.



NEUROENDOCRINE RESPONSES TO STRESS General Stress Reactions If you examine the functions of the sympathetic nervous system listed in Table 4.1, it is fairly obvious that increased arousal of the sympathetic nervous system prepares an organism for action. Blood is diverted from the intestines and other vegetative activities and is transferred to the brain and the striated muscles. Blood pressure, heart rate, and respira tion rate increase, allowing more oxygen to flow to the brain and mus cles. The increase in blood sugar provides more energy, and the increase in blood clotting defends against cuts. These changes enable greater physical and mental effort on the part of the organism. (Piloerection is 37 38 STRESS, COPING, AND DEVELOPMENT TABLE 4.1. Functions of the Autonomic Nervous System Sympathetic nervous system • Increases blood pressure, heart rate, respiration rate, and perspiration. • Increases blood sugar and blood clotting. • Dilates pupils. • Causes piloerections (goose bumps). • Decreases saliva, mucus, and gastrointestinal motility. • Diverts blood from intestines to brain and striated muscles. Parasympathetic nervous system • Controls digestion. • Maintains and conserves bodily resources. • Decreases blood pressure, heart rate, respiration rate, etc. • Generally opposes sympathetic activation but sometimes acts in consort.



important for furred species. Hair standing on end makes a cat, for ex ample, look much larger and intimidating, and also provides protection against bites.) Walter Cannon (1939) termed this type of sympathetic nervous sys tem arousal the “fight–flight” reaction. In response to a threat or stress, the fight–flight reaction makes it possible for an organism to more effec tively meet such challenges through mobilizing its mental and physical



abilities. People often find that they run much faster when being chased by a dog than when out for their morning jog; athletes talk about “get ting pumped up” or “getting the adrenaline flowing” to achieve peak performances. Indeed, that is exactly what happens. As early as 1915, Cannon showed that when cats are exposed to barking dogs, epinephrine or adren aline is released into their bloodstream. Cannon hypothesized that the per ception of a threat activates the thalamus (now we know it is the hypothal amus), which stimulates the pituitary gland to release hormones that activate the adrenal glands, which lie on top of the kidneys. The adrenal medulla, or center, releases epinephrine (adrenaline) and norepinephrine (noradrenaline), which stimulate sympathetic nervous system activation (see Figure 4.1)—hence, the fight–flight reaction. Once the threat is re moved, parasympathetic activation returns the body to homeostasis by de creasing blood pressure, heart rate, and respiratory rate, returning the body to a vegetative state that promotes gastrointestinal activity. The effect of a sudden sympathetic nervous system arousal on someone with underlying cardiovascular disease may lead to a stroke or myocardial infarction (heart attack). However, prolonged sympathetic nervous system arousal can lead to serious physical problems and death in even relatively healthy individuals. Cannon described the case of an The Physiology of Stress 39 Hypothalamus Pituitary Gland Anterior Lobe Posterior Lobe Growth hormone (GH) Vasopressin Thyrotropic hormone (TH) Antidiuretic hormone (ADH) Follicle-stimulating hormone (FSH) Oxcytocin Luteinizing hormone (LH) Prolactin or Luteotropic hormone (LTH) Melanocyte-stimulating hormone (MSH) Adrenocorticotropic hormone (ACTH) Adrenal Glands Adrenal Medulla Adrenal Cortex Catecholamines Steroids Epinephrine (adrenaline) Norepinephrine (noradrenaline) Corticosteroids (cortisone, cortisol)



Glucocorticoids Mineralocorticoids



FIGURE 4.1. Components of the neuroendocrine system.



Australian aborigine who was cursed by a local “witch doctor” and who died a few days later of no obvious organic cause, such as disease. Can non termed this phenomenon “voodoo death” (despite the fact that vodun is only found in the Caribbean and Brazil) and thought that it de rived from overactivation of the sympathetic nervous system. Essentially, increased blood pressure decreases circulating blood volume by forcing liquids out



of the vascular system and into the surrounding tissues. If this process goes on long enough, the blood volume is eventually insuffi cient to sustain adequate blood pressure levels, the arterioles dilate in an attempt to increase blood flow, and blood pressure can drop dramati cally, leading to shock and cardiovascular arrest. This reaction may be aggravated by lack of food and drink (aborigines so cursed may stop in gesting food and liquids), but, nonetheless, it is a direct effect of stress. Thus, one can literally be “scared to death.” Animals can also be frightened to death. For example, transporta tion of animals, even domesticated ones, can result in death (Backstrom & Kauffman, 1995). Among pigs this is called porcine stress syndrome; mortality rates are even higher among wild animals. Paradoxically, try ing to protect deer in an overpopulated area from hunting by transport ing them to other areas usually results in the death of those animals 40 STRESS, COPING, AND DEVELOPMENT



transported, in part from stress. I even remember reading a London Times article about an okapi in the Berlin zoo that died of fright during a Wagner music festival. Apparently “Ride of the Valkyries” is simply too scary! Cannon believed that any threat resulted in the fight–flight reaction and that such a reaction is a general response to any stress, physical or social. He believed that the body responds to all threats in a similar man ner, whether or not that manner is immediately relevant. That is, we re spond with the same sympathetic activation to negative performance evaluations from our supervisors as our ancestors did to carnivorous predators. In reacting to sudden physical threats, it makes a great deal of sense for the body to be able to run away very quickly, or even to chal lenge the predator with enhanced strength (and blood clotting ability). However, the same physiological response is not generally appropriate to social and verbal challenges (although increased blood flow to the brain should—but does not always—help with witty repartees). Physical vio lence is not an appropriate response to employers' chastisements (al though work-related violence is unfortunately on the rise). Forty years ago, Dubos (1965) argued that the necessity to suppress direct physiological response to modern challenges results in diseases of adaptation. For example, increases in blood pressure and blood clotting without the physical release of actually running or fighting may eventu ally result in hypertension and cardiovascular disease. Thus, Dubos be lieved that the current epidemic of cardiovascular disease has resulted in part from the body's response to verbal and social challenges as if they were direct physical threats without the attendant release from physical activity. Hans Selye's (1956) “physiology of dirt” expanded on Cannon's flight–fight theory in two ways. First of all, Selye focused attention on the corticosteroids, which are released by the adrenal cortex, or top layer of the adrenal glands. He also expanded on Cannon's homeostatic pro cess by describing three stages in reaction to stress. The first, or alarm, stage is similar to Cannon's fight–flight reaction but involves the adrenal glands as well as the hypothalamic–pituitary axis. However, Selye no ticed that some organisms became inured to the stressor. In the second stage, adaptation, there is a return to physiological homeostasis, or per haps



augmented functioning. In the third stage, exhaustion, the organ ism may fall ill or die if the stress continues. The models of Cannon and Selye are similar in that they posit gen eral or universal reactions to stress. Thus, heightened sympathetic reac tion will occur regardless of whether the stressor is a physical predator or a college exam and whether the organism being stressed is a man or a mouse. More recent researchers, however, have suggested that there are The Physiology of Stress 41



more specific reactions to stress that can vary depending on the stressor or the individual.



