Misplaced Pages

A mental disorder is an impairment of the mind disrupting normal thinking, feeling, mood, behavior, or social interactions, and accompanied by significant distress or dysfunction. The causes of mental disorders are very complex and vary depending on the particular disorder and the individual. Although the causes of most mental disorders are not fully understood, researchers have identified a variety of biological, psychological, and environmental factors that can contribute to the development or progression of mental disorders. Most mental disorders result in a combination of several different factors rather than just a single factor.

Research results

Risk factors for mental illness include psychological trauma, adverse childhood experiences, genetic predisposition, and personality traits. Correlations between mental disorders and substance use are also found to have a two way relationship, in that substance use can lead to the development of mental disorders and having mental disorders can lead to substance use/abuse. This effect is stronger and more reliable in some substance use than others, such as smoking.

Mental illnesses have risk factors, for instance including unequal parental treatment, adverse life events and drug use in depression, migration and discrimination, childhood trauma, loss or separation in families, and cannabis use in schizophrenia and psychosis, and parenting factors, child abuse, family history (e.g. of anxiety), and temperament and attitudes (e.g. pessimism) in anxiety. Many psychiatric disorders include problems with impulse and other emotional control.

In February 2013, a study found genetic links between five major psychiatric disorders: autism, ADHD, bipolar disorder, major depressive disorder, and schizophrenia. Abnormal functioning of neurotransmitter systems is also responsible for some mental disorders, including serotonin, norepinephrine, dopamine, and glutamate system's abnormal functioning. Differences have also been found in the size or activity of specific brain regions in some cases. Psychological mechanisms have also been implicated, such as cognitive (e.g. reasoning) biases, emotional influences, personality dynamics, temperament, and coping style. Studies have indicated that variation in genes can play an important role in the evolution of mental disorders, although the reliable identification of connections between specific genes and specific disorders has proven more difficult. Environmental events surrounding pregnancy (such as maternal hypertension, preeclampsia, or infection) and birth have also been implicated. Traumatic brain injury may increase the risk of developing certain mental disorders. Throughout the years, there have been inconsistent links found to certain viral infections, substance misuse, and general physical health that have been false.

Adverse experiences affect a person's mental health, including abuse, neglect, bullying, social stress, traumatic events, and other overwhelming life experiences. The specific risks and pathways to particular disorders are less clear, however. Aspects of the wider community have also been implicated, including employment problems, socioeconomic inequality, lack of social cohesion, problems linked to migration, and features of particular societies and cultures. Mental stress is a common cause of mental illnesses, so finding a coping solution to cope with mental stress would be beneficial. Many solutions that have helped reduce stress are yoga, exercise, and some medications that may help.

Theories

General theories

This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (October 2024) (Learn how and when to remove this message)

Several theories or models seek to explain the causes (etiology) of mental disorders. These theories may differ in regards to how they explain the cause of the disorder, how to treat the disorder, and how they classify mental disorders. Theories also differ about the philosophy of mind they accept; that is, whether the mind and brain are identical or not.

During most of the 20th century, mental illness was ascribable to problematic relationships between children and their parents. This view was held well into the late 1990s, in which people still believed this child-parent relationship was a large determinant of severe mental illness, such as depression and schizophrenia. In the 21st century, additional factors have been identified such as genetic contributions, though experience also plays a role. So, the perceived causes of mental illness have changed over time and will most likely continue to alter while more research develops throughout the years.

Outside the West, community approaches remain a focus.

A practical mixture of models will explain particular issues and disorders, although there may be difficulty defining boundaries for indistinct psychiatric syndromes.

Medical or biomedical model

An overall distinction is also commonly made between a "medical model" (also known as a biomedical or disease model) and 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, along with latter focusing on hypothesized social constructionism and social contexts.

Biological psychiatry has tended to follow a biomedical model focused on organic or "hardware" pathology of the brain, where many mental disorders are conceptualized as disorders of brain circuits shaped by a complex interplay of genetics and experience.

The social and medical models of mental disorders each work to identify and study distinct aspects, solutions, and potential therapies of disorders. The intersection and cross reference between the two models can further be used to develop more holistic models of mental disorders. Many criticisms historically of each model is the exclusivity of the other perspective. Therefore, intersectional research improved the impact and importance of future findings.

Biopsychosocial model

The primary model of contemporary mainstream Western psychiatry is the biopsychosocial model (BPS), which integrates biological, psychological, and social factors. The Biopsychosocial model was first conceptualised by George Engel in 1977, suggesting that to understand a person's medical condition it is not simply the biological factors to consider, but also the psychological and social factors . The biopsychosocial approach systematically considers biological, psychological, and social factors and their complex interactions in understanding health, illness, and health care delivery. Biological, psychological, and social factors exist along a continuum of natural systems. The factors within the model contain the following:

• Biological (physiological pathology)
• Psychological (thoughts emotions and behaviours such as psychological distress, fear/avoidance beliefs, current coping methods and attribution)
• Social (socio-economical, socio-environmental, and cultural factors such as work issues, family circumstances and benefits/economics)

This model is commonly used for case conceptualization of psychological disorders as well as chronic pain, with the view that the pain is a psychophysiological behavior pattern that cannot be categorised into biological, psychological, or social factors alone.

A related view, the diathesis-stress model, posits that mental disorders result from genetic dispositions and environmental stressors, combining to cause patterns of distress or dysfunction. The model is one way to explain why some individuals are more vulnerable to mental disorders than others. Additionally, it explains why some people may develop a mental disorder after exposure to stressful life events while others do not.

Psychoanalytic theories

Psychoanalytic theories focus on unresolved internal and relational conflicts. These theories have been predicated as explanations of mental disorders. Many psychoanalytic groups are said to adhere to the biopsychosocial model and to accept an eclectic mix of subtypes of psychoanalysis. Sigmund Freud developed the psychoanalytic theory. This theory focuses on the impact of unconscious forces on human behavior. According to Freud, a personality has three parts: the id, ego, and superego. The id operates under the pleasure principle, the ego operates under the reality principle, and the superego is the "conscience" and incorporates what is and is not socially acceptable into a person's value system. According to the psychoanalytic theory, there are five stages of psychosexual development that everyone goes through the oral stage, anal stage, phallic stage, latency stage, and genital stage. Mental disorders can be caused by an individual receiving too little or too much gratification in one of the psychosexual developmental stages. When this happens, the individual is said to be in that developmental stage.

Attachment theory

Attachment theory is a kind of evolutionary-psychological approach sometimes applied in the context of 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. According to this theory, a child's attachment is to a nurturing adult, the more likely that child will maintain healthy relationships with others in their life. As found by the Strange Situation experiment run by Mary Ainsworth based on the formulations of John Bowlby, there are four patterns of attachment: secure attachment, avoidant attachment, disorganized attachment, and ambivalent attachment. Later research found the fourth pattern of attachment is known as disorganized disoriented attachment. Secure attachments reflect trust in the child-caretaker relationship while insecure attachment reflects mistrust. The security of attachment in a child affects the child's emotional, cognitive, and social competence later in life.

Evolutionary psychology

Evolutionary psychology and evolutionary psychiatry posit that mental disorders involve the dysfunctional operation of mental modules adapted to ancestral physical or social environments but not necessarily to modern ones. Behavioral abnormalities that resemble human mental illness have been found in related species (great apes).

Other theories suggest that mental illness could have evolutionary advantages for the species, including enhancing creativity and stress to enhance survival by activating the flight-or-fight response in anticipation of danger.

Mania and depression could have benefited from seasonal changes by helping to increase energy levels during times of plenty and rejuvenating energy during times of scarcity. In this way, mania was set in motion during the spring and summer to facilitate energy for hunting; depression worked best during the winter, similar to how bears hibernate to recover their energy levels. This may explain the connection between circadian genes and Bipolar Disorder and explain the relationship between light and seasonal affective disorder.

Biological factors

Biological factors consist of anything physical that can cause adverse effects on a person's mental health. Biological factors include genetics, prenatal damage, infections, exposure to toxins, brain defects or injuries, and substance abuse. Many professionals believe that the cause of mental disorders is the biology of the brain and the nervous system.

Mind mentions genetic factors, long-term physical health conditions, and head injuries or epilepsy (affecting behavior and mood) as factors that may trigger an episode of mental illness.

Genetics

Some rare mental disorders are caused only by genetics such as Huntington's disease.

Family linkage and some twin studies have indicated that genetic factors often play a role in the heritability of mental disorders. The reliable identification of specific genetic variation can cause indication of higher risk to particular disorders, through linkage, Genome Wide Association Scores or association studies, has proven difficult. This is due to the complexity of interactions between genes, environmental events, and early development or the need for new research strategies. No specific gene results in a complex trait disorder, but specific variations of alleles result in higher risk for a trait. The heritability of behavioral traits associated with a mental disorder may be in permissive than in restrictive environments, and susceptibility genes probably work through both "within-the-skin" (physiological) pathways and "outside-the-skin" (behavioral and social) pathways. Investigations increasingly focus on links between genes and endophenotypes because they are more specific traits. Some include neurophysiological, biochemical, endocrinological, neuroanatomical, cognitive, or neuropsychological, rather than disease categories. Concerning a well-known mental disorder, schizophrenia, it is said with certainty that alleles (forms of genes) were responsible for this disorder. Some research has indicated only multiple, rare mutations are thought to alter neurodevelopmental pathways that can ultimately contribute to schizophrenia; virtually every rare structural mutation was different in each individual.

Research has shown that many conditions are polygenic meaning there are multiple defective genes rather than only one that is responsible for a disorder, and these genes may also be pleiotropic meaning that they cause multiple disorders, not just one. Schizophrenia and Alzheimer's are both examples of hereditary mental disorders. When exonic genes encode for proteins, these proteins do not just affect one trait. The pathways that contribute to complex traits and phenotypes interact with multiple systems, even though proteins have specific functions. brain plasticity (neuroplasticity) raises questions of whether some brain differences may be caused by mental illnesses or by pre-existing and then causing them.

Attention deficit hyperactivity disorder

In November 1999, Biological Psychiatry published a literature review by psychiatrists Joseph Biederman and Thomas Spencer found the average heritability estimate of ADHD from twin studies to be 0.8, while a subsequent family, twin, and adoption studies literature review published in Molecular Psychiatry in April 2019 by psychologists Stephen Faraone and Henrik Larsson that found an average heritability estimate of 0.74. Additionally, evolutionary psychiatrist Randolph M. Nesse has argued that the 5:1 male-to-female sex ratio in the epidemiology of ADHD suggests that ADHD may be the end of a continuum where males are overrepresented at the tails, citing clinical psychologist Simon Baron-Cohen's suggestion for the sex ratio in the epidemiology of autism as an analogue.

Natural selection has been acting against the genetic variants for ADHD over the course of at least 45,000 years, indicating that it was not an adaptive trait in ancient times. The disorder may remain at a stable rate by the balance of genetic mutations and removal rate (natural selection) across generations; over thousands of years, these genetic variants become more stable, decreasing disorder prevalence. Throughout human evolution, the EFs involved in ADHD likely provide the capacity to bind contingencies across time thereby directing behaviour toward future over immediate events so as to maximise future social consequences for humans.

ADHD has a high heritability of 74%, meaning that 74% of the presence of ADHD in the population is due to genetic factors. There are multiple gene variants which each slightly increase the likelihood of a person having ADHD; it is polygenic and thus arises through the accumulation of many genetic risks each having a very small effect. The siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder.

The association of maternal smoking observed in large population studies disappears after adjusting for family history of ADHD, which indicates that the association between maternal smoking during pregnancy and ADHD is due to familial or genetic factors that increase the risk for the confluence of smoking and ADHD.

ADHD presents with reduced size, functional connectivity and activation as well as low noradrenergic and dopaminergic functioning in brain regions and networks crucial for executive functioning and self-regulation. Typically, a number of genes are involved, many of which directly affect brain functioning and neurotransmission. Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH. Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF. A common variant of a gene called latrophilin 3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication. The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioural phenotypes, including ADHD symptoms reflecting split attention. The DRD4 gene is both linked to novelty seeking and ADHD. The genes GFOD1 and CDH13 show strong genetic associations with ADHD. CDH13's association with ASD, schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene. Another candidate causative gene that has been identified is ADGRL3. In zebrafish, knockout of this gene causes a loss of dopaminergic function in the ventral diencephalon and the fish display a hyperactive/impulsive phenotype.

Bipolar disorder

Behavioral genetic studies have suggested that many chromosomal regions and candidate genes are related to bipolar disorder susceptibility with each gene exerting a mild to moderate effect. The risk of bipolar disorder is nearly ten-fold higher in first-degree relatives of those with bipolar disorder than in the general population; similarly, the risk of major depressive disorder is three times higher in relatives of those with bipolar disorder than in the general population.

Although the first genetic linkage finding for mania was in 1969, linkage studies have been inconsistent. Findings point strongly to heterogeneity, with different genes implicated in different families. Robust and replicable genome-wide significant associations showed several common single-nucleotide polymorphisms (SNPs) are associated with bipolar disorder, including variants within the genes CACNA1C, ODZ4, and NCAN. The largest and most recent genome-wide association study failed to find any locus that exerts a large effect, reinforcing the idea that no single gene is responsible for bipolar disorder in most cases. Polymorphisms in BDNF, DRD4, DAO, and TPH1 have been frequently associated with bipolar disorder and were initially associated in a meta-analysis, but this association disappeared after correction for multiple testing. On the other hand, two polymorphisms in TPH2 were identified as being associated with bipolar disorder.

Due to the inconsistent findings in a genome-wide association study, multiple studies have undertaken the approach of analyzing SNPs in biological pathways. Signaling pathways traditionally associated with bipolar disorder that have been supported by these studies include corticotropin-releasing hormone signaling, cardiac β-adrenergic signaling, phospholipase C signaling, glutamate receptor signaling, cardiac hypertrophy signaling, Wnt signaling, Notch signaling, and endothelin 1 signaling. Of the 16 genes identified in these pathways, three were found to be dysregulated in the dorsolateral prefrontal cortex portion of the brain in post-mortem studies: CACNA1C, GNG2, and ITPR2.

Prenatal damage

Any damage that occurs to a fetus while still in its mother's womb is considered prenatal damage. Mental disorders can develop if the pregnant mother uses drugs or alcohol or is exposed to illnesses or infections during pregnancy. Environmental events surrounding pregnancy and birth have increased the development of mental illness in the offspring. Some events may include maternal exposure to stress or trauma, conditions of famine, obstetric birth complications, infections, and gestational exposure to alcohol or cocaine. These factors have been hypothesized to affect areas of neurodevelopment, general development, and restrict neuroplasticity.

Infection, disease and toxins

Infection

There have been some findings of links between infection by the parasite Toxoplasma gondii and schizophrenia.

AIDS has been linked to some mental disorders. Research shows that infections and exposure to toxins such as HIV and streptococcus cause dementia. This HIV infection that makes its way to the brain is called encephalopathy which spreads itself through the brain leading to dementia. The infections or toxins that trigger a change in the brain chemistry can develop into a mental disorder.

Depression and emotional liability may be also be caused by babesiosis.

There is some evidence that there may be a relationship between BoDV-1 infection and psychiatric disease.

The research on Lyme disease caused by a deer tick and toxins is expanding the link between bacterial infections and mental illness.

Disease

Depression, anxiety, mania, psychosis, vegetative symptoms, cognitive deficit and consciousness impairment may be caused by internal disease as well as endocrine and metabolic disorders, deficiency states and neurologic disorders.

Injury and brain defects

This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources in this section. Unsourced material may be challenged and removed. (October 2024) (Learn how and when to remove this message)

Any damage to the brain can cause a mental disorder. The brain is the control system for the nervous system and the rest of the body. Without it, the body cannot function properly.

Increased mood swings, insane behavior, and substance abuse disorders are traumatic brain injury (TBI) examples. Findings on the relationship between TBI severity and prevalence of subsequent psychiatric disorders have been inconsistent, and occurrence relates to prior mental health problems. Direct neurophysiological effects in a complex interaction with personality, attitude, and social influences.

Head trauma classifies as either open or closed head injury. In open head injury, the skull is punctured and the brain tissue is demolished. Closed head injury is more common, the skull is not punctured because there is an impact of the brain against the skull that creates permanent structural damage (subdural hematoma). With both types, symptoms may disappear or persist over time. Typically the longer the length of time spent unconscious and the length of post-traumatic amnesia the worse the prognosis for the individual. The cognitive residual symptoms of head trauma are associated with the type of injury (either an open head injury or closed head injury) and the amount of tissue destroyed. Closed injury head trauma symptoms include; Deficits in abstract reasoning ability, judgment, memory, and marked personality changes. Open injury head trauma symptoms tend to be the experience of classic neuropsychological syndromes like aphasia, visual-spatial disorders, and types of memory or perceptual disorders.

Brain tumors are classified as either malignant and benign, and as intrinsic (directly infiltrate the parenchyma of the brain) or extrinsic (grows on the external surface of the brain and produces symptoms as a result of pressure on the brain tissue). Progressive cognitive changes associated with brain tumors may include confusion, poor comprehension, and even dementia. Symptoms tend to depend on the location of the tumor in the brain. For example, tumors on the frontal lobe tend to be associated with the sign of impairment of judgment, apathy, and loss of the ability to regulate/modulate behavior.

Findings have indicated abnormal functioning of brainstem structures in individuals with mental disorders such as schizophrenia, and other disorders that have to do with impairments in maintaining sustained attention. Some abnormalities in the average size or shape of some regions of the brain have been found in some disorders, reflecting genes and experiences. 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 medication use or substance use. Some studies have also found reduced hippocampal volumes in major depression, possibly worsening with time depression.

Neurotransmitter systems

Abnormal levels of dopamine activity correspond with several disorders (reduced in ADHD and OCD, and increased in schizophrenia). The dysfunction in serotonin and other monoamine neurotransmitters (norepinephrine and dopamine) correspond with certain mental disorders and their associated neural networks. Some include major depression, obsessive-compulsive disorder, phobias, post-traumatic stress disorder, and generalized anxiety disorder. Studies of depleted levels of monoamine neurotransmitters show an association with depression and other psychiatric disorders, but "... it should be questioned whether 5-HT represents just one of the final and not the main, factors in the neurological chain of events underlying psychopathological symptoms...."

Simplistic "chemical imbalance" explanations for mental disorders have never received empirical support; and most prominent psychiatrists, neuroscientists, and psychologists have not espoused such ill-defined, facile etiological theories. Instead, neurotransmitter systems have been understood in the context of the diathesis-stress or biopsychosocial models. The following 1967 quote from renowned psychiatric and neuroscience researchers exemplifies this more sophisticated understanding (in contrast to the woolly "chemical imbalance" notion).

Whereas specific genetic factors may be of importance in the etiology of some, and possibly all, depressions, it is equally conceivable that early experiences of the infant or child may cause enduring biochemical changes, that may predispose some individuals to depressions in adulthood. It is not likely that changes in the metabolism of the biogenic amines alone will account for the complex phenomena of normal or pathological affect.

Substance abuse

This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (October 2024) (Learn how and when to remove this message)

Substance abuse, especially long-term abuse, can cause or exacerbate many mental disorders. Alcoholism is linked to depression while abuse of amphetamines and LSD can leave a person feeling paranoid and anxious.

Correlations of mental disorders with drug use include cannabis, alcohol, and caffeine. At more than 300 mg, caffeine may cause anxiety or worsen anxiety disorders. Illicit drugs can stimulate particular parts of the brain that can affect development in adolescence. Cannabis has also been found to worsen depression and lessen an individual's motivation. Alcohol has the potential to damage "white matter" in the brain that affects thinking and memory. Alcohol is a problem in many countries due to many people participating in excessive drinking or binge drinking.

Environmental factors

The term "environment" is very loosely defined in the context of mental illnesses. Unlike biological and psychological causes, environmental causes denote a wide range of stressors that individuals experience in everyday life. They are more psychologically than biologically based. Events that evoke feelings of loss are the most likely to cause a mental disorder to develop in an individual.

Environmental factors include but are not limited to dysfunctional home life, poor interpersonal relationships, substance abuse, not meeting social expectations, low self-esteem, and poverty. The British charity organisation Mind lists childhood abuse, trauma, violence, neglect, social isolation, discrimination, grief, stress, homelessness, social disadvantage, debt, unemployment, caring for a family member or friend, and significant trauma as an adult (such as war, an accident, or being the victim of a violent crime) as possible triggers of an episode of mental illness.

Repeating generational patterns, behaviors that are passed down through different familial generations, are also a risk factor for mental illness, especially in children.

Life events and emotional stress

Mistreatment in childhood or adulthood (including sexual-, physical-, and emotional abuse, domestic violence, and bullying) has been linked to the onset of mental disorders through an interaction of societal, familial, psychological, and biological factors. More generally, negative or stressful life events have been implicated in the development of a range of disorders, including mood and anxiety disorders.

The main risks appear to be from the accumulation of such experiences over time, although a single major trauma can sometimes lead to disorders, especially post-traumatic stress disorder. Resilience to such experiences varies; a person may be resistant to some stressors but not to others. The psychological resilience of an individual can be affected by genetics, temperamental characteristics, cognitive flexibility, coping strategies, and previous experiences. For example, in the case of bipolar disorder, stress is not a specific cause but does place genetically and biologically vulnerable people at risk for more severe forms of the illness.

Adverse childhood experiences

The Adverse Childhood Experiences Study has shown a strong dose–response relationship between adverse childhood experiences or ACEs (such as physical and/or emotional neglect, abuse, poverty, malnutrition, and traumatic experiences) and numerous health, social, and behavioral problems including suicide attempts and the frequency of depressive episodes. Several such experiences can cause toxic stress.

ACEs may affect the structural and functional development of the brain and lead to abnormalities, and chronic trauma can disrupt immune responses and cause lasting dysregulated inflammatory response. A child's neurological development can be disrupted when chronically exposed to stressful events, and his/her cognitive functioning and/or ability to cope with negative emotions can diminish. Over time, the child may adopt various harmful coping strategies that contribute to later mental and physical problems. Findings have been mixed, but some studies suggest that cognitive deficit is more related to neglect than other forms of adversity.

Poor parenting is a risk factor for depression and anxiety. Separation, grief in families, and other forms childhood trauma are risk factors for schizophrenia. Children are more susceptible to psychological harm from traumatic events than adults, but their reaction does vary by individual child, age, the type of event, and the length of exposure.

Neglect is a form of mistreatment in which the responsible caretakers fail to provide the necessary age-appropriate care, supervision, and protection. It is different from abuse in that it is, in this context, not intentional in causing harms. The long-term effects of neglect can be reduced physical, emotional, and mental health throughout the victim's life.

Familial and close relationships

Parental divorce, death, absence, or the lack of stability appears to increase the risk of mental disorders in a child. Early social privation, and the lack of "ongoing, harmonious, secure, committed" relationships have been implicated in the development of mental illnesses. Continuous conflict with friends, one's support system, and family can all increase the risk of developing a mental illness or can worsen one's mental health.

Divorce is a factor that affects adults as well as children. Divorcees may have emotional adjustment problems due to a loss of intimacy and social connections; however, new statistics show that the negative effects of divorce have been overstated.

Social expectations and self-esteem

Having both too low or too high self-esteem can be detrimental to an individual's mental health. Low self-esteem in particular can result in aggression, self-deprecating behavior, anxiety, and other mental disorders. Being perceived as someone who does not "fit in" can result in bullying and other types of emotional abuse, which can lead to the victim experiencing depression, anger, and loneliness.

Poverty

Studies show that there is a direct correlation between poverty and mental illness: the lower the socioeconomic status of an individual, the higher the risk of mental illness. Impoverished people in England, defined as those who live in the lowest 20% income bracket, are two to three times more likely to develop mental illness than those of a higher economic class. This increased risk remains consistent for all poor individuals regardless of any in-group demographic differences, as all disadvantaged families experience economic stressors such as unemployment or lack of housing. A lower or more insecure educational, occupational, economic, or social position is generally linked to more mental disorders. Children from these backgrounds may have low levels of self-efficiency and self-worth. Studies have also shown a strong relationship between poverty and substance abuse, another risk factor in the onset of mental disorders.

Problems in one's community or culture including poverty, unemployment or underemployment, a lack of social cohesion, and migration have been associated with the development of mental disorders. Personal resources, community factors, and interactions between individual and regional-level income levels have been implicated. Socioeconomic deprivation in neighborhoods can cause worsen mental health, even after accounting for genetic factors. According to a 2009 meta-analysis by Paul and Moser, countries with high income inequality and poor unemployment protections have worse mental health outcomes among the unemployed.

The effects of different socioeconomic factors varies by country. Minority ethnic groups, including first or second-generation immigrants, are at a greater risk of developing mental disorders. This has been attributed to the insecurities in their lives and their disadvantages, including racism. There have been alternate models, such as the drift hypothesis to account for the complex relationship between an individual's social status and mental health.

Psychological and individual factors, including resilience

Some clinicians believe that psychological characteristics alone determine mental disorders. Others speculate that abnormal behavior can be explained by a mix of social and psychological factors. In many examples, environmental and psychological triggers complement one another resulting in emotional stress, which in turn activates a mental illness. Each person is unique in how they will react to psychological stressors. What may break one person may have little to no effect on another. Psychological stressors, which can trigger mental illness, are as follows: emotional, physical, or sexual abuse, loss of a significant loved one, neglect, and being unable to relate to others.

The inability to relate to others is also known as emotional detachment. Emotional detachment makes it difficult for an individual to empathize with others or to share their feelings. These individuals tend to stress the importance of their independence and tend to struggle relating to others. An emotionally detached person may try to rationalize or apply logic to a situation to which there is no logical explanation. Often, the inability to relate to others stems from a traumatic event.

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; or an individual's overall personality, temperament, or coping style or the extent of protective factors or "positive illusions" such as optimism, personal control and a sense of meaning.

See also

• Air pollution
• Correlates of crime
• Diseases of poverty
• Social medicine
• Winner and loser culture

References

1. "Mental, behavioural or neurodevelopmental disorders". International Classification of Diseases for Mortality and Morbidity Statistics, 11th rev. (ICD-11 MMS). World Health Organization. April 2019. Retrieved 2019-10-30. Mental, behavioural and neurodevelopmental disorders are syndromes characterized by clinically significant disturbance in an individual's cognition, emotional regulation, or behaviour that reflects a dysfunction in the psychological, biological, or developmental processes that underlie mental and behavioural functioning. These disturbances are usually associated with distress or impairment in personal, family, social, educational, occupational, or other important areas of functioning.
2. Webster's Third New International Dictionary, (Springfield, MA: Merriam-Webster, 1961, rev. 2016), ("mental illness noun, variants: or mental disorder or less commonly mental disease, Definition of mental illness: any of a broad range of medical conditions (such as major depression, schizophrenia, obsessive compulsive disorder, or panic disorder) that are marked primarily by sufficient disorganization of personality, mind, or emotions to impair normal psychological functioning and cause marked distress or disability and that are typically associated with a disruption in typical thinking, feeling, mood, behavior, interpersonal interactions, or daily functioning").
3. American Heritage Dictionary of the English Language, 5th ed. (Boston: Houghton Mifflin Harcourt, 2011, rev. 2018), ("mental disorder, n. - Any of various disorders, such as schizophrenia, bipolar disorder, or autism spectrum disorder, characterized by a distressing or disabling impairment of an individual's cognitive, emotional, or social functioning.")
4. Oxford English Dictionary, 3rd ed. (Oxford, UK: Oxford University Press, September 2001), ("II. Senses relating to the mind in an unhealthy or abnormal state. 5. a. Designating a temporary or permanent impairment of the mind due to inherited defect, injury, illness, or environment, usually needing special care or rehabilitation. Esp. in mental breakdown, mental deficiency, mental disease, mental disorder, mental incapacity, mental retardation, etc.; see also mental illness n. at Compounds. ... mental illness n. a condition which causes serious abnormality in a person's thinking or behaviour, esp. one requiring special care or treatment; a psychiatric illness. Now somewhat dated, and sometimes avoided as being potentially offensive.").
5. Arango C, Díaz-Caneja CM, McGorry PD, Rapoport J, Sommer IE, Vorstman JA, et al. (July 2018). "Preventive strategies for mental health". The Lancet. Psychiatry. 5 (7): 591–604. doi:10.1016/S2215-0366(18)30057-9. hdl:11370/92f1a79c-f53d-47ae-be92-7a4c8d4b4e25. PMID 29773478. S2CID 21703364.
6. Clark LA, Cuthbert B, Lewis-Fernández R, Narrow WE, Reed GM (September 2017). "Three Approaches to Understanding and Classifying Mental Disorder: ICD-11, DSM-5, and the National Institute of Mental Health's Research Domain Criteria (RDoC)". Psychological Science in the Public Interest. 18 (2): 72–145. doi:10.1177/1529100617727266. PMID 29211974. S2CID 206743519. ... research has shown that psychopathology generally arises from multiple biological, behavioral, psychosocial, and cultural factors, all interacting in complex ways and filtered through an individual's lifetime of experience. Research also has shown that the outcomes of these factors and their interactions are not clearly definable, distinct diseases, but are instead complex and variable combinations of psychological problems.
7. Read, John; Bentall, Richard P. (February 2012). "Negative childhood experiences and mental health: theoretical, clinical and primary prevention implications". British Journal of Psychiatry. 200 (2): 89–91. doi:10.1192/bjp.bp.111.096727. ISSN 0007-1250. PMID 22297585.
8. Kurbatfinski, Stefan; Dosani, Aliyah; Dewey, Deborah M.; Letourneau, Nicole (2024-09-12). "Proposed Physiological Mechanisms Underlying the Association between Adverse Childhood Experiences and Mental Health Conditions: A Narrative Review". Children. 11 (9): 1112. doi:10.3390/children11091112. ISSN 2227-9067. PMC 11430311. PMID 39334644.
9. Treur, Jorien L.; Munafò, Marcus R.; Logtenberg, Emma; Wiers, Reinout W.; Verweij, Karin J. H. (July 2021). "Using Mendelian randomization analysis to better understand the relationship between mental health and substance use: a systematic review". Psychological Medicine. 51 (10): 1593–1624. doi:10.1017/S003329172100180X. ISSN 0033-2917. PMC 8327626. PMID 34030749.
10. Gatt JM, Burton KL, Williams LM, Schofield PR (January 2015). "Specific and common genes implicated across major mental disorders: a review of meta-analysis studies". Journal of Psychiatric Research. 60: 1–13. doi:10.1016/j.jpsychires.2014.09.014. PMID 25287955.
11. Lahti-Pulkkinen M, Girchenko P, Tuovinen S, Sammallahti S, Reynolds RM, Lahti J, et al. (June 2020). "Maternal Hypertensive Pregnancy Disorders and Mental Disorders in Children". Hypertension. 75 (6). Ovid Technologies (Wolters Kluwer Health): 1429–1438. doi:10.1161/hypertensionaha.119.14140. hdl:20.500.11820/02b77370-a4e8-4dbe-bbcf-879222a3420b. PMID 32306771. S2CID 216028720.
12. Rice F, Harold GT, Boivin J, van den Bree M, Hay DF, Thapar A (February 2010). "The links between prenatal stress and offspring development and psychopathology: disentangling environmental and inherited influences". Psychological Medicine. 40 (2): 335–345. doi:10.1017/S0033291709005911. PMC 2830085. PMID 19476689. S2CID 13752317.
13. ^ Bhugra D, Becker MA (February 2005). "Migration, cultural bereavement and cultural identity". World Psychiatry. 4 (1): 18–24. PMC 1414713. PMID 16633496.
14. ^ Ghaemi SN (November 2006). "Paradigms of psychiatry: eclecticism and its discontents". Current Opinion in Psychiatry. 19 (6): 619–624. doi:10.1097/01.yco.0000245751.98749.52. PMID 17012942. S2CID 22068456.
15. Insel TR, Wang PS (May 2010). "Rethinking mental illness". JAMA. 303 (19): 1970–1971. doi:10.1001/jama.2010.555. PMID 20483974. S2CID 8210144.
16. Hogan A. J. (2019). Social and medical models of disability and mental health: evolution and renewal. CMAJ: Canadian Medical Association journal, 191(1), E16–E18. https://doi.org/10.1503/cmaj.181008
17. Engel GL (April 1977). "The need for a new medical model: a challenge for biomedicine". Science. 196 (4286): 129–136. Bibcode:1977Sci...196..129E. doi:10.1126/science.847460. PMID 847460.
18. Miaskowski C, Blyth F, Nicosia F, Haan M, Keefe F, Smith A, Ritchie C (September 2020). "A Biopsychosocial Model of Chronic Pain for Older Adults". Pain Medicine. 21 (9): 1793–1805. doi:10.1093/pm/pnz329. PMID 31846035.
19. Murthy RS, et al. (2002) . The World Health Report 2001: Mental Health, New Understanding, New Hope (Reprint ed.). Geneva: World Health Organization. ISBN 9789241562010.
20. Nyongesa A (2018-09-23). Tintinnabulation of Literary Theory: Traversing Genres to Contemporary Experience. Mwanaka Media and Publishing. doi:10.2307/j.ctvh9vxtv.8. ISBN 978-1-77906-514-8. JSTOR j.ctvh9vxtv. S2CID 239252932.
21. Saygin D, Tabib T, Bittar HE, Valenzi E, Sembrat J, Chan SY, et al. (2005). "Transcriptional profiling of lung cell populations in idiopathic pulmonary arterial hypertension". Pulmonary Circulation. 10 (1): 54–77. doi:10.1111/j.1527-2001.2005.tb00373.x. PMC 7052475. PMID 32166015. S2CID 143641177.
22. Keller H (November 2018). "Universality claim of attachment theory: Children's socioemotional development across cultures". Proceedings of the National Academy of Sciences of the United States of America. 115 (45): 11414–11419. Bibcode:2018PNAS..11511414K. doi:10.1073/pnas.1720325115. PMC 6233114. PMID 30397121.
23. ^ Waters E, Hamilton CE, Weinfield NS (2000). "The stability of attachment security from infancy to adolescence and early adulthood: general introduction". Child Development. 71 (3): 678–683. doi:10.1111/1467-8624.00175. JSTOR 1132385. PMID 10953933.
24. Fearon RP, Bakermans-Kranenburg MJ, van Ijzendoorn MH, Lapsley AM, Roisman GI (2010). "The significance of insecure attachment and disorganization in the development of children's externalizing behavior: a meta-analytic study" (PDF). Child Development. 81 (2): 435–456. doi:10.1111/j.1467-8624.2009.01405.x. JSTOR 40598991. PMID 20438450.
25. Nettle, Daniel; Clegg, Helen (2006-03-07). "Schizotypy, creativity and mating success in humans". Proceedings of the Royal Society B: Biological Sciences. 273 (1586): 611–615. doi:10.1098/rspb.2005.3349. ISSN 0962-8452. PMC 1560060. PMID 16537133.
26. Rantala, Markus J.; Luoto, Severi; Krams, Indrikis; Karlsson, Hasse (2018-03-01). "Depression subtyping based on evolutionary psychiatry: Proximate mechanisms and ultimate functions". Brain, Behavior, and Immunity. 69: 603–617. doi:10.1016/j.bbi.2017.10.012. ISSN 0889-1591. PMID 29051086. S2CID 3975281.
27. https://www.genome.gov/genetics-glossary/Genome-Wide-Association-Studies Genome-wide association studies (GWAS). Genome.gov. (n.d.). Retrieved August 8, 2022
28. Lu H, Qiao J, Shao Z, Wang T, Huang S, Zeng P (December 2021). "A comprehensive gene-centric pleiotropic association analysis for 14 psychiatric disorders with GWAS summary statistics". BMC Medicine. 19 (1): 314. doi:10.1186/s12916-021-02186-z. PMC 8667366. PMID 34895209.
29. Lynch M. (2005). Simple evolutionary pathways to complex proteins. Protein science: a publication of the Protein Society, 14(9), 2217–2227. https://doi.org/10.1110/ps.041171805
30. Biederman J, Spencer T (November 1999). "Attention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder". Biological Psychiatry. 46 (9). Elsevier: 1234–1242. doi:10.1016/S0006-3223(99)00192-4. PMID 10560028. S2CID 45497168.
31. Faraone SV, Larsson H (April 2019). "Genetics of attention deficit hyperactivity disorder". Molecular Psychiatry. 24 (4). Nature Research: 562–575. doi:10.1038/s41380-018-0070-0. PMC 6477889. PMID 29892054.
32. Baron-Cohen S (June 2002). "The extreme male brain theory of autism". Trends in Cognitive Sciences. 6 (6). Elsevier: 248–254. doi:10.1016/S1364-6613(02)01904-6. PMID 12039606. S2CID 8098723. Archived from the original on 3 July 2013. Retrieved 9 July 2020.
33. Nesse RM (2005). "32. Evolutionary Psychology and Mental Health". In Buss DM (ed.). The Handbook of Evolutionary Psychology (1st ed.). Hoboken, NJ: Wiley. p. 918. ISBN 978-0-471-26403-3.
34. Nesse RM (2016) . "43. Evolutionary Psychology and Mental Health". In Buss DM (ed.). The Handbook of Evolutionary Psychology, Volume 2: Integrations (2nd ed.). Hoboken, NJ: Wiley. p. 1019. ISBN 978-1-118-75580-8.
35. Esteller-Cucala P, Maceda I, Børglum AD, Demontis D, Faraone SV, Cormand B, Lao O (May 2020). "Genomic analysis of the natural history of attention-deficit/hyperactivity disorder using Neanderthal and ancient Homo sapiens samples". Scientific Reports. 10 (1): 8622. Bibcode:2020NatSR..10.8622E. doi:10.1038/s41598-020-65322-4. PMC 7248073. PMID 32451437.
36. Keller MC (December 2008). "The evolutionary persistence of genes that increase mental disorders risk". Current Directions in Psychological Science. 17 (6): 395–399. doi:10.1111/j.1467-8721.2008.006 (inactive 1 November 2024).{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
37. Barkley RA (2004). "Attention-deficit/hyperactivity disorder and self-regulation: Taking an evolutionary perspective on executive functioning.". In Baumeister RF, Vohs KD (eds.). Handbook of self-regulation: Research, theory, and applications. The Guilford Press. pp. 301–323.
38. ^ Faraone SV, Banaschewski T, Coghill D, Zheng Y, Biederman J, Bellgrove MA, Newcorn JH, Gignac M, Al Saud NM, Manor I, Rohde LA, Yang L, Cortese S, Almagor D, Stein MA, Albatti TH, Aljoudi HF, Alqahtani MM, Asherson P, Atwoli L, Bölte S, Buitelaar JK, Crunelle CL, Daley D, Dalsgaard S, Döpfner M, Espinet S, Fitzgerald M, Franke B, Gerlach M, Haavik J, Hartman CA, Hartung CM, Hinshaw SP, Hoekstra PJ, Hollis C, Kollins SH, Sandra Kooij JJ, Kuntsi J, Larsson H, Li T, Liu J, Merzon E, Mattingly G, Mattos P, McCarthy S, Mikami AY, Molina BS, Nigg JT, Purper-Ouakil D, Omigbodun OO, Polanczyk GV, Pollak Y, Poulton AS, Rajkumar RP, Reding A, Reif A, Rubia K, Rucklidge J, Romanos M, Ramos-Quiroga JA, Schellekens A, Scheres A, Schoeman R, Schweitzer JB, Shah H, Solanto MV, Sonuga-Barke E, Soutullo C, Steinhausen HC, Swanson JM, Thapar A, Tripp G, van de Glind G, van den Brink W, Van der Oord S, Venter A, Vitiello B, Walitza S, Wang Y (September 2021). "The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder". Neuroscience and Biobehavioral Reviews. 128. Elsevier BV: 789–818. doi:10.1016/j.neubiorev.2021.01.022. ISSN 0149-7634. PMC 8328933. PMID 33549739.
39. Faraone SV, Larsson H (April 2019). "Genetics of attention deficit hyperactivity disorder". Molecular Psychiatry. 24 (4). Springer Science and Business Media LLC: 562–575. doi:10.1038/s41380-018-0070-0. PMC 6477889. PMID 29892054.
40. Nolen-Hoeksema S (2013). Abnormal Psychology (6th ed.). McGraw-Hill Education. p. 267. ISBN 978-0-07-803538-8.
41. Skoglund C, Chen Q, D'Onofrio BM, Lichtenstein P, Larsson H (January 2014). "Familial confounding of the association between maternal smoking during pregnancy and ADHD in offspring". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 55 (1): 61–68. doi:10.1111/jcpp.12124. PMC 4217138. PMID 25359172.
42. Obel C, Zhu JL, Olsen J, Breining S, Li J, Grønborg TK, Gissler M, Rutter M (April 2016). "The risk of attention deficit hyperactivity disorder in children exposed to maternal smoking during pregnancy - a re-examination using a sibling design". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 57 (4): 532–537. doi:10.1111/jcpp.12478. PMID 26511313.
43. Biederman J (June 2005). "Attention-deficit/hyperactivity disorder: a selective overview". Biological Psychiatry. 57 (11): 1215–1220. doi:10.1016/j.biopsych.2004.10.020. PMID 15949990.
44. Hinshaw SP (May 2018). "Attention Deficit Hyperactivity Disorder (ADHD): Controversy, Developmental Mechanisms, and Multiple Levels of Analysis". Annual Review of Clinical Psychology. 14 (1): 291–316. doi:10.1146/annurev-clinpsy-050817-084917. PMID 29220204.
45. Barkley RA (2011). "Attention-deficit/hyperactivity disorder, self-regulation, and executive functioning.". In Vohs KD, Baumeister RF (eds.). Handbook of self-regulation: Research, theory, and applications (2nd ed.). The Guilford Press. pp. 551–563.
46. Antshel KM, Hier BO, Barkley RA (2014). "Executive Functioning Theory and ADHD". In Goldstein S, Naglieri JA (eds.). Handbook of Executive Functioning. New York, NY: Springer. pp. 107–120. doi:10.1007/978-1-4614-8106-5_7. ISBN 978-1-4614-8106-5.
47. Kebir O, Joober R (December 2011). "Neuropsychological endophenotypes in attention-deficit/hyperactivity disorder: a review of genetic association studies". European Archives of Psychiatry and Clinical Neuroscience. 261 (8): 583–594. doi:10.1007/s00406-011-0207-5. PMID 21409419. S2CID 21383749.
48. Berry MD (January 2007). "The potential of trace amines and their receptors for treating neurological and psychiatric diseases". Reviews on Recent Clinical Trials. 2 (1): 3–19. CiteSeerX 10.1.1.329.563. doi:10.2174/157488707779318107. PMID 18473983. Although there is little direct evidence, changes in trace amines, in particular PE, have been identified as a possible factor for the onset of attention deficit/hyperactivity disorder (ADHD). ... Further, amphetamines, which have clinical utility in ADHD, are good ligands at trace amine receptors. Of possible relevance in this aspect is modafanil, which has shown beneficial effects in ADHD patients and has been reported to enhance the activity of PE at TAAR1. Conversely, methylphenidate, ...showed poor efficacy at the TAAR1 receptor. In this respect it is worth noting that the enhancement of functioning at TAAR1 seen with modafanil was not a result of a direct interaction with TAAR1.
49. Sotnikova TD, Caron MG, Gainetdinov RR (August 2009). "Trace amine-associated receptors as emerging therapeutic targets". Molecular Pharmacology. 76 (2): 229–235. doi:10.1124/mol.109.055970. PMC 2713119. PMID 19389919.
50. Gizer IR, Ficks C, Waldman ID (July 2009). "Candidate gene studies of ADHD: a meta-analytic review". Human Genetics. 126 (1): 51–90. doi:10.1007/s00439-009-0694-x. PMID 19506906. S2CID 166017.
51. Arcos-Burgos M, Muenke M (November 2010). "Toward a better understanding of ADHD: LPHN3 gene variants and the susceptibility to develop ADHD". Attention Deficit and Hyperactivity Disorders. 2 (3): 139–147. doi:10.1007/s12402-010-0030-2. PMC 3280610. PMID 21432600.
52. Nikolaidis A, Gray JR (June 2010). "ADHD and the DRD4 exon III 7-repeat polymorphism: an international meta-analysis". Social Cognitive and Affective Neuroscience. 5 (2–3): 188–193. doi:10.1093/scan/nsp049. PMC 2894686. PMID 20019071.
53. ^ Grimm O, Kranz TM, Reif A (February 2020). "Genetics of ADHD: What Should the Clinician Know?". Current Psychiatry Reports. 22 (4): 18. doi:10.1007/s11920-020-1141-x. PMC 7046577. PMID 32108282.
54. ^ Zayats T, Neale BM (12 February 2020). "Recent advances in understanding of attention deficit hyperactivity disorder (ADHD): how genetics are shaping our conceptualization of this disorder". F1000Research. 8: 2060. doi:10.12688/f1000research.18959.2. PMC 6896240. PMID 31824658.
55. ^ Kerner B (February 2014). "Genetics of bipolar disorder". Appl Clin Genet. 7: 33–42. doi:10.2147/tacg.s39297. PMC 3966627. PMID 24683306.
56. ^ Barnett JH, Smoller JW (November 2009). "The genetics of bipolar disorder". Neuroscience. 164 (1): 331–343. doi:10.1016/j.neuroscience.2009.03.080. PMC 3637882. PMID 19358880.
57. Reich T, Clayton PJ, Winokur G (April 1969). "Family history studies: V. The genetics of mania". The American Journal of Psychiatry. 125 (10): 1358–1369. doi:10.1176/ajp.125.10.1358. PMID 5304735. S2CID 33268.
58. Segurado R, Detera-Wadleigh SD, Levinson DF, Lewis CM, Gill M, Nurnberger JI, et al. (2003). "Genome Scan Meta-Analysis of Schizophrenia and Bipolar Disorder, Part III: Bipolar Disorder". The American Journal of Human Genetics. 73 (1): 49–62. doi:10.1086/376547. PMC 1180589. PMID 12802785.
59. ^ Craddock N, Sklar P (May 2013). "Genetics of bipolar disorder". Lancet. 381 (9878): 1654–1662. doi:10.1016/S0140-6736(13)60855-7. PMID 23663951. S2CID 9502929.
60. Seifuddin F, Mahon PB, Judy J, Pirooznia M, Jancic D, Taylor J, Goes FS, Potash JB, Zandi PP (July 2012). "Meta-analysis of genetic association studies on bipolar disorder". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 159B (5): 508–518. doi:10.1002/ajmg.b.32057. PMC 3582382. PMID 22573399.
61. Gao J, Jia M, Qiao D, Qiu H, Sokolove J, Zhang J, Pan Z (March 2016). "TPH2 gene polymorphisms and bipolar disorder: A meta-analysis". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 171B (2): 145–152. doi:10.1002/ajmg.b.32381. PMID 26365518. S2CID 9467242.
62. Torkamani A, Topol EJ, Schork NJ (November 2008). "Pathway analysis of seven common diseases assessed by genome-wide association". Genomics. 92 (5): 265–272. doi:10.1016/j.ygeno.2008.07.011. PMC 2602835. PMID 18722519.
63. Pedroso I, Lourdusamy A, Rietschel M, Nöthen MM, Cichon S, McGuffin P, Al-Chalabi A, Barnes MR, Breen G (August 2012). "Common genetic variants and gene-expression changes associated with bipolar disorder are over-represented in brain signaling pathway genes". Biological Psychiatry. 72 (4): 311–317. doi:10.1016/j.biopsych.2011.12.031. PMID 22502986. S2CID 30065607.
64. Nurnberger JI, Koller DL, Jung J, Edenberg HJ, Foroud T, Guella I, Vawter MP, Kelsoe JR (June 2014). "Identification of pathways for bipolar disorder: a meta-analysis". JAMA Psychiatry. 71 (6): 657–664. doi:10.1001/jamapsychiatry.2014.176. PMC 4523227. PMID 24718920.
65. Raza MU, Tufan T, Wang Y, Hill C, Zhu MY (August 2016). "DNA Damage in Major Psychiatric Diseases". Neurotox Res. 30 (2): 251–267. doi:10.1007/s12640-016-9621-9. PMC 4947450. PMID 27126805.
66. Contopoulos-Ioannidis DG, Gianniki M, Ai-Nhi Truong A, Montoya JG (2022). "Toxoplasmosis and Schizophrenia: A Systematic Review and Meta-Analysis of Prevalence and Associations and Future Directions". Psychiatric Research and Clinical Practice. 4 (2). American Psychiatric Association Publishing: 48–60. doi:10.1176/appi.prcp.20210041. PMC 9558922. PMID 36254187. S2CID 248354624.
67. ^ "HIV and Dementia". www.hopkinsmedicine.org. Baltimore MD: The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System. 2021-08-08. Archived from the original on 2020-08-03. Retrieved 2022-05-04.
68. Ebert S, Goos M, Rollwagen L, Baake D, Zech WD, Esselmann H, et al. (April 2010). "Recurrent systemic infections with Streptococcus pneumoniae do not aggravate the course of experimental neurodegenerative diseases". Journal of Neuroscience Research. 88 (5): 1124–1136. doi:10.1002/jnr.22270. PMID 19859962. S2CID 35148634.
69. "Lyme Disease and Mental Health". 17 August 2018.
70. A, Testa; R, Giannuzzi; S, Daini; L, Bernardini; L, Petrongolo; N, Gentiloni Silveri (February 2013). "Psychiatric emergencies (part III): psychiatric symptoms resulting from organic diseases". European Review for Medical and Pharmacological Sciences. 17 (Suppl 1). Eur Rev Med Pharmacol Sci: 86–99. ISSN 1128-3602. PMID 23436670. Retrieved 2023-08-11.
71. "Brain Death - Brain, Spinal Cord, and Nerve Disorders". MSD Manual Consumer Version. Retrieved 2023-03-24.
72. Schmidt CW (August 2007). "Environmental connections: a deeper look into mental illness". Environmental Health Perspectives. 115 (8): A404, A406–A404, A410. doi:10.1289/ehp.115-a404. PMC 1940091. PMID 17687431.
73. "What causes mental health problems?". mind.org.uk. October 2017.
74. Landstedt, Evelina; Almquist, Ylva B. (December 2019). "Intergenerational patterns of mental health problems: the role of childhood peer status position". BMC Psychiatry. 19 (1): 286. doi:10.1186/s12888-019-2278-1. ISSN 1471-244X. PMC 6749655. PMID 31533680.
75. Phillips, Anna C.; Carroll, Douglas; Der, Geoff (2015-07-04). "Negative life events and symptoms of depression and anxiety: stress causation and/or stress generation". Anxiety, Stress, & Coping. 28 (4): 357–371. doi:10.1080/10615806.2015.1005078. ISSN 1061-5806. PMC 4772121. PMID 25572915.
76. Hassanzadeh, Akbar; Heidari, Zahra; Feizi, Awat; Hassanzadeh Keshteli, Ammar; Roohafza, Hamidreza; Afshar, Hamid; Adibi, Payman (2017). "Association of Stressful Life Events with Psychological Problems: A Large-Scale Community-Based Study Using Grouped Outcomes Latent Factor Regression with Latent Predictors". Computational and Mathematical Methods in Medicine. 2017: 1–12. doi:10.1155/2017/3457103. ISSN 1748-670X. PMC 5625761. PMID 29312459.
77. Vella, Shae-LeighCynthia; Pai, NageshB (2019). "A theoretical review of psychological resilience: Defining resilience and resilience research over the decades". Archives of Medicine and Health Sciences. 7 (2): 233. doi:10.4103/amhs.amhs_119_19. ISSN 2321-4848. S2CID 209406511.
78. Anderson, Ian M.; Haddad, Peter M.; Scott, Jan (2012-12-27). "Bipolar disorder". BMJ. 345: e8508. doi:10.1136/bmj.e8508. ISSN 1756-1833. PMID 23271744. S2CID 22156246.
79. Kerner, Berit (February 2014). "Genetics of bipolar disorder". The Application of Clinical Genetics. 7: 33–42. doi:10.2147/TACG.S39297. ISSN 1178-704X. PMC 3966627. PMID 24683306.
80. Felitti, Vincent J; Anda, Robert F; Nordenberg, Dale; Williamson, David F; Spitz, Alison M; Edwards, Valerie; Koss, Mary P; Marks, James S (May 1998). "Relationship of Childhood Abuse and Household Dysfunction to Many of the Leading Causes of Death in Adults". American Journal of Preventive Medicine. 14 (4): 245–258. doi:10.1016/S0749-3797(98)00017-8. PMID 9635069. S2CID 26055600.
81. Bucci, Monica; Marques, Sara Silvério; Oh, Debora; Harris, Nadine Burke (August 2016). "Toxic Stress in Children and Adolescents". Advances in Pediatrics. 63 (1): 403–428. doi:10.1016/j.yapd.2016.04.002. ISSN 0065-3101. PMID 27426909. S2CID 37342598.
82. Crick, Daisy C.P.; Halligan, Sarah L.; Howe, Laura D.; Lacey, Rebecca E.; Khandaker, Golam M.; Burgner, David; Herbert, Annie; Suderman, Matthew; Anderson, Emma L.; Fraser, Abigail (February 2022). "Associations between Adverse Childhood Experiences and the novel inflammatory marker glycoprotein acetyls in two generations of the Avon Longitudinal Study of Parents and Children birth cohort". Brain, Behavior, and Immunity. 100: 112–120. doi:10.1016/j.bbi.2021.11.001. PMC 8791601. PMID 34793940.
83. Morgan, Cyleen A.; Chang, Yun-Hsuan; Choy, Olivia; Tsai, Meng-Che; Hsieh, Shulan (2021-12-31). "Adverse Childhood Experiences Are Associated with Reduced Psychological Resilience in Youth: A Systematic Review and Meta-Analysis". Children. 9 (1): 27. doi:10.3390/children9010027. ISSN 2227-9067. PMC 8773896. PMID 35053652.
84. Sheffler, Julia L.; Piazza, Jennifer R.; Quinn, Jamie M.; Sachs-Ericsson, Natalie J.; Stanley, Ian H. (2019-09-03). "Adverse childhood experiences and coping strategies: identifying pathways to resiliency in adulthood". Anxiety, Stress, & Coping. 32 (5): 594–609. doi:10.1080/10615806.2019.1638699. ISSN 1061-5806. PMC 6824267. PMID 31288568.
85. Gould, Felicia; Clarke, Jennifer; Heim, Christine; Harvey, Philip D.; Majer, Matthias; Nemeroff, Charles B. (April 2012). "The effects of child abuse and neglect on cognitive functioning in adulthood". Journal of Psychiatric Research. 46 (4): 500–506. doi:10.1016/j.jpsychires.2012.01.005. PMC 3307950. PMID 22336639.
86. Berthelot, Nicolas; Paccalet, Thomas; Gilbert, Elsa; Moreau, Isabel; Mérette, Chantal; Gingras, Nathalie; Rouleau, Nancie; Maziade, Michel (September 2015). "Childhood abuse and neglect may induce deficits in cognitive precursors of psychosis in high-risk children". Journal of Psychiatry and Neuroscience. 40 (5): 336–343. doi:10.1503/jpn.140211. ISSN 1180-4882. PMC 4543096. PMID 26035064.
87. Popovic, David; Schmitt, Andrea; Kaurani, Lalit; Senner, Fanny; Papiol, Sergi; Malchow, Berend; Fischer, Andre; Schulze, Thomas G.; Koutsouleris, Nikolaos; Falkai, Peter (2019-03-21). "Childhood Trauma in Schizophrenia: Current Findings and Research Perspectives". Frontiers in Neuroscience. 13: 274. doi:10.3389/fnins.2019.00274. ISSN 1662-453X. PMC 6448042. PMID 30983960.
88. Peterson, Sarah (2018-02-01). "Effects". The National Child Traumatic Stress Network. Retrieved 2023-07-02.
89. Gonzalez, Dulce; Bethencourt Mirabal, Arian; McCall, Janelle D. (2023), "Child Abuse and Neglect", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 29083602, retrieved 2023-07-02
90. Petersen, Anne C.; Joseph, Joshua; Feit, Monica (2014-03-25), "Consequences of Child Abuse and Neglect", New Directions in Child Abuse and Neglect Research, National Academies Press (US), retrieved 2023-07-02
91. Horwath, Jan (2007), "Living with Child Neglect: The Impact on Children", Child Neglect: Identification and Assessment, London: Macmillan Education UK, pp. 41–68, doi:10.1007/978-0-230-20982-4_3 (inactive 1 November 2024), ISBN 978-1-4039-3346-1, retrieved 2023-07-02{{citation}}: CS1 maint: DOI inactive as of November 2024 (link)
92. Tashjian S, Mullins J (May 16, 2018). "Parenting Styles and Child Behavior". Psychology in Action. Archived from the original on October 17, 2018.
93. "Relationships". Mental Health America. Retrieved 8 August 2022.
94. Marquis P (October 1992). "Family dysfunction as a risk factor in the development of antisocial behavior". Psychological Reports. 71 (2): 468–470. doi:10.2466/pr0.1992.71.2.468. PMID 1410104. S2CID 8826585.
95. Sander S, Strizzi JM, Øverup CS, Cipric A, Hald GM (2020-11-30). "When Love Hurts - Mental and Physical Health Among Recently Divorced Danes". Frontiers in Psychology. 11: 578083. doi:10.3389/fpsyg.2020.578083. PMC 7734469. PMID 33329227.
96. Simpson, J.; Hillman, R.; Crawford, T.; Overton, P. G. (2010-12-01). "Self-esteem and self-disgust both mediate the relationship between dysfunctional cognitions and depressive symptoms". Motivation and Emotion. 34 (4): 399–406. doi:10.1007/s11031-010-9189-2. ISSN 1573-6644. S2CID 145371730.
97. Baumeister, Roy F.; Smart, Laura; Boden, Joseph M. (1996). "Relation of threatened egotism to violence and aggression: The dark side of high self-esteem". Psychological Review. 103 (1): 5–33. doi:10.1037/0033-295X.103.1.5. ISSN 1939-1471. PMID 8650299.
98. Sowislo, Julia Friederike; Orth, Ulrich (January 2013). "Does low self-esteem predict depression and anxiety? A meta-analysis of longitudinal studies". Psychological Bulletin. 139 (1): 213–240. doi:10.1037/a0028931. ISSN 1939-1455. PMID 22730921.
99. Hoover, John H.; Oliver, Ronald L.; Thomson, Keith A. (December 1993). "Perceived Victimization by School Bullies: New Research and Future Direction". The Journal of Humanistic Education and Development. 32 (2): 76–84. doi:10.1002/j.2164-4683.1993.tb00133.x.
100. Nansel, Tonja R.; Overpeck, Mary; Pilla, Ramani S.; Ruan, W. June; Simons-Morton, Bruce; Scheidt, Peter (2001-04-25). "Bullying Behaviors Among US Youth: Prevalence and Association With Psychosocial Adjustment". JAMA. 285 (16): 2094–2100. doi:10.1001/jama.285.16.2094. ISSN 0098-7484. PMC 2435211. PMID 11311098.
101. Rivara, Frederick; Menestrel, Suzanne Le; Prevention, Committee on the Biological and Psychosocial Effects of Peer Victimization: Lessons for Bullying; Board on Children, Youth; Justice, Committee on Law and; Education, Division of Behavioral and Social Sciences and; Division, Health and Medicine; National Academies of Sciences, Engineering (2016-09-14), "Consequences of Bullying Behavior", Preventing Bullying Through Science, Policy, and Practice, National Academies Press (US), retrieved 2023-07-02
102. Marmot MG. Fair Society Healthy Lives : The Marmot Review ; Strategic Review of Health Inequalities in England Post-2010. London: Marmot Review; 2010.
103. Perry, Melissa J. (1996-09-01). "The relationship between social class and mental disorder". Journal of Primary Prevention. 17 (1): 17–30. doi:10.1007/BF02262736. ISSN 1573-6547. PMID 24254919. S2CID 144679736.
104. Doi, Satomi; Fujiwara, Takeo; Isumi, Aya; Ochi, Manami (2019). "Pathway of the Association Between Child Poverty and Low Self-Esteem: Results From a Population-Based Study of Adolescents in Japan". Frontiers in Psychology. 10: 937. doi:10.3389/fpsyg.2019.00937. ISSN 1664-1078. PMC 6511812. PMID 31133920.
105. Manhica, Hélio; Straatmann, Viviane S.; Lundin, Andreas; Agardh, Emilie; Danielsson, Anna-Karin (July 2021). "Association between poverty exposure during childhood and adolescence, and drug use disorders and drug-related crimes later in life". Addiction. 116 (7): 1747–1756. doi:10.1111/add.15336. ISSN 0965-2140. PMC 8247994. PMID 33197093.
106. Breedvelt, Josefien J. F.; Tiemeier, Henning; Sharples, Evelyn; Galea, Sandro; Niedzwiedz, Claire; Elliott, Iris; Bockting, Claudi L. (July 2022). "The effects of neighbourhood social cohesion on preventing depression and anxiety among adolescents and young adults: rapid review". BJPsych Open. 8 (4): e97. doi:10.1192/bjo.2022.57. ISSN 2056-4724. PMC 9230698. PMID 35642359.
107. Sareen, Jitender; Afifi, Tracie O.; McMillan, Katherine A.; Asmundson, Gordon J. G. (2011-04-01). "Relationship Between Household Income and Mental Disorders: Findings From a Population-Based Longitudinal Study". Archives of General Psychiatry. 68 (4): 419–427. doi:10.1001/archgenpsychiatry.2011.15. ISSN 0003-990X. PMID 21464366. S2CID 39076836.
108. Raphael, Eva; White, Justin S.; Li, Xinjun; Cederin, Klas; Glymour, M. Maria; Sundquist, Kristina; Sundquist, Jan; Hamad, Rita (May 2020). "Neighborhood Deprivation and Mental Health Among Immigrants to Sweden". Epidemiology. 31 (3): e25–e27. doi:10.1097/EDE.0000000000001160. ISSN 1044-3983. PMC 7138696. PMID 31977591.
109. "The toll of job loss". www.apa.org. Retrieved 2023-11-26.
110. Currie, Janet; Stabile, Mark (2003-11-01). "Socioeconomic Status and Child Health: Why Is the Relationship Stronger for Older Children?". American Economic Review. 93 (5): 1813–1823. doi:10.1257/000282803322655563. ISSN 0002-8282. PMID 29058847.
111. Cameron, Lisa; Williams, Jenny (2009-05-01). "Is the relationship between socioeconomic status and health stronger for older children in developing countries?". Demography. 46 (2): 303–324. doi:10.1353/dem.0.0054. ISSN 0070-3370. PMC 2831276. PMID 21305395.
112. Kirmayer, L. J.; Narasiah, L.; Munoz, M.; Rashid, M.; Ryder, A. G.; Guzder, J.; Hassan, G.; Rousseau, C.; Pottie, K.; for the Canadian Collaboration for Immigrant and Refugee Health (CCIRH) (2011-09-06). "Common mental health problems in immigrants and refugees: general approach in primary care". Canadian Medical Association Journal. 183 (12): E959–E967. doi:10.1503/cmaj.090292. ISSN 0820-3946. PMC 3168672. PMID 20603342.
113. Fox, John W. (December 1990). "Social Class, Mental Illness, and Social Mobility: The Social Selection-Drift Hypothesis for Serious Mental Illness". Journal of Health and Social Behavior. 31 (4): 344–353. doi:10.2307/2136818. ISSN 0022-1465. JSTOR 2136818. PMID 2135936.
114. Schneiderman N, Ironson G, Siegel SD (2005). "Stress and health: psychological, behavioral, and biological determinants". Annual Review of Clinical Psychology. 1: 607–628. doi:10.1146/annurev.clinpsy.1.102803.144141. PMC 2568977. PMID 17716101.

• Causes of mental disorders
• Biology of bipolar disorder
• Cause (medicine)
• Biology of attention deficit hyperactivity disorder
• Biology of obsessive–compulsive disorder