Causes of mental disorders
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The causes of mental disorders are complex, and interact and vary according to the particular disorder and individual. Genetics, early development, drugs, disease or injury, neurocognitive and psychological mechanisms, and life experiences, society and culture can all contribute to the development or progression of different mental disorders.
Theoretical perspectives
There are a number of theories or models, seeking to integrate and explain diverse findings on mental disorders. The field is complicated by the fact that many psychiatric disorders could still be classified as syndromes - patterns of symptoms that do not have an accepted or consistent cause[citation needed]. Different disorders may require different explanations and are likely to have their own etiology (pattern of causation). The most common view is that disorders tend to result from genetic vulnerabilities and environmental stressors combining to cause patterns of dysfunction or trigger disorders (Diathesis-stress model). A practical mixture of models may often be used to explain particular issues and disorders, but the primary focus of contemporary mainstream Western psychiatry has been said to be the biopsychosocial (BPS) model[citation needed]- incorporating or merging together biological, psychological and social factors - although this may be commonly neglected or misapplied in practice due to being too broad or relativistic.[1] and, in reality, biopsychiatry has tended to follow a biomedical model, focusing on "organic" or "hardware" pathology of the brain. Psychoanalytic theories, focused on unresolved internal and relational conflicts, have been posited as overall explanations of mental disorder, although today most psychoanalytic groups are said to adhere to the biopsychosocial model and to accept an eclectic mix of subtypes of psychoanalysis.[1] Evolutionary psychology (or more specifically evolutionary psychopathology or psychiatry) has also been proposed as an overall theory, positing that many mental disorders involve the dysfunctional operation of mental modules adapted to ancestral physical or social environments but not necessarily to modern ones.[2][3][4] Attachment theory is another kind of evolutionary-psychological approach sometimes applied in the context for mental disorders, which focuses on the role of early caregiver-child relationships, responses to danger, and the search for a satisfying reproductive relationship in adulthood.[5] An overall distinction is also commonly made between a "medical model" (also known as a biomedical or disease model) or a "social model" (also known as an empowerment or recovery model) of mental disorder and disability, with the former focusing on hypothesized disease processes and symptoms, and the latter focusing on hypothesized social constructionism and social contexts.[6]
Genes
Family-linkage and twin studies have indicated that genetic factors often play an important role in the development of mental disorders. The reliable identification of specific genetic susceptibility to particular disorders, through linkage or association studies, has proven difficult.[7][8] This has been reported to be likely due to the complexity of interactions between genes, environmental events, and early development[9] or to the need for new research strategies.[10] The heritability of behavioral traits associated with mental disorder may be greater in permissive than in restrictive environments, and susceptability genes probably work through both "within-the-skin" (physiological) pathways and "outside-the-skin" (behavioral and social) pathways.[11] Investigations increasingly focus on links between genes and endophenotypes - more specific traits (including neurophysiological, biochemical, endocrinological, neuroanatomical, cognitive, or neuropsychological) - rather than disease categories.[12][13]
Pregnancy and birth
Environmental events surrounding pregnancy and birth have been linked to an increased development of mental illness in the offspring. This includes maternal exposure to serious psychological stress or trauma, conditions of famine, obstetric birth complications, infections, and gestational exposure to alcohol or cocaine. Such factors have been hypothesized to affect specific areas of neurodevelopment within the general developmental context and to restrict neuroplasticity.[14]
People with developmental disabilities, such as mental retardation, are more likely to experience mental illness than those in the general community.[15]
Disease, injury and infection
Higher rates of mood, psychotic, and substance abuse disorders have been found following traumatic brain injury (TBI). Findings on the relationship between TBI severity and prevalence of subsequent psychiatric disorders have been inconsistent, and occurrence has been linked to prior mental health problems as well as direct neurophysiological effects, in a complex interaction with personality and attitude and social influences.[16]
A number of psychiatric disorders have often been tentatively linked with microbial pathogens, particularly viruses; however while there have been some suggestions of links from animal studies, and some inconsistent evidence for infectious and immune mechanisms (including prenatally) in some human disorders, infectious disease models in psychiatry are reported to have not yet shown significant promise except in isolated cases.[17] There have been some inconsistent findings of links between infection by the parasite Toxoplasma gondii and human mental disorders such as schizophrenia, with the direction of causality unclear.[18][19][20] A number of diseases of the white matter can cause symptoms of mental disorder.[21]
Poorer general health has been found among individuals with severe mental illnesses, thought to be due to direct and indirect factors including diet, bacterial infections, substance use, exercise levels, effects of medications, socioeconomic disadvantages, lowered help-seeking or treatment adherence, or poorer healthcare provision.[22] Some chronic general medical conditions have been linked to some aspects of mental disorder, such as AIDS-related psychosis.
The current research on Lyme's Disease caused by a deer tick, and related toxins, is expanding the link between bacterial infections and mental illness.[citation needed]
Individual characteristics
Mental characteristics of individuals, as assessed by both neurological and psychological studies, have been linked to the development and maintenance of mental disorders. This includes cognitive or neurocognitive factors, such as the way a person perceives, thinks or feels about certain things;[23][24][25][26][27] or an individual's overall personality, temperament or coping style[28][29][30] or the extent of protective factors or 'positive illusions' such as optimism, personal control and a sense of meaning.[31][32]
Abnormal levels of dopamine activity have been implicated in a number of disorders (e.g., reduced in ADHD, increased in Schizophrenia), thought to be part of the complex encoding of the importance of events in the external world.[33] Dysfunction in serotonin and other monoamine neurotransmitters such as norepinephrine and dopamine has also been centrally implicated in mental disorders, including clinical depression as well as obsessive compulsive disorder, phobias, posttraumatic stress disorder, and generalized anxiety disorder, although the limitations of a simple "monoamine hypothesis" have been highlighted[34] and studies of depleted levels of monoamine neurotransmitters have tended to indicate no simple or directly causal relation with mood or major depression, although features of these pathways may form trait vulnerabilities to depression.[35] Dysfunction of the central gamma-aminobutyric (GABA) system following stress has also been associated with anxiety spectrum disorders and there is now a body of clinical and preclinical literature also indicating an overlapping role in mood disorder.[36]
Findings have indicated abnormal functioning of brainstem structures in disorders such as schizophrenia, related to impairments in maintaining sustained attention.[37] Some abnormalities in the average size or shape of some regions of the brain have been found in some disorders, reflecting genes and/or experience. Studies of schizophrenia have tended to find enlarged ventricles and sometimes reduced volume of the cerebrum and hippocampus, while studies of (psychotic) bipolar disorder have sometimes found increased amygdala volume. Findings differ over whether volumetric abnormalities are risk factors or are only found alongside the course of mental health problems, possibly reflecting neurocognitive or emotional stress processes and/or medication use or substance use.[38][39] Some studies have also found reduced hippocampal volumes in major depression, possibly worsening with time depressed.[40]
Life events, stresses and relationships
It is reported that there is good evidence on the importance of psychosocial influences on psychopathology in general, although less known about the specific risk and protective mechanisms.[41] Maltreatment in childhood and in adulthood, including sexual abuse, physical abuse, emotional abuse, domestic violence and bullying, has been linked to the development of mental disorder, through a complex interaction of societal, family, psychological and biological factors.[42][43][44][45][46][47] Negative or stressful life events more generally have been implicated in the development of a range of disorders, including mood and anxiety disorders. The main risks appear to be from a cumulative combination of such experiences over time, although exposure to a single major trauma can sometimes lead to psychopathology, including PTSD. Resilience to such experiences varies, and a person may be resistant to some forms of experience but susceptible to others. Features associated with variations in resilience include genetic vulnerability, temperamental characteristics, cognitive set, coping patterns, and other experiences.