Specific Reactions to Stress In many ways, the field of psychosomatic medicine is predicated upon individual differences in reaction to stress. Alexander (1950) proposed that different emotional states underlie different psychosomatic illnesses. For example, heart disease was thought to be related to underlying chronic patterns of hostility, while asthma involved unconscious anguish due to separation from the mother. Different types of environmental stress could result in particular emotional conflicts, which in turn pro voked specific under- or overarousal of particular systems, eventually leading to organic problems. Given the difficulty in establishing the presence of underlying un conscious conflicts, this psychosomatic theory developed the “weak organ” theory—namely, that stress resulted in different illnesses, depending upon the physiological (genetic) weaknesses of the individual (see Wiener, 1977). In this model, stress is thought to result in either heart disease or asthma, depending upon the constitutional weaknesses of the individual. For example, individuals high in hostility exhibit greater in creases in blood pressure under stress than those low in hostility, thus providing a possible mechanism through which hostility can result in heart disease (Hardy & Smith, 1988). Early work by Lazarus and his colleagues (reviewed in Lazarus, Averill, & Opton, 1974) suggested that there are individual differences in physiological reactions to stress. They investigated the effect of stress on end organs, or the outward manifestations of sympathetic arousal. These include heart rate, respiratory rate, and galvanic skin response (GSR), which reflects the amount of perspiration on the skin. They found individual differences in the patterning of responses. For example, some individuals' heart rates increased in response to stress, whereas other individuals' heart rates decreased though they perspired more. While sympathetic arousal did occur, the manifestation of this arousal varied across individuals. Thus, there may be individual differences in the patterns of physiological reactions to stress. Further, there was early evidence that different types of stressors may evoke different physiological reactions. Mason (1971) subjected rats and monkeys to different types of stress, including hunger, inade quate nutrition, and cold. He found that there were “stressor profiles,” such as specific neuroendocrine reactions that varied depending on types of stress, and concluded that reactions to stress were specific, not gen eral.



42 STRESS, COPING, AND DEVELOPMENT



It is now well established that there are both individual differences in as well as situation-specific responses to stress, and that the physiol ogy of stress is much more complicated than originally thought. For ex ample, within the sympathetic nervous system (SNS), there are different subsystems that can be activated independently (Jänig & McLachlan, 1992). Further, we know much more about the timing of and interaction between different stress-regulating systems in the body. The SNS constitutes the immediate reaction to stressors, and con sists of two major subsystems (Gevirtz, 2000), both of which result in the release of catecholamines (epinephrine and norepinephrine, also called adrenaline and noradrenaline). In the first system, the SNS neu rons use norepinephrine to stimulate target organs and to immediately increase the heart and respiratory rates and decrease gastrointestinal ac tivity, which allow more circulating blood to reach the muscles more quickly, giving them more nutrients and taking away toxins such as lac tic acid generated by motor activity. Norepinephrine also serves to in crease muscle strength and mental activity. The second system also re sults in the release of catecholamines, but indirectly via the adrenal medulla. In the sympathetic–adrenomedullary (SAM) system, the sympa thetic nerves directly stimulate the adrenal medulla to release both epi nephrine and norepinephrine into the bloodstream, which then also af fect the target organs (see Figure 4.2). The pathways are, in fact, redundant, which signals the importance of being able to respond imme diately to stress for adaptation.



FIGURE 4.2. Two pathways in the stress activation of the sympathetic nervous system.



The Physiology of Stress 43



Hypothalamic–Pituitary–Adrenocortical Axis and the Anabolic/Catabolic Balance



Catecholamines are toxic, and too prolonged an exposure damages the organs that are being activated (Sapolsky, 1998). Thus, activation of the hypothalamic–pituitary–adrenocortical (HPA) axis occurs not simply as a stress response, but is a way in which the body tries to reduce the toxic effects of SNS exposure. For example, SNS stimulates the inflammatory response of the immune system (see below), which, if prolonged, can damage various organ systems. HPA activation suppresses the immune system in an attempt to prevent this damage. The HPA axis is presented in Figure 4.3. The stressor, which in cludes chemical toxins, mechanical stress (such as physical exertion or exposure to heat or cold), and psychosocial problems (more precisely, the perception of threat or harm), stimulates the hypothalamus to se crete corticotropin-releasing hormone (CRH). In turn, CRH stimulates the anterior lobe of the pituitary to release adrenocorticotropic hormone (ACTH) into the bloodstream. The adrenal cortex, or outer part of the adrenal gland, releases corticosteroids, which are fat-soluble molecules that use cholesterol as a component. Cell walls are also made up in part by cholesterol. This allows them to cross cell membranes and enter every cell in the body. This is why stress can affect nearly every organ system. Corticosteroids include both glucocorticoids and mineral corticoids. Glucocorticoids have a wide range of effects. They can suppress immune



FIGURE 4.3. Stress activation of the hypothalamic–pituitary–adrenocortical axis (HPA).



44 STRESS, COPING, AND DEVELOPMENT



function, raise metabolic rates, and stimulate the release of glucose into the body. They can also affect sex hormones and thus influence fertility. Depending upon the duration of the stressor, they can either stimulate or suppress growth hormone (Sapolsky, 1998). Mineral corticoids regulate systems such as calcium metabolism. HPA activation is a slower system, taking about 20 minutes to acti vate, but it allows for a more sustained response to stressors. The prob



lem is that prolonged exposure to glucocorticoids also has toxic effects. Long-term immune suppression can leave us vulnerable to infectious agents such as bacteria or viruses and may also interfere with the im mune system's surveillance against cancer cells. Thus, there are feedback mechanisms set up to decrease glucocorticoid levels if they get too high. For example, there are receptors in the hippocampus that monitor and help regulate the amount of cortisol in the blood system. However, pro longed or repeated exposure to high levels of cortisol can damage these receptors. Sapolsky (1992, 1999) proposed that this may result in poorer regulation of cortisol and may be a result in hippocampal damage, lead ing to memory problems in late life. However, sometimes individuals exposed to prolonged chronic stress, such as those who have posttraumatic stress disorder, have lower levels of cortisol (Yehuda, 2000) because cortisol levels have simply been depleted, exhausting their ability to mount a stress response. Ini bisa sangat serius. For example, these individuals may be chronically fatigued and unable to exercise precisely because this requires increases in blood pressure and blood glucose levels. With a functioning stress response, these systems simply cannot respond, and the person is easily fatigued (Gruenewald & Matsumoto, 1999). Epel, Burke, and Wolkowitz (2007) have argued that a systems ap proach needs to be taken to properly understand neuroendocrine re sponses to stress. In particular, increased levels of any one hormone may be less important than the “anabolic/catabolic balance.” In general, ana bolic processes are those that result in healthy growth in bone, muscle, skin, and other tissues, while the complementary catabolic processes break down components for fuel or as a process of continual restructur ing. For example, bone density reflects a dynamic process in which cal cium is deposited in bone cells (anabolic process) but taken from bone cells when needed for other functions such as muscle contraction (cata bolic process). Cortisol and catecholamines are catabolic because they break down substances to generate energy, while other hormones such as growth hormone and the sex hormones (estrogen and testosterone) are anabolic because they increase bone mass and muscle size, deposit fat in the appropriate cells, and so on. Prolonged exposure to stress (and high levels of cortisol) may disrupt the anabolic/catabolic balance, resulting in The Physiology of Stress 45



decreased muscle mass, bone density, and fat deposits in the abdomen (Dallman, Pecoraro, & la Fleur, 2005).



Flight, Fight—or Affiliate? Cannon's now famous “fight–flight” response has been criticized as being too simplistic and ignoring the social component of the stress response. Taylor et al. (2000) have hypothesized that women's responses to stress may be more characterized by the oxytocin–estrogen–endogenous opioid system, which constitutes the neurological underpinnings of the attach ment and caregiving systems. Oxytocin is a hormone secreted by the hypothalamus as well as the



ovaries and testes. It initially was identified as a major factor in lactation and nursing behavior as well as “maternal responsiveness.” However, it is also found in men and may play a role in sperm ejaculation and sexual behavior. While oxytosin is suppressed by stress and cortisol, it has also been shown to reduce the adverse effects of stress and to be an antianxiolytic, especially in the presence of social support (Heinrichs, Baumgartner, Kirschbaum, & Ehlert, 2003). Taylor et al. (2000) argue that fleeing under stress may be difficult or impossible for pregnant women or mothers of infants and also may put their offspring at risk. Therefore, they suggest that it was evolu tionarily important for women to tend first to infants if there were exter nal stressors. Further, experimental research shows that women are much more likely than men to seek social support under stress. There fore, they added a “tend and befriend” dimension to Cannon's original fight–flight dichotomy. Elsewhere (Aldwin & Gilmer, 2004), we suggested that this type of affiliation may also be important in men's adaptation. Certainly field studies show that men often have larger social networks than women and also seek social support in stressful situations, albeit to a somewhat lesser extent than women (Taylor, 2007). Men also feel protective of their families and friends under stress. Still, this recognition of the social aspect of stress responses is an important extension of Cannon's original twodimensional response. Therefore, we proposed a triune model of stress responses, which includes fight, fight, and affiliate. This three dimensional space allows for a more complex understanding of individ ual differences in response to stress, as well as for personality, gender, and contextual influences. For example, one could easily hypothesize that individuals who are hostile may be more likely to fight in response to stress while those who are shy may be more likely to flee. Women may be more likely to affiliate under stress, but both men and women may change their stress responses to be more protective if young children are 46 STRESS, COPING, AND DEVELOPMENT



involved. Of course, in such extreme cases as, for example, the collapse of the World Trade Center towers, individuals may find themselves run ning blindly without any recollection of how long they have been run ning. Whether this triune model is a useful way to organize the stress field, however, remains to be seen.



IMMUNE RESPONSES TO STRESS The immune system is an extremely complex mechanism that regulates the body's reaction both to external threats and to internal malfunctions (for overviews of this topic, see Aldwin & Gilmer, 2004; Cohen & Her bert, 1996; Gruenewald & Kemeny, 2007; Kiecolt-Glaser et al., 2002; Rabin, 1999). External threats include bacteria, viruses, parasites, and toxins; internal threats consist of malfunctioning cells. One of the great wonders of the immune system is that it learns to differentiate between self and other. Each cell in the human body has an identifier unique to that person, called a human leukocyte-associated (HLA) molecule. These are on the



cell membrane, are genetically determined, and allow the immune system to readily distinguish its own cells from those of invaders, which include bacteria, viruses, and parasites. For example, bacteria proliferating in the bloodstream are recognized by the immune system as foreign and then attacked. Viruses cannot proliferate on their own; rather, they work by taking over the DNA or RNA of a cell to manufacture copies of themselves. Usually this results in a change on the surface of the cell membrane, which alerts the immune system to the in vader. However, the AIDS virus is particularly deadly because not only does it take over an immune system component, the T cells, but it hides within the cell and does not appear to make easily recognizable mem brane changes—so it is difficult for a person's own immune system to recognize these dangerous cells. The immune system can also be activated by inert molecules such as pollen or dust. Thus, an antigen is anything that activates the immune system. The immune system can also recognize cells that have started malfunctioning, such as precancerous cells.



Innate Immunity The simplest type of immune reaction to invaders is called innate immu nity, or nonspecific defenses, and may include fevers, vomiting, defeca tion, and urination, which rid the body of pathogens (see Dantzer, 2004). This type of defense, however, can be extremely costly. High fe vers (those that are 105 degrees Fahrenheit or above) can result in blind The Physiology of Stress 47



ness, brain damage, and death. Vomiting and diarrhea can be very effec tive ways of ridding the body of food- or water-borne illnesses, but the resulting dehydration and electrolytic imbalance can be fatal. Indeed, one of the leading causes of infant mortality in developing nations is di arrhea. Thus, the immune system also has a more effective and less costly form of defense, called “cellular immunity.” In innate immunity, cells such as phagocytes (including granulo cytes, monocytes, and neutrophils) recognize invaders and literally “eat” them—hence “phagos,” which is Greek for “eat.” These cells roam the circulatory system or are sometimes embedded in membranes such as those lining the nose, and they engulf whatever invader they come across. Macrophages (big eaters) are similar but much more effective be cause they can be directed by the lymphocytes toward specific types of cells and can eat 10 times the number of cells as, say, neutrophils (Guyton & Hall, 1996). Basophils do not eat cells but instead secrete noxious chemicals to kill invaders such as parasites.



Acquired Immunity In contrast to innate immunity, “acquired immunity” reflects the fact that the immune system “learns” to identify specific types of antigens and develops tools that are specific to that antigen. Further, the immune system has a memory. Once a specific type of immune response is learned, it remembers which components are neces



sary for combating the antigen, and it will manufacture more of that specific component when challenged. This is one reason why young children seem so susceptible to every infection that comes along—their immune systems are literally learning the “vocabulary” of bacteria and viruses. Until they have been exposed to a particular type of bacteria or virus, they will not have the appropriate antibody in their repertoire (un less they are nursing and can utilize their mothers' immune defenses). Vaccinations work by administering either a dead or very weak ver sion of bacteria or virus so that a child's immune system can learn to make the correct antibodies without much risk of the child's becoming seriously ill. Some vaccinations, such as gamma globulin shots for hepa titis, work by directly providing the immune system with copies of the appropriate antibody (IgG). However, viruses can mutate very rapidly, and the immune system must always be developing new antibodies for the mutations, which is why one needs to get a flu shot every year. Bacte ria can also mutate rapidly, and the overuse and incorrect use of antibi otics may result in drug-resistant strains of bacteria. If a person does not take the full complement of antibiotics, for example, all of the bacteria may not be killed, and the surviving ones will be more drug-resistant. 48 STRESS, COPING, AND DEVELOPMENT



Further, if a particular strain of bacteria or virus is provided with very hospitable vectors, or hosts, it can develop into a much stronger (or more virulent) version (Whiteside et al., 1993). For example, the home less are very hospitable vectors for tuberculosis (TB). Due to nutritional deprivation, loss of sleep, and stress, the homeless often have highly weakened immune systems. The TB virus is airborne, and being exposed to coughs in a crowded shelter is often a perfect environment for the transmission of TB. Due to lack of medical care, the homeless may not seek treatment until the TB is fairly far advanced, and their chaotic liv ing conditions may make it difficult for them to consistently take their antibiotics for the requisite number of months to completely destroy the infection. Some public health officials worry that our neglect of the health and well-being of the homeless may result in a dramatic increase in particularly virulent forms of TB (Villarino, Geiter, & Simone, 1992). Thus, the immune system has to be constantly learning to recognize new enemies and manufacture new antibodies. However, errors can arise in learning, and the immune system may attack normal cells, resulting in autoimmune diseases such as rheumatoid arthritis. Sometimes viruses manufacture antigens that are very similar to a naturally occurring pro tein, and the immune system may get confused and attack a “good” pro tein. It is thought that multiple sclerosis (MS) and some types of Type 1 (insulin-dependent) diabetes, especially when it arises in adulthood, are due to invading viruses that generate antigens that the immune system confuses with the nerve sheaths (in MS) or the beta cells that manufac ture insulin (in diabetes). Thus, the viruses can disable an organism by getting the immune system to attack a crucial function. There are a great many components to the immune system, and re searchers are still identifying subcomponents. However, the components of acquired immunity are generally categorized into two broad divisions: humoral immunity, which includes antibodies or immunoglobulins, and



cellular immunity, which includes a variety of cell types (T cells and NK cells) that either directly challenge invaders (or malfunctioning cells) or mediate humoral immunity (B cells). While both T and B cells derive from precursor cells in the bone marrow, T cells are matured in the thy mus.



Humoral Immunity Unlike phagocytes (or T cells), B cells do not engulf or lyse (break open) antigens but instead generate antibodies. Also called immunoglobulins, these are complex protein chains that specifically agglutinate or bind an tigens together so that they can be more easily removed from the body. Other antibodies serve to identify antigens to T cells or to basinophils, The Physiology of Stress 49



which then destroy the antigens by lysing their cells (often by using hydrogen peroxide). At other times, the macrophages or T cells can iden tify antigens to B cells and stimulate them to produce antibodies, which then agglutinate this specific type of antigen. There are five major types of antibodies or immunoglobulins: IgA, IgD, IgE, IgG, and IgM. (I use the acronym MADGE to remember these, despite the different order of presentation.) Note that there are also many subtypes of each antibody. Antibodies are generally specific to par ticular antigens, although if the molecular shape of antigens is similar enough, some cross-reactivity may occur. Sometimes an antibody may react to more than one antigen, which is called multispecificity.



Cellular Immunity Cellular immunity refers to activated or mature T cells. Through a pro cess that is still poorly understood, the thymus processes the immature or “naive” T cells (also called rosettes), differentiates them into specific types of T cells, and selects those that can recognize a particularly anti gen. The thymus also destroys T cells that would self-react. There are many different types of cells and somewhat different naming conventions for them. Some types of T cells, such as cytotoxic T cells (cT), directly recognize and lyse cells that are abnormal in some way, either because they are infected with bacteria or viruses, are cancer cells, or in general have the wrong HLA complex on their cell mem branes (such as those in transplanted organs). These are also called effector cells. In contrast, helper T cells, also known as CD4+ cells, do not directly lyse cells but instead generate molecules called cytokines that stimulate other parts of the immune system. Cytokines, also known as interleukins, have different functions but in general help in communi cating between and regulating the different parts of the immune system. For example, interleukin-4 (IL-4) stimulates B cells to produce antibod ies, whereas interleukin-2 (IL-2) assists in cell maturation. Macrophages can also release interleukin-1 (IL-1), which causes T cells to proliferate. IL-6 is involved in inflammatory processes. When an organism is exposed to antigens, there is a massive in crease in the number of T cells (as well as other components of the immune system), in part due to the stimulating influence of helper T cells



and macrophages. This results in inflammation and other immune symp toms. For example, the fevers, aches, runny nose, and lethargy com monly associated with colds or the flu are actually side effects of the actions of the immune system against the invading virus. The same is true of the redness, tenderness, and swelling associated with bee bites. Allergic reactions and asthma are caused by an inappropriate or exces 50 STRESS, COPING, AND DEVELOPMENT



sive proliferation of IgE. Similarly, phlegm and pus in wounds are largely dead bacteria and immune cells. The massive increase in T cells is physi ologically very costly, and it is thought that the immune system induces lethargy so that it can redirect available energy supplies to producing T cells. While inflammatory responses are necessary in the short run, in the long term they are in and of themselves toxic and may result in problems such as autoimmune disorders, chronically inflamed nerves, and even heart disease, which is now largely thought of as an inflammatory pro cess. Thus, the immune system uses suppressor T cells, also known as CD8 cells, to decrease immune reactions. In many ways, the ratio of CD4+ to CD8 cells may be a better indicator of the healthiness of the immune system than is the absolute level of any one component. Memory T cells constitute the “library” that the immune system consults in order to see if it can recognize a particular antigen. If a par ticular antigen is in its library, the immune system can thus stimulate the appropriate cell proliferation much more rapidly than if the thymus has to take the time to figure out the precise antibodies needed to repel that specific invader. This allows the immune system to prevent the occur rence of illness—that is, it can overwhelm the invaders before they have a chance to proliferate too widely. Thus, in some ways, the immune sys tem actually becomes more efficient with age—at least until very late in life, when there are fewer rosettes and the immune system takes much longer to mount challenges to new invaders that it has not seen before (Weksler & Szabo, 2000). Natural killer (NK) cells have been receiving increasing attention as an important immune system component. Unlike T and B cells, they can independently attack viruses and parasites without requiring presensi tization (Murasko & Bernstein, 1999). Low levels of NK cells have also been associated with chronic virus infection and autoimmune disease (Whiteside, Bryant, Day, & Herberman, 1990). More importantly, NK cells have a surveillance function in the fight against tumor proliferation. By a currently unknown mechanism, NK cells have the capacity to iden tify cells that are mutating into tumor cells. By destroying these cells, NK cells help fight against cancer. Depending upon the circumstances, pre cancerous cells can arise very frequently, and thus a weakened NK cell system can have serious consequences.



Immune System Assays There are two basic kinds of immune system assays: structural and func tional measures. Structural assays refer to counts of the number of par The Physiology of Stress 51



ticular types of immune system antibodies or cells and constitute the most common and reliable way to assess immune function (Virella, 1993). However, simple counts of B and T cells may not be good indica tors of immunocompetence; it may be more important to determine how well these cells are functioning. B cell functioning is generally deter mined by how many antibodies they produce when stimulated by mitogens (usually PHA or con A—hence, the term “con A proliferation assay”). Researchers determine what proportion of cells NK cells can lyse and also examine CD4+/CD8 reactivity. However, reactivity may be hard to quantify consistently, and some of the assays may be not only less than reliable but also subject to lab drift (differences across labs or across time within labs).



Stress and Immune Function The relationship between stress and immune system functioning is com plex, but stress and other psychosocial factors have been associated with the functioning of various components of the immune system, including antigens, CD4+/CD8 ratios, and NK cells (for reviews, see Aldwin & Gilmer, 2004; Cohen & Herbert, 1996; Gruenewald & Kemeny, 2007; Kiecolt-Glaser et al., 2002; Rabin, 1999; Solomon & Benton, 2001). In part, the impact of stress depends upon the duration and intensity of the stressor. Very short-term stimulation, such as laboratory stressors, may actually increase or stimulate immune functioning, but acute stressors, such as students' examinations, suppress a variety of immune functions. The influence of chronic stress is most profound and long-lasting. For example, there is an extensive literature on caregiving stress that sug gests that immunosuppression may last long after the stressor has ended (Glaser et al., 1998). Nevertheless, while experimentally creating a stress-immune sys tem-illness chain has proven difficult (Kaplan, 1991), a number of carefully controlled studies have started constructing this chain. Co hen, Tyrrell, & Smith (1991) conducted an experiment in which differ ent types of stress were related to the “success” of a viral infection (how much the cold virus proliferated after exposure) and cold symp toms. Further, Cohen et al. (1998) showed that individuals who re ported chronic interpersonal stress were more likely to come down with a cold following exposure to a rhinovirus. Kiecolt-Glaser, Page, Marucha, MacCallum, & Glaser (1998) showed that students under stress had lower levels of cytokines (which regulate the inflammation and healing process) and small experimentally induced wounds took longer to heal. However, most of the work, especially in humans, is 52 STRESS, COPING, AND DEVELOPMENT



correlational instead of causal—and thus must be viewed with cau tion. It many ways, it is easier to show stress, immune-suppression, and illness links in individuals who are already ill. Zautra et al. (1998) stud ied women with rheumatoid arthritis and showed that interpersonal stressors were associated with immune system changes in T cells and IL-2, which in turn were associated with physician ratings of disease activity. Similarly, stress has been associated with lower CD4+ cell counts in HIV



positive men, which in turn is often associated with a more rapid pro gression of the disease (Nott & Vedhara, 1999). While the mechanisms through which stress affects the immune sys tem are not clearly understood at this point, the central nervous system and the immune system have complex bidirectional relationships, and there is evidence, at least in animals, that the brain monitors immune system processes (Dunn, 1989). Given that the various components of the immune system need to communicate in order to function, it is not surprising that there are receptor sites for neurotransmitters on immune system cells. (Neurotransmitters may be more aptly termed “communi cation peptides,” since they are found in nearly every organ in the body and do not seem to be limited simply to transmitting neuronal com mands.) Further, changes in the immune system may also have cognitive and psychological effects (for reviews, see Dunn, 1989; Smith, 1991). Thus, stress-induced emotions, neuroendocrine functions, and the im mune system may usefully be examined in a transactional framework.



CELLULAR RESISTANCE TO STRESS Cells can also be stressed, which can lead to their malfunctioning and even to death. There are a large number of factors that can create stress at the cellular level, including exposure to biochemical toxins, radiation, heat, and cold. Perhaps the most pervasive source of stress is reactive ox ygenating species (ROS), the so-called free radicals. Free radicals are molecules, usually oxygen, that have an imbalance in their number of electrons. These are generated when processing oxygen for energy in the cell, or by the immune system when it seeks to destroy bacteria and other invaders by squirting them with ROS such as hydrogen peroxide or superoxides. ROS can seriously disrupt the functioning of the cell, of ten by damaging the conformation of proteins, especially in sensitive organelles like mitochondria, which are the power houses of the cell. There are a number of ways in which cells can protect themselves from stress. There are naturally occurring antioxidants such as super The Physiology of Stress 53



oxide dismutase (SOD), which can absorb or distribute extra electrons, thereby counteracting ROS. Other chemicals such as vitamin C, lipoic acid, and acetylcarnitine also act as antioxidants and serve to protect the cell (Calabrese, Giuffrida, Calvani, & Butterfield, 2006; Hagen, Moreau, Suh, & Visioli, 2002). Other stress-protective mechanisms at the cellular level include DNA repair mechanisms and heat shock proteins (hsps). Hsps have a number of functions, including refolding damaged proteins back into their proper structure and regulating the enzymes necessary for repair (Sartori & Scherrer, 2003). Hsps received their name because they were first identified in plants that were subjected to heat stress. The impor tance of these DNA repair mechanisms and Hsps is underscored by the fact that they are highly conserved across species, that is, they can be found in nearly all living cells from bacteria through mammals and may be a major regulator of the aging process (Calabrese et al., 2006; Jurivich, Qiu, &



Welk, 1997). As mentioned earlier, only one article has examined psychosocial factors and hsps (Lewthwaite et al., 2002). They found elevated levels of hsps in individuals with low SES, high social isolation, and (for women only) high levels of psychosocial distress. How psychosocial factors can impact stress resistance and vulnerability at the cellular level is, at this point, unknown.



SUMMARY There are many complex ways in which the body responds to and coun teracts the effects of stress, include neuroendocrine responses, immune responses, and cellular responses. In a sense, the approaches that empha size general and specific reactions to stress are complementary rather than competing. Stress does involve mobilization of the SAM and the HPA axis as well as the immune system and cellular responses. However, within that general framework, there may be variations due to individ ual differences in patterns of reactivity or to stressor characteristics. Which approach is appropriate depends upon the specific stressors or responses to stress under investigation. Different types of problems or stressors require different levels of analysis. For example, obtaining very precise neuroendocrine profiles in reac tion to stress may be nearly impossible in a field setting. Confounding factors such as sleep patterns, nutrition, and activity level cannot be con trolled. In such settings, more general measures of sympathetic nervous system arousal may be more appropriate. However, more precise physio 54 STRESS, COPING, AND DEVELOPMENT



logical measurements may be necessary for studies that seek to define mechanisms between personality, stressors, and specific disease out comes, such as hostility and coronary heart disease. Nonetheless, stress clearly affects the whole body, and the roles that psychosocial factors such as coping play in moderating the effects of stress will take up the re mainder of this book.



STRESS, COPING, AND DEVELOPMENT Design and Measurement Issues



CHAPTER 5



Design and Measurement Issues in Stress Research



The sheer amount of research on the effects of stress during the past quarter-century has been extraordinary. A review by Vingerhoets and Marcelissen (1988) counted nearly 10,000 articles published during the decade between 1976 and 1985. Since 1986, more than 60,000 arti cles on stress have been published in psychology! A search of PubMed yielded more than 238,000 articles in total! Obviously, a review of all of this literature is beyond the scope of this (or any) book. However, there are a few general observations that can be made. Further, a number of extremely crucial research design issues have emerged, an understanding of which is essential to conducting adequately designed studies on stress. In this chapter, the different types of stress instruments are briefly re viewed.



GENERAL OBSERVATIONS It has been established, beyond doubt, that stress is associated with neg ative health outcomes in almost a bewildering array of illnesses, ranging from backaches and headaches to heart disease and, perhaps, cancer. (For reviews of the health effects of stress for various illnesses, see Aldwin & Gilmer, 2004; Duijts, Zeegers, & Borne, 2003; Krantz & McCeney, 2002; Turner & Wheaton, 1995; Vitaliano, Zhang, & Scanlan, 2003). The mechanisms for this broad spectrum effect of stress almost 55 56 STRESS, COPING, AND DEVELOPMENT



certainly lie within the neuroendocrine and immune systems (see Chap ter 4), but the specific details are still being worked out. A number of general observations, however, can be made. Contrary to Holmes and Rahe's (1967) initial hypothesis, positive stressful events per se do not appear to have adverse health effects. Most research shows that negative or undesirable rather than positive events precipitate symptoms (Rabkin & Streuning, 1976; Turner & Wheaton, 1995). In fact, there are some studies suggesting that positive events may buffer or mitigate the adverse effects of negative or undesirable events, although there is a great deal of inconsistency in the findings (Doyle, Wolchik, Dawson-McClure, & Sandler, 2003; Reich & Zautra, 1981). Thoits (1983) cautioned that undesirable events may be better predictors of psychological symptoms, but total events may be better predictors of physical health symptoms. This may be because the so-called positive events may have many negative characteristics. A promotion or a new job may initially entail an increase in workload, or a new marriage may get off to a rocky start. In general, going through a negative event, like a divorce, may have more serious health consequences than experiencing a positive event such as marriage. Further, stressors that are thought to be uncontrollable are generally more distressing than those that are more likely to be under an individ ual's control (Reich & Zautra, 1981). For example, quitting a job may be less stressful than being fired. Similarly, initiating a divorce from a spouse



may be less stressful than being divorced (Wilder & Chiriboga, 1991). The uncontrollability of the event may explain why natural disas ters and other types of trauma are so stressful. Perhaps the most important thing to remember about stress re search is that the relations between stress and health outcomes, although broad in scope, are relatively modest in effect sizes. The correlations be tween stress and health outcomes are typically in the .20s–.40 range. Overall, this is a positive finding, because it suggests as a species that we are rather resilient to stress. Unlike some laboratory rats, we tend not to become ill at the slightest bit of adversity! However, the relatively modest relation between stress and health increases the difficulty in establishing a definitive causal relationship between a stressor and a particular disease, because not everyone who experiences stress will become ill, and if he or she does become ill, the type of illness developed may depend upon the degree of exposure to pathogens, genetic propensities to disease, nutritional status, and so on. It is much easier to establish a relationship between stress and flare-ups of existing conditions, such as rheumatoid arthritis (Revenson & Felton, 1989), than it is to implicate stress in the etiology of a new illness (but see Cohen et al., 1991). While the link between stress and incidence of Design and Measurement Issues 57



cardiovascular disease is relatively weak and somewhat inconsistent, there is a stronger relationship between stress and poor outcomes in in dividuals who are already ill (Aldwin & Gilmer, 2004).



DESIGN ISSUES IN STRESS RESEARCH There are additional problems to be considered in the design of any stress and health study. First, what is the timing of the event under study, and what is the particular health outcome? Any specific disease, espe cially chronic illnesses such as heart disease or cancer, may take decades to develop. How reasonable is it to propose that a particular stressor may affect this etiology?—unless, of course, stress can be seen as a trigger that helps to precipitate full-blown disease from underlying preclinical pathologies, in which case it would be reasonable to expect a relation ship between stress and disease, if—and only if—there existed such pa thologies. Similarly, it is also unreasonable to expect that illnesses with relatively short incubation periods, such as colds, will be greatly affected by an event that could have occurred up to a year earlier unless that event has ongoing ramifications for day-to-day existence (which many do). Thus, for any study it is critical to consider issues regarding the tim ing of the stressor and the probable etiology of the particular illness un der study. The second major issue for consideration is whether the appropriate types of stressors have been identified for the particular age or ethnic group being studied. The inappropriateness of items to particular popu lations may lead to incorrect conclusions about the relationship between stress and health outcomes in various groups. For example, an early re view by Paykel (1983) found little relationship between stress and health



among the elderly, primarily because the types of events then studied were more relevant to younger groups than to older ones. Only when agespecific inventories were developed did the relationship between stress and health emerge (Aldwin, 1990). Given that life stage, social structures, and cultural values may determine both the occurrence of particular types of stressors and the ways in which various events are perceived (See Chapters 13 and 14), it is imperative that the stress mea sure used in any given research project be both culturally and develop mentally appropriate. An additional issue that has yet to be resolved is whether the effects of stress on well-being are cumulative (ie, additive) or multiplicative. Most stress research assumes that stress is cumulative: There is a direct linear increase in symptoms, negative affect, and so forth coincident with incremental increases in stress. This is indicated by the fact that we 58 STRESS, COPING, AND DEVELOPMENT



sum the number of life events checked or add up the ratings and then correlate them with an outcome measure. However, it is entirely possible that the effects of stress are multiplicative. That is, having two stressful life events may multiply the stress effects by more than a factor of two. Early work by Rutter (1981), for example, found that most children could cope readily with one major stressful event, such as the death of a parent. However, the death of a parent in conjunction with other stress ful circumstances, such as poverty or mental illness in the remaining par ent, often proved overwhelming. (See Aldwin, Levenson, and Spiro, 1994, for a corroborating example of the nonlinear effects of combat ex posure on mental health in later life.) It is equally possible that stress may have an asymptotic effect, that is, after three or more stressors, the increase in symptoms would reach its maximum possible level. The point is that we simply do not know what the dose–response curve is between stress and various health out comes; nor do we know how that curve varies among individuals, although studies by Brown and Harris (1989) and Surtees (1989) have begun to address some of those issues. Nonetheless, cumulative stress is thought to have more adverse consequences than isolated life events (Ev ans, 2004). Even the duration of stress effects is a matter of some debate. The general wisdom holds that the psychiatric effects of stressful life events usually dissipate within 6 months to 1 year (Depue & Monroe, 1986; Norris & Murrell, 1987), while the effects of mere hassles dissipate within a day or two (DeLongis, Folkman, & Lazarus, 1988). However, some of the trauma literature suggests that posttraumatic stress disor ders may linger for decades, as with Pearl Harbor survivors (Wilson, Harel, & Kahana, 1989) and World War II prisoners of war (Page, Engdahl, & Eberly, 1991). Even studies of regular soldiers suggest that the effects of combat exposure can be detected even after 50 years have passed (Aldwin & Levenson, 2005; Spiro, Schnurr, & Aldwin, 1994). Much of the work in stress research has been directed toward the conceptualization and measurement of stress and, to a large extent, to overcoming barriers in the larger scientific community concerning the physiological effects of psychosocial phenomena. Thus, it is not surpris



ing that such elemental questions as dose-response and timing of stress effects have not yet been definitively delineated. In fairness, it should also be acknowledged that stress effects are highly probabilistic phenom ena, being dependent on myriad contextual and personal factors. Thus, it may not be possible to develop clear-cut curves. At best, one can deter mine population risk rates, such as the temporary increase in deaths due to coronary heart disease (CHD) during the first year of widowhood, documented by Parkes and Weiss (1983). However, it is also understood Design and Measurement Issues 59



that generalizing from a population risk to an individual risk is not pos sible, at least not without committing the ecological fallacy. Clearly, most of the recent work in stress research has emphasized individual dif ferences in response to stress, and, as we shall see later, many have ar gued that how individuals cope with stress is more important in develop ing psychological and physical reactions to stress than is simple exposure to a stressor.



PROBLEMS IN CAUSAL DIRECTIONALITY One of the thorniest design issues in stress research remains the interrela tions among stress, personality, and health. Despite the strong evidence that stress is related to health, assessing the causal directionality in this relation remains problematic. On the one hand, higher stress scores may reflect rather than cause poor health. Someone with a chronic disabling illness, for example, may well experience more hassles in the struggle to do everyday chores; more role strain in relation to finances, work, and marriage; and may even be subject to more negative life events. On the other hand, a serious problem in studies that rely primarily on self reports of stress and health may be that a third factor, personality style, is confounded with both types of assessment and creates a spurious asso ciation. Both of these problems with causal directionality have resulted in a series of classical interchanges in the literature. Lazarus and his col leagues (DeLongis, Coyne, Dakof, Folkman, & Lazarus, 1982; Kanner, Coyne, Schaefer, & Lazarus, 1981; Lazarus & Folkman, 1984) have consistently argued that subjective appraisals of stress are more effective in predicting health outcomes because they take into account the mean ing of the event to the individual. Individual characteristics (ie, beliefs, values, and commitments) and contextual factors (ie, the timing and duration of the stressor) may conjointly influence the degree to which any particular event may be stressful. Due to a variety of factors, being laid off a job provides an excellent example of the lack of uniformity in stress effects. For example, the degree to which being laid off is stressful may depend upon personal factors such as age and commitment to the lost job (eg, losing a job at McDonald's when one is 16 years old is much less stressful than losing a managerial position when one is 50 years old). Or losing a job may be particularly stressful depending upon contextual factors, such as a high general unemployment rate that may increase the duration of unemploy



ment, the recent purchase of a house that has depleted one's savings, or a spouse who is also laid off. Thus, Lazarus argued that the so-called ob 60 STRESS, COPING, AND DEVELOPMENT



jective ratings of life-event stress that assign “life-change units” to spe cific life events do not take into account these individual differences, and thus subjective ratings of stress are inherently better predictors of health outcomes than these “objective” ratings. This emphasis on individual differences in the meaning of events was underscored by a prospective study of bereavement by Wortman and Silver (1989). They found that nearly one-third of bereaved spouses did not appear to be distressed at any point up to a year after the death, contrary to general expectations of extreme distress traditionally associ ated with conjugal bereavement. In a challenge to the position championed by Lazarus and his col leagues, Dohrenwend, Dohrenwend, Dodson, and Shrout (1984) criti cized as potentially confounded with prior mental health status subjec tive measures of stress that rely upon individual appraisals. That is, individuals who are depressed or who have high levels of emotionality, for example, may be more likely to perceive everyday occurrences as stressful. We all are familiar with individuals who “catastrophize” and overreact to very minor problems. Thus, the Dohrenwends have argued that subjective indices of stress such as hassles may be reflecting rather than causing mental health problems. Only objective stress measures, in their view, can demonstrate that psychosocial stress causes problems in both psychological and physical health. In response, Lazarus, DeLongis, Folkman, and Gruen (1985) had clinical psychologists identify the items that potentially reflected mental health problems and reanalyzed their data omitting these items. They still found that these “uncontaminated” hassles were better predictors of physical health than life events, a finding confirmed by Rowlison and Felner (1989). In an escalation of the conflict, Schroeder and Costa (1984) at tacked life events (and stress measures in general) for being confounded with personality characteristics as well as with preexisting health status. They separated “contaminated” life events—that is, those judged to re flect prior health status or personality—from “uncontaminated” ones. For example, “trouble paying bills” was judged to be contaminated by neuroticism, while “being laid off” was thought to be a more objective stressor. They found that only the “contaminated” life events were asso ciated with health outcomes and concluded that “contamination factors . . . inflated the overall event–illness correlation” (p. 860). In turn, Maddi, Bartone, and Pucetti (1987) criticized the Schroeder and Costa rating scheme for both its lack of theoretical rationale and its lack of clarity in the grouping procedure used. They pointed out, for ex ample, that difficulty in paying bills may derive from being laid off— and, thus, terming one “contaminated” and the other as “uncontami Design and Measurement Issues 61



nated” makes a spurious and insupportable distinction. They used their own grouping procedure and found that “uncontaminated” life events were



actually better predictors of health, both cross-sectionally and lon gitudinally, than were so-called contaminated events. The problem with both sets of arguments is, of course, that none of these studies actually assessed the factors with which the stressors were thought to be confounded, namely, prior mental health and emotional ity. On the basis of self-report data, it is impossible to determine whether an event was due primarily to environmental happenstance or an indi vidual's prior maladaptation. Someone may be laid off through no fault of his or her own but because his or her firm lost a big contract; another person might have had a problem with alcohol and the supervisor used an economic slowdown as an excuse to lay off the troublesome em ployee. Only longitudinal data with assessments of the putative con founding agent can answer the questions raised by the Dohrenwends and Costa and his colleagues. My colleagues and I examined these issues in two longitudinal stud ies. In the first study, we examined the relationship between mental health and economic stress (Aldwin & Revenson, 1987). We had base line measures of mental health and economic stress and obtained follow up measures a year later, during which time the unemployment rate had risen by several points. We showed that people with poorer mental health at Time 1 were more likely to report economic strain at Time 2 when the economy had worsened, demonstrating that people with poorer mental health were more likely to experience stress. Nonetheless, even controlling for mental health at Time 1, economic stress did have adverse health effects at Time 2, especially if the economic problems ap peared to be chronic. This demonstrated that stress could have adverse effects in and of itself, not due to its acknowledged confound with prior mental health status. A subsequent study also used longitudinal data to examine the issue of personality, stress, and mental health (Aldwin, Levenson, Spiro, & Bossé, 1989). Drawing upon the Normative Aging Study archives, we utilized a measure of emotionality assessed in 1975 and administered life events, hassles, and mental health measures in 1985 to a large sample of older men. We showed that both life events and hassles were correlated at about the same level (~.20) with the personality assessment 10 years earlier, partially confirming the concerns of the Dohrenwends, Schroeder, and Costa. That is, individuals higher in emotionality were more likely to report hassles, even 10 years later, but they were also more likely to report life events. Nonetheless, both life events and hassles contributed independent variance to mental health, even controlling for preexisting emotionality. 62 STRESS, COPING, AND DEVELOPMENT



In other words, personality, stress, and health are, to a certain ex tent, confounded with one another. While this confound needs to be rec ognized in studies, especially cross-sectional ones, longitudinal studies confirm that stress can cause negative health outcomes, regardless of prior personality and health status. The debate over causal directionality between personality, stress, and health has also provided useful insights into the nature of the stress process. Rather than thinking of the stress process only in terms of con



founds, the bidirectionality (or rather, multidirectionality) between per sonality, stress, and health actually provides strong support for the transactionist viewpoint. Once again, by focusing on unidirectional causality (does stress cause health problems or only reflect them? or is personality causing everything?), only parts of the process are being highlighted. Yes, the concerns of the Dohrenwends and the personality psychologists are real: The perception of stress is in part a reflection of prior personality and mental health. However, that is precisely the point of a transactionist perspective. Appraisal is a function of both the person and the environment. Nonetheless, that does not diminish the very real and independent contribution that stress makes to mental and physical health —and, perhaps, even to changes in personality (see, eg, Aldwin, Sutton, & Lachman, 1996b; Schnurr, Rosenberg, & Friedman, 1993). These issues in the design of stress research and causal directionality should be borne in mind as we consider the various ways that stress can be measured.



DIFFERENT APPROACHES TO STRESS MEASUREMENT How a researcher chooses to measure stress depends upon both the re search question and the way in which stress is conceptualized. Generally, researchers who define stress in terms of environmental demands study extremely stressful environments or individual life events, while those preferring definitions emphasizing the transaction between the person and the environment tend to study everyday stressors or hassles. Stress can also be studied in a laboratory situation, using standardized stress ors such as mental math or cold pressor tests, in which pain is induced by immersing an arm in very cold water. The overall goals of the differ ent approaches are usually similar—to determine the manner in which stress relates to some health outcome, whether it is physical or mental health, through either self-report or some physiological indicator of stress (except, of course, for those studies that seek to examine the pre cursors of stress or its distribution in a population). Design and Measurement Issues 63



In truth, the differences between various approaches to stress mea surement are not necessarily clear-cut, and there is much overlap at both the conceptual level and the measurement level. The distinction between hassles and chronic role strain can be blurred, as is that between life events and trauma. Clinicians who study PTSD among combat veterans argue that there is a qualitative difference between the two categories, with trauma leading to a physiological state characterized by flashbacks, nightmares, and hyperreactivity, whereas life events “just” lead to de pression and anxiety. Are the differences simply a matter of degree of stressfulness? When is a motor vehicle accident a traumatic experience, a life event, or just a “hassle”? In part, the various conceptions of stress can be differentiated using a two-dimensional space defined by duration on the x-axis and severity on the y-axis (see Figure 5.1). Traumas tend to be of relatively short duration and characterized by life-threatening severity, either to oneself or others.



On the other hand, conditions lasting for long periods of time that are not immediately life-threatening can be considered chronic role strain. Some life circumstances such as living in a war-torn area or an impoverished violent barrio are a combination of chronic stress punctu ated by short periods of trauma. Life events may be of varying duration, but they differ from role strain in having clearly defined endpoints. On going marital problems, for example, are role strain; divorce is a life



FIGURE 5.1. Comparison of the duration and severity of different conceptions of stress.