Mental Disability across the Life Span
June 30, 2008 – 7:29 pmBy LeVonder Brinkley
Summary and Abstract
An estimated 26.2 % of Americans suffer from a diagnosable mental disorder in a given year. Approximately 30% of adults and 17% of the children and adolescents in the United States display serious emotional psychological disturbance. The field of behavioral genetics studies the effects of genetics on behavior and psychological characteristics. This paper examines research that supports the author’s contention that the etiology of most mental disabilities is genetically influenced. The author researches forms of psychopathology of various disabilities and their etiology that supports her contention. Disabilities examined occur across the developmental stages of the life span. The author seeks to answer the question, “Nature or nurture?” Findings reveal that nature predisposes and nurture determines manifestation and severity of the disability.
Introduction
The author chose to research mental disability as it occurs throughout life stages because of the prevalence of mental illness in her family, and her life’s dedication to the vocation of mental health. The author’s great-grandfather suffered depression and committed suicide; grandfather endured depression and developed an addiction to alcohol; mother endured depression and developed dementia; the author (great-granddaughter) has a diagnosis of situational depression, and her children have been diagnosed with depression. This generational history spans more than 120 years and five generations. The author precludes that a causal factor for depression and other mental disabilities is genetics.
The author received certification as a cross-categorical special education teacher and taught children with various mental and developmental disabilities. She specialized in teaching children with autistic disorder; and worked as the primary therapist and case manager with persons dually diagnosed with mental illness and developmental disabilities. Society stigmatizes individuals who carry a mental disability label. The author supported the students and clients in their right for self -direction of their lives.
A mental illness is any disease or condition affecting the brain that influences the way one thinks, feels, behaves and/or relates to others and to the environment. A person with an untreated mental illness often is unable to cope with life’s daily routines and demands.
It is estimated that of 100 adults: 13 have a significant anxiety disorder, six suffer from serious depression, five display a personality disorder involving maladaptive tendencies that cause distress or impaired functioning, one is schizophrenic, one suffers from Alzheimer’s disease, and 10 abuse drugs or alcohol (Chiu, Demler, Kessler & Walters, 2005). This data suggests that psychological and behavioral disorders are a major problem in our society. Individuals with mental illness are a part of the norm due to its prevalence.
This paper discusses the disorders that significantly affect a given life stage. Those examined are: anxiety, cognitive, communication, disruptive behavior, eating, mood and psychosis. It gives a general description of several of the most prevalent mental disabilities; organizes the disabilities by onset as it relates to stages of development over the life span; and examines research that discusses causal factors for each disability. The author attempts to answer the question, “nature or nurture?” The field of behavioral genetics revealed surprising answers.
Mental Disability across the Life Span
Prenatal/ infancy/ toddlerhood (conception to three years)
Psychosis
Schizophrenia. Schizophrenia is categorized as psychosis. A chronic neurological disorder, it affects 1% of the general population. The onset of behavioral characteristics occurs in early adulthood around age 25. The author chose to discuss in the prenatal stage of development due to studies indicating etiology. Epidemiological studies indicate that viral infections during the second trimester of gestation increase the likelihood that the offspring will go on to develop schizophrenia in adulthood (Wolff & Bilkey, 2008).
It appears likely that multiple genes are involved in creating a predisposition to develop the disorder. In addition, factors such as prenatal difficulties like intrauterine starvation or viral infections, perinatal complications, and various nonspecific stressors, seem to influence the development of schizophrenia. However, it is not yet understood how the genetic predisposition is transmitted, and it cannot yet be accurately predicted whether a given person will or will not develop the disorder (Wolff & Bilkey, 2008).
Several regions of the human genome were investigated to identify genes that may confer susceptibility for schizophrenia. The strongest evidence to date leads to chromosomes 13 and 6 but remains unconfirmed. Identification of specific genes involved in the development of schizophrenia will provide important clues into what goes wrong in the brain to produce and sustain the illness and will guide the development of new and better treatments. Neurotransmitters, substances that allow communication between nerve cells, have long been thought to be involved in the development of schizophrenia. It is likely, although not yet certain, that the disorder is associated with some imbalance of the complex, interrelated chemical systems of the brain, perhaps involving the neurotransmitters dopamine and glutamate ( Wolff & Bilkey, 2008) .