Relationship issues have been consistently linked to the development of mental disorders, with continuing debate on the relative importance of the home environment or work/school and peer group. Issues with parenting skills or parental depression or other problems may be a risk factor. Parental divorce appears to increase risk, perhaps only if there is family discord or disorganization, although a warm supportive relationship with one parent may compensate. Details of infant feeding, weaning, toilet training etc do not appear to be importantly linked to psychopathology. Early social privation, or lack of ongoing, harmonious, secure, committed relationships, have been implicated both in childhood (including in institutional care) and also through the lifespan.in social relations and the experience of loneliness, particularly during adolescence, and the development of mental disorder.[48][49]
Society and culture
Problems in the wider community or culture - such as poverty, unemployment or underemployment, lack of social cohesion, migration - have been implicated in the development of mental disorder.[6][41] Mental illnesses have been linked to particular social and cultural systems.[50][51][52][53][54]
Stresses and strains related to socioeconomic position (socioeconomic status (SES) or social class) have been linked to the occurrence of major mental disorders, with a lower or more insecure educational, occupational, economic or social position generally linked to more mental disorder.[55] There have been mixed findings on the nature of the links and on the extent to which pre-existing personal characteristics influence the links. Both personal resources and community factors have been implicated, as well as interactions between individual-level and regional-level income levels.[56] The causal role of different socioeconomic factors may vary by country.[57]
Minority ethnic groups, including first or second-generation immigrants, have been found to be at greater risk for developing mental disorders, which has been attributed to various kinds of life insecurities and disadvantages, including racism.[58]
See also
References
- ↑ 1.0 1.1 Seyyed Nassir Ghaemi (2006) Paradigms of Psychiatry: Eclecticism and Its Discontents Curr Opin Psychiatry. ;19(6):619-624.
- ↑ Baron-Cohen, S. (Ed.) (1997) The Maladapted Mind: Classic Readings in Evolutionary Psychopathology ISBN 9780863774607
- ↑ Brune, M. (2002) Toward an integration of interpersonal and biological processes: evolutionary psychiatry as an empirically testable framework for psychiatric research. Psychiatry. 2002 Spring;65(1):48-57.
- ↑ Nesse, R. (2002) Evolutionary biology: a basic science for psychiatry World Psychiatry. 2002 February; 1(1): 7–9.
- ↑ Crittenden (2002) Attachment, information processing, and psychiatric disorder World Psychiatry. June; 1(2): 72–75.
- ↑ 6.0 6.1
- ↑ Insel, TR. & Collins, FS. (2003) Psychiatry in the Genomics Era Am J Psychiatry 160:616-620
- ↑ Bearden CE, Reus VI, Freimer NB. (2004) Why genetic investigation of psychiatric disorders is so difficult. Curr Opin Genet Dev. Jun;14(3):280-6
- ↑ Kas MJ, Fernandes C, Schalkwyk LC, Collier DA. (2007) Genetics of behavioural domains across the neuropsychiatric spectrum; of mice and men. Mol Psychiatry. Apr;12(4):324-30.
- ↑ Burmeister, M. (2006) Genetics of Psychiatric Disorders: A Primer Focus 4:317
- ↑ Kendler KS. (2001) Twin studies of psychiatric illness: an update. Arch Gen Psychiatry. 2001 Nov;58(11):1005-14.
- ↑ Bearden, CE. & Freimer, NB. (2006) Endophenotypes for psychiatric disorders: ready for primetime? Trends Genet. Jun;22(6):306-13.
- ↑ Glahn, DC., Thompson, PM. & Blangero J. (2007) Neuroimaging endophenotypes: strategies for finding genes influencing brain structure and function. Hum Brain Mapp. 2007 Jun;28(6):488–501. doi:10.1002/hbm.20401. PMID 17440953.
- ↑ Fumagalli, F., Molteni, R., Racagni, G., Riva, MA. (2007). Stress during development: Impact on neuroplasticity and relevance to psychopathology. Prog Neurobiol. Mar;81(4):197-217.
- ↑ Learning about Intellectual Disabilities and Health URL last accessed on August 24 2006.
- ↑ Fann JR, Burington B, Leonetti A, Jaffe K, Katon WJ, Thompson RS. (2004) Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. Jan;61(1):53-61.
- ↑ Pearce, B.D. (2003) Modeling the role of infections in the etiology of mental illness Clinical Neuroscience Research Volume 3, Issues 4-5 , December 2003, Pages 271-282
- ↑ Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors
- ↑ Thomas HV, Thomas DR, Salmon RL, Lewis G, Smith AP. (2004) Toxoplasma and coxiella infection and psychiatric morbidity: a retrospective cohort analysis. BMC Psychiatry. Oct 18;4:32.
- ↑ Alvarado-Esquivel C, Alanis-Quinones OP, Arreola-Valenzuela MA, Rodriguez-Briones A, Piedra-Nevarez LJ, Duran-Morales E, Estrada-Martinez S, Martinez-Garcia SA, Liesenfeld O. (2006) Seroepidemiology of Toxoplasma gondii infection in psychiatric inpatients in a northern Mexican city. BMC Infect Dis. Dec 19;6:178.
- ↑ Walterfang M, Wood SJ, Velakoulis D, Copolov D, Pantelis C. (2005) Diseases of white matter and schizophrenia-like psychosis. Aust N Z J Psychiatry. Sep;39(9):746-56.
- ↑ Phelan, M., Stradins, L., Morrison, S. (2001) Physical health of people with severe mental illness BMJ 322:443-444
- ↑ Iacoviello BM, Alloy LB, Abramson LY, Whitehouse WG, Hogan ME. (2006) The course of depression in individuals at high and low cognitive risk for depression: a prospective study. J Affect Disord. Jul;93(1-3):61-9. PMID 16545464
- ↑ Peer JE, Rothmann TL, Penrod RD, Penn DL, Spaulding WD. (2004) Social cognitive bias and neurocognitive deficit in paranoid symptoms: evidence for an interaction effect and changes during treatment. Schizophr Res. Dec 1;71(2-3):463-71.PMID 15474917
- ↑ Bell V, Halligan PW, Ellis HD. (2006) Explaining delusions: a cognitive perspective. Trends Cogn Sci. May;10(5):219-26.PMID 16600666
- ↑ Weems CF, Costa NM, Watts SE, Taylor LK, Cannon MF. (2007) Cognitive errors, anxiety sensitivity, and anxiety control beliefs: their unique and specific associations with childhood anxiety symptoms. Behav Modif. Mar;31(2):174-201. PMID 17307934
- ↑ Brunelin J, d'Amato T, Brun P, Bediou B, Kallel L, Senn M, Poulet E, Saoud M. (2007) Impaired verbal source monitoring in schizophrenia: an intermediate trait vulnerability marker? Schizophr Res. Jan;89(1-3):287-92.PMID 17029909
- ↑ Gil S, Caspi Y. (2006) Personality traits, coping style, and perceived threat as predictors of posttraumatic stress disorder after exposure to a terrorist attack: a prospective study.Psychosom Med. Nov-Dec;68(6):904-9. PMID 17079704
- ↑ Brandes M, Bienvenu OJ. (2006) Personality and anxiety disorders. Curr Psychiatry Rep. Aug;8(4):263-9. PMID 16879789
- ↑ Christensen MV, Kessing LV. (2006) Do personality traits predict first onset in depressive and bipolar disorder? Nord J Psychiatry. ;60(2):79-88. PMID 16635925
- ↑ Shelley E. Taylor and Annette L. Stanton (2007) Coping Resources, Coping Processes, and Mental Health. Annual Review of Clinical Psychology Vol. 3: 377-401
- ↑ Andrew Mathews and Colin MacLeod (2004)Cognitive vulnerability to emotional disorders Annual Review of Clinical Psychology vol. 1: 167-195
- ↑ Iversen SD, Iversen LL. (2007) Dopamine: 50 years in perspective. Trends Neurosci. Mar 15
- ↑ Hindmarch, I. (2002) Beyond the monoamine hypothesis: mechanisms, molecules and methods Eur Psychiatry. Jul;17 Suppl 3:294-9.
- ↑ Ruhe HG, Mason NS, Schene AH. (2007) Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion studies. Mol Psychiatry. Apr;12(4):331-59.
- ↑ Kalueff, AV. & Nutt, DJ. (2006) Role of GABA in anxiety and depression. Depress Anxiety. Nov 20
- ↑ Mirsky A.F., & Duncan, C.C. (2005). Pathophysiology of mental illness: a view from the fourth ventricle. International Journal of Psychophysiology: 58, 162.
- ↑ McDonald C, Marshall N, Sham PC, Bullmore ET, Schulze K, Chapple B, Bramon E, Filbey F, Quraishi S, Walshe M, Murray RM. (2006) Regional brain morphometry in patients with schizophrenia or bipolar disorder and their unaffected relatives. Am J Psychiatry. Mar;163(3):478-87.
- ↑ Velakoulis D, Wood SJ, Wong MT, McGorry PD, Yung A, Phillips L, Smith D, Brewer W, Proffitt T, Desmond P, Pantelis C. (2006) Hippocampal and amygdala volumes according to psychosis stage and diagnosis: a magnetic resonance imaging study of chronic schizophrenia, first-episode psychosis, and ultra-high-risk individuals. Arch Gen Psychiatry. Feb;63(2):139-49.
- ↑ Colla M, Kronenberg G, Deuschle M, Meichel K, Hagen T, Bohrer M, Heuser I. (2007) Hippocampal volume reduction and HPA-system activity in major depression. J Psychiatr Res. Oct;41(7):553-60.
- ↑ 41.0 41.1 Rutter, M. (2000). Psychosocial influences: critiques, findings, and research needs. Dev Psychopathol. Summer;12(3):375-405.PMID 11014744
- ↑ Spataro J, Mullen PE, Burgess PM, Wells DL, Moss SA. (2004) Impact of child sexual abuse on mental health: prospective study in males and females. Br J Psychiatry. 2004 May;184:416-21.
- ↑ Maughan, B. & McCarthy, G. (1997) Childhood adversities and psychosocial disorders. Br Med Bull. Jan;53(1):156-69.
- ↑ Teicher MH, Samson JA, Polcari A, McGreenery CE. (2006) Sticks, stones, and hurtful words: relative effects of various forms of childhood maltreatment. Am J Psychiatry. Jun;163(6):993-1000.
- ↑ Kessler RC, Davis CG, Kendler, KS. (1997) Childhood adversity and adult psychiatric disorder in the US National Comorbidity Survey. Psychol Med. 1997 Sep;27(5):1101-19.
- ↑ Pirkola S, Isometsa E, Aro H, Kestila L, Hamalainen J, Veijola J, Kiviruusu O, Lonnqvist J. (2005) Childhood adversities as risk factors for adult mental disorders: results from the Health 2000 study. Soc Psychiatry Psychiatr Epidemiol. Oct;40(10):769-77.
- ↑ MacMillan HL, Fleming JE, Streiner DL, Lin E, Boyle MH, Jamieson E, Duku EK, Walsh CA, Wong MY, Beardslee WR. (2001) Childhood abuse and lifetime psychopathology in a community sample. Am J Psychiatry. Nov;158(11):1878-83.
- ↑ Heinrich, LM & Gullone, E. (2006) The clinical significance of loneliness: a literature review. Clin Psychol Rev. Oct;26(6):695-718. PMID 16952717
- ↑ Hara Estroff Marano (2003) The Dangers of Loneliness Psychology Today
- ↑ Fee, D. (2000). Pathology and the Postmodern: Mental Illness as Discourse and Experience. London: Sage Publications Ltd.
- ↑ Al-Issa, I. (1995). Handbook of culture and mental illness. Connecticut: International Universities Press.
- ↑ Krause, I. (2006). Hidden Points of View in Cross-cultural Psychotherapy and Ethnography. Transcultural Psychiatry, 43, 181-203.
- ↑ Richards, P.S. & Bergin, A. E. (2000). Handbook of Psychotherapy and Religious Diversity. Washington D.C.: American Psychological Association.
- ↑ Littlewood, R. (1997). Aliens and Alienists: Ethnic Minorities and Psychiatry. London: Routledge.
- ↑ Muntaner C, Eaton WW, Miech R, O'Campo P. (2004) Socioeconomic position and major mental disorders. Epidemiol Rev. 26:53-62.
- ↑ V. Lorant1,, D. Deliège1, W. Eaton2, A. Robert3, P. Philippot4 and M. Ansseau (2003) Socioeconomic Inequalities in Depression: A Meta-Analysis Am J Epidemiol 157:98-112.
- ↑ R Araya1, G Lewis1, G Rojas2 and R Fritsch (2003) Education and income: which is more important for mental health? Journal of Epidemiology and Community Health 57:501-505
- ↑ Chakraborty, A. & McKenzie, K (2002) Does racial discrimination cause mental illness? The British Journal of Psychiatry 180: 475-477