Many studies of people with schizophrenia have found abnormalities in brain structure, enlargement of the fluid-filled cavities, called the ventricles, in the interior of the brain, and decreased size of certain brain regions for example, or function, decreased metabolic activity in certain brain regions. These abnormalities are quite subtle and are not characteristic of all people with schizophrenia, nor do they occur only in individuals with this illness (Wolff & Bilkey, 2008).
Microscopic studies of brain tissue after death have also shown small changes in distribution or number of brain cells in people with schizophrenia. It showed that many of these changes are present before an individual becomes ill, and schizophrenia may be, in part, a disorder in development of the brain. Developmental neurobiologists funded by the National Institute of Mental Health (NIMH) have found that schizophrenia may be a developmental disorder resulting when neurons form inappropriate connections during fetal development. These errors may lie dormant until puberty, when changes in the brain that occur normally during this critical stage of maturation interact adversely with the faulty connections (Wolff & Bilkey, 2008).
This research has spurred efforts to identify prenatal factors that may have some bearing on the apparent developmental abnormality. In other studies, investigators using brain-imaging techniques have found evidence of early biochemical changes that may precede the onset of disease symptoms, prompting examination of the neural circuits that are most likely to be involved in producing those symptoms. Meanwhile, scientists working at the molecular level are exploring the genetic basis for abnormalities in brain development and in the neurotransmitter systems regulating brain function (Wolff & Bilkey, 2008).
Wolff and Bilkey (2008) hypothesized that an increase in proinflammatory cytokines in response to infection alters fetal neurodevelopment in a way that increases vulnerability to the disease. They used an animal model to induce maternal immune activation (MIA) during mid gestation. Offspring of the animals showed normal behavior as juveniles and behavioral features of schizophrenia in adulthood.
Communication
Autism. Autism is a developmental disorder characterized by impairments in language and social interaction and by excessively repetitive and ritualistic behaviors. Onset is before the age of three, and though severity of symptoms may change over time, they typically persist in some form throughout life. A recent study reported the prevalence of autism in 3-10 year-olds to be about 3.4 cases per 1000 children. Autism is part of a group of disorders called autism spectrum disorders (ASDs), also known as pervasive developmental disorders. ASDs range in severity, with autism being the most debilitating form while other disorders, such as Asperger syndrome, produce milder symptoms (Boyle, Doernberg, Karapurkar, Murphy, Rice & Yeargin-Allsopp, 2003).
Estimating the prevalence of Autism is difficult and controversial due to differences in the ways cases are identified and defined, differences in study methods, and changes in diagnostic criteria. Autism is about four times more common in boys than girls. Girls with the disorder, however, tend to have more severe symptoms and greater cognitive impairment. (Boyle et al, 2003).
Abraham and Geshwind (2008) examined autism for genetic linkage, genotyping 350 markers in 75 autism affected sibling pair families. They found strengthened evidence for linkage of autism to chromosomes 1q, 13p, 16q, and Xq, and diminished evidence for linkage to 7q and 13q. Family and twin studies suggest that autism arises from interactions of multiple genetic variants, and that different combinations of variants may be causative in different groups of people. This study suggests genetics as a causal factor for Autism disorder.
Preschool/Middle childhood (3-12 years)
Disruptive Behaviors Disorder
Attention Deficit Hyperactivity Disorder. Attention Deficit Hyperactivity Disorder (ADHD) is one of the most common mental disorders in children and adolescents. ADHD usually becomes evident in preschool or early elementary years. The median age of onset of ADHD is seven years, although the disorder can persist into adolescence and occasionally into adulthood. It is hard for these children to control their behavior and/or pay attention. It is estimated that between 3 and 5 percent of children have ADHD, or approximately 2 million children in the United States. This means that in a classroom of 25 to 30 children, it is likely that at least one will have ADHD (Chiu et al, 2005).
The principal characteristics of ADHD are inattention, hyperactivity, and impulsivity. These symptoms appear early in a child’s life. Because many normal children may have these symptoms, but at a low level, or the symptoms may be caused by another disorder, it is important that the child receive a thorough examination and appropriate diagnosis by a well-qualified professional. A child who “can’t sit still” or is otherwise disruptive will be noticeable in school, but the inattentive daydreamer may be overlooked. The impulsive child who acts before thinking may be considered a “discipline problem,” while the passive child may be viewed as unmotivated. Yet both may have attention deficit disorders (Chiu et al, 2005).
Hay, Martin, and Piek (2006) researched the role that genes play in the susceptibility to ADHD. Family, twin, and adoption studies provide compelling evidence that genes play a strong role in one’s susceptibility to ADHD. Many gene studies of ADHD have produced evidence implicating several genes in the etiology of the disorder. These studies are also consistent with the idea that the genetic vulnerability to ADHD is mediated by many genes of small effects. Results of Behavioral genetic and molecular genetic studies have converged to suggest that both genetic and nongenetic factors contribute to the development of attention deficit hyperactivity disorder.
McGiffen, Plomin, Riley (2001) say ADHD is among the most recognized genetic-based disorders in psychiatry. In their studies families, they found that relatives of ADHD children are at high risk for ADHD, comorbid psychiatric disorders, school failure, learning disability, and impairments in intellectual functioning. In later life stages, ADHD may comorbid with depression, bipolar, and substance use.
Additional lines of evidence from twin, adoption, and segregation analysis studies suggest that the familial aggregation of ADHD has a substantial genetic component. Their results suggest that the heritability of ADHD ranges from 0.88 to 1.0, suggesting a substantial role for genetic factors in its etiology (Hay et al, 2006).
Adolescence/young adulthood (12-20 years)
Eating disorders.
Eating Disorders are also a type of mental illness. Females are much more likely than males to develop an eating disorder. Only an estimated 5-15% of people with anorexia or bulimia and an estimated 35% of those with binge-eating disorder are male. The three main types of eating disorders are anorexia nervosa (AN), bulimia nervosa, and binge-eating disorder (BED). In their lifetime, an estimated 0.5 to 3.7% of females suffer from anorexia, and an estimated 1.1 to 4.2% suffers from bulimia. Individuals with ED have a complex of puzzling symptoms, for which there has been no neurobiological explanation (Walter, 2008).
BED. Community surveys have estimated that between 2 percent and 5 percent of Americans experience binge-eating disorder in a 6-month period. A family history study design (Lilenarchian, Ringham, Kalarchian & Marcus, 2008) was used to examine patterns of comorbidity and family psychopathology in women with and without BED and to assess whether any other forms of psychopathology may share a common etiology with BED. Elevated lifetime rates of major depressive disorder, dysthymic disorder, any depressive disorder, social phobia, and any anxiety disorder were found among women with BED compared with control women without BED.
Upon examination of psychopathology among first-degree relatives based upon reports by study participants serving as informants. Lienarchian et al found elevated lifetime rates of mood disorders (bipolar disorder, any depressive disorder), nearly all anxiety disorders (social phobia, specific phobia, obsessive-compulsive disorder, panic disorder, agoraphobia, any anxiety disorder), and eating disorders (any eating disorder) among the relatives of women with BED compared with the relatives of control women. All disorders that occurred at elevated rates in relatives followed a pattern of independent transmission from BED. The elevated lifetime rates of BED and any eating disorder reported among the first-degree relatives of women with BED compared with the first-degree relatives of women without BED are in accord with findings from other researchers.
Berry, Bulik, Crow & Hudson (2006) in a similar study of obese individuals, found that BED aggregated strongly in families, independent of obesity. The findings of these studies suggest that BED is familial. Although biological and other factors may be related, genetics may be a causal factor for BED.
Anorexia and Bulimia Nervosa. Anorexia nervosa (AN) and bulimia nervosa (BN) are related disorders of unknown etiology that most commonly begin during adolescence in women. The mortality rate among people with anorexia estimated at 0.56 % per year, or approximately 5.6 % per decade, which is about 12 times higher than the annual death rate due to all causes of death among females ages 15-24 in the general population (US Census, 2005).
AN and BN have unique and puzzling symptoms, such as restricted eating or binge-purge behaviors, body image distortions, denial of emaciation (extreme loss of flesh), and resistance to treatment. These are often chronic and relapsing disorders. AN has the highest death rate of any psychiatric disorder. The lack of understanding of the pathogenesis of this illness has hindered the development of effective interventions, particularly for AN (Walter, 2008).
Symptoms are frequently chronic and often disabling conditions that are characterized by
aberrant patterns of feeding behavior and weight regulation, and deviant attitudes and perceptions toward body weight and shape. AN, fear of weight gain and unrelenting obsession with fatness, even in the face of increasing cachexia (loss of weight, muscle, and appetite), accounts for extreme medical and psychological morbidity, and standardized mortality rates exceeding those of all other psychiatric disorders. BN usually emerges after a period of food restriction, which may or may not have been associated with weight loss. Binge eating is followed by either self-induced vomiting, or by some other means of compensation for the excess of food ingested (Walter, 2008).
Walter (2008) reviewed findings in brain chemistry and neuroimaging that shed new light on understanding the psychopathology of these disorders. The relationship of insular disturbance and interoceptive awareness in individuals with AN was examined. The insular is thought to play an important role in processing interoceptive information, which can be defined as the sense of the physiological condition of the entire body.
Aside from taste, interoceptive information includes sensations such as temperature, touch, muscular sensations, and hunger. The role of the insular is focused on how stimuli might affect the body state. Interoception is critical for self-awareness because it provides the link between cognitive and affective processes and the current body state. Many of the symptoms commonly found in AN, such as distorted body image, lack of recognition of the symptoms of malnutrition, could be related to disturbed interoceptive awareness. In support of this possibility, only the controls showed positive relationship between self-ratings of pleasantness and the intensity of the signal for sugar in the insular (Walter, 2008).
In addition, studies have consistently found that AN and BN individuals have elevated pain thresholds and is potentially a marker of altered interoceptive awareness. Those with AN fail to accurately recognize and incorporate affective and social stimuli in the environment. Individuals with AN have enhanced ability to pay attention to detail or use a logical/analytic approach, but exhibit worse performance with global strategies (Walter, 2008).
Brain imaging studies show that disturbances of 5-HT function occur when people are ill, and persist after recovery from AN and BN. It is possible that a trait related disturbance of 5-HT neuronal modulation predates the onset of AN and contributes to premorbid symptoms of anxiety, obsessions, and inhibition. This dysphoric temperament may involve dysregulation of emotional and reward pathways, which also mediate aspects of feeding, thus making these individuals vulnerable to disturbed appetitive behaviors (Walter, 2008).
In the treatment of AN, restricting food intake may become powerfully reinforcing because it provides a temporary respite from dysphoric mood. Several factors may act on these vulnerabilities to cause AN to start in adolescence. First, puberty-related female gonadal steroids ( age-related changes) may exacerbate 5-HT dysregulation. Second, stress and/or cultural and societal pressures may contribute by increasing anxious and obsessional temperament. Individuals with AN may discover that reduced
dietary intake, by reducing plasma tryptophan availability, is a means by which they can modulate brain 5-HT functional activity and anxious mood. People with AN enter a vicious cycle which accounts for the chronicity of this disorder because caloric restriction results in a brief respite from dysphoric mood. However, malnutrition and weight loss, in turn, produce alterations in many neuropeptides and monoamine function, perhaps in the service of conserving energy, but which also exaggerates dysphoric mood (Walter, 2008).
Anxiety Disorders
The etiology of child and adolescent anxiety may be of a biological and/or learned nature. Indeed, researchers propose that anxiety arises from a complex interaction of specific characteristics related to the child (e.g., biological, psychological, and genetic factors) and his or her environment (e.g., conditioning, observational learning, family relations, traumatic events (Stickle & Weems, 2005).
Within a biological model of etiology, researchers have investigated genetic influences as well as neurobiological structures and circuits. A recent meta-analysis of the genetic epidemiology of anxiety disorders demonstrated that PD, phobias, OCD, and GAD aggregate in families and concluded that genetic factors have a moderate influence on the
development of anxiety disorders. Research suggests that genetic factors may help us understand why certain individuals exposed to similar experiences have different responses and outcomes concerning the development of pathological anxiety (Stickle & Weems, 2005).
Research aimed at identifying specific brain areas and circuits underlying anxiety disorders has provided support for neurobiological influences in anxiety. The most support for neuroanatomical influences has come from research investigating the amygdala’s role in fear conditioning. Research in this area has implicated the amygdala in the pathophysiology of anxiety disorders (Rauch, Shin, & Wright, 2003).
Neurochemical factors have also been implicated in the development of anxiety symptoms. Abnormal function of serotonin, norepinephrine, dopamine, and γ-aminobutyric acid systems as well as abnormal chemoreceptor reactivity have all been implicated in anxiety ( Rauch et al, 2003).
Obsessive-Compulsive Disorder. Obsessive-Compulsive Disorder, also known as, OCD, is another type of anxiety disorder. Approximately 2.2 million American adults, 18 and older, have OCD (Chiu, 2005). The first symptoms of OCD often begin during childhood or adolescence, however, the median age of onset is 19.5. Obsessive-Compulsive Disorder (OCD) is an anxiety disorder where a person has recurrent and unwanted ideas or impulses (called obsessions) and an urge or compulsion to do something to relieve the discomfort caused by the obsession.
The obsessive thoughts range from the idea of losing control, to themes surrounding religion or keeping things or parts of one’s body clean all the time. Repetitive behaviors such as hand washing, counting, checking, or cleaning are often performed with the hope of preventing obsessive thoughts or making them go away. Performing these so-called “rituals,” however, provides only temporary relief, and not performing them markedly increases anxiety. They may be obsessed with germs or dirt, and wash their hands repeatedly. They may be filled with doubt and feel the need to check things repeatedly (Chiu et al, 2005).
Compulsions are behaviors that help reduce the anxiety surrounding the obsessions. Most people (90%) who have OCD have both obsessions and compulsions. The thoughts and behaviors a person with OCD has are senseless, repetitive, distressing, and sometimes harmful, but they are also difficult to overcome. OCD is more common than schizophrenia, bipolar disorder, or panic disorder. Yet, it is still commonly overlooked by mental health professionals, mental health advocacy groups, and people who themselves have the problem. Many people still carry the misperception that they somehow caused themselves to have these compulsive behaviors and obsessive thoughts. (National Institute of Mental Health (NIMH), 2001).
OCD is likely the cause of a number of intertwined and complex factors which include genetics, biology, personality development, and how a person learns to react to the environment around them. What scientists today do know is that it is not a sign of a character flaw or a personal weakness. OCD is a serious mental disorder, which is more treatable than ever. Without the appropriate treatment, it affects a person’s ability to function in everyday activities, one’s work, one’s family, and one’s social life (NIMH, 2001).
Other compulsive behaviors include counting (often while performing another compulsive action such as hand washing), repeating, hoarding, and endlessly rearranging objects in an effort to keep them in precise alignment with each other. Cognitive problems, such as mentally repeating phrases, list making, or checking, are also common (NIMH, 2001).
An epidemiological study of OCD (Reiger, Robins, 1991) revealed that 84% of youth diagnosed with OCD had comorbid disorders, including major depression (62%), social phobia (38%), alcohol dependence (24%), and dysthymia, (22%), The most common comorbid diagnoses include other anxiety disorders and depressive disorders. Additionally, children with anxiety disorders frequently experience other psychiatric conditions, including attention-deficit/hyperactivity disorder and disruptive disorders. etiology of child and adolescent anxiety may be of a biological and/or learned nature.
Researchers (Stickle and Weems, 2005) have investigated genetic influences as well as neurobiological structures and circuits. A recent meta-analysis of the genetic epidemiology of anxiety disorders demonstrated that PD, phobias, OCD, and GAD aggregate in families and concluded that genetic factors have a moderate influence on the development of anxiety disorders. Researchers have suggested that, although clearly not the only contributing influences, genetic factors may help us understand why certain individuals exposed to similar experiences have different responses and outcomes concerning the development of pathological anxiety.
Young adulthood/middle adulthood (20-65 years)
Anxiety disorders
Post traumatic stress disorder. Post-Traumatic Stress Disorder (PTSD) is an anxiety disorder that affects approximately 3.6% of U.S. adults aged 18 to 54 (5.2 million people) each year. An estimated 7.8 percent of Americans will experience PTSD at some point in their lives, with women (10.4%) twice as likely as men (5%) to develop PTSD (Chui et al, 2005).
Posttraumatic Stress Disorder, or PTSD, is a psychiatric disorder that can occur following the experience or witnessing of life-threatening events such as military combat, natural disasters, terrorist incidents, serious accidents, or violent personal assaults like rape. Fairbank, Hough, Jordan, Kulka, Marmar, Schlemager & Weiss ( 2005) report that the traumatic events most often associated with PTSD for men are rape, combat exposure, childhood neglect, and childhood physical abuse. The most traumatic events for women are rape, sexual molestation, physical attack, being threatened with a weapon, and childhood physical abuse. PTSD can develop at any age. It can develop in childhood but research shows that the median age of onset is 23 years of age.
About 30% of Vietnam veterans experience PTSD at some point after the war. This disorder also frequently occurs after violent personal assaults such as rape, mugging, or domestic violence; terrorism; natural or human-caused disasters; and accidents. Most survivors of trauma return to normal given a little time. However, some people will have stress reactions that do not go away on their own, or may even get worse over time. These individuals may develop PTSD. People who suffer from PTSD often relive the experience through nightmares and flashbacks, have difficulty sleeping, and feel detached or estranged, and these symptoms can be severe enough and last long enough to significantly impair the person’s daily life (Fairbank et al, 2005).
PTSD is marked by clear biological changes as well as psychological symptoms. PTSD is complicated by the fact that it frequently occurs in conjunction with related disorders such as depression, substance abuse, problems of memory and cognition, and other problems of physical and mental health. The disorder is also associated with impairment of the person’s ability to function in social or family life, including occupational instability, marital problems and divorces, family discord, and difficulties in parenting (Fairbank et al, 2005).
About 30 percent of the men and women who have spent time in war zones experience PTSD. An additional 20 to 25 percent have had partial PTSD at some point in their lives. More than half of all male Vietnam veterans and almost half of all female Vietnam veterans have experienced “clinically serious stress reaction symptoms. PTSD has also been detected among veterans of the Gulf War, with some estimates running as high as 8 percent. Careful research and documentation of PTSD began in earnest after the Vietnam War. The National Vietnam Veterans Readjustment Study estimated in 1988 that the prevalence of PTSD in that group was 15.2% at that time and that 30% had experienced the disorder at some point since returning from Vietnam (Fairbank et al, 2005).
PTSD has subsequently been observed in all veteran populations that have been studied, including World War II, Korean conflict, and Persian Gulf populations, and in United Nations peacekeeping forces deployed to other war zones around the world. There are substantially similar findings of PTSD in military veterans in other countries. PTSD is not only a problem for veterans, however. Although there are unique cultural- and gender-based aspects of the disorder, it occurs in men and women, adults and children, Western and non-Western cultural groups, and all socioeconomic strata. A national study of American civilians conducted in 1995 estimated that the lifetime prevalence of PTSD was 5% in men and 10% in women. A revision of this study done in 2005, reports that PTSD occurs in about 8% of all Americans (Fairbank et al, 2005).
PTSD is associated with a number of distinctive neurobiological and physiological changes. PTSD may be associated with stable neurobiological alterations in both the central and autonomic nervous systems, such as altered brainwave activity, decreased volume of the hippocampus, and abnormal activation of the amygdala. Both the hippocampus and the amygdala are involved in the processing and integration of memory. The amygdala has also been found to be involved in coordinating the body’s fear response. Psycho-physiological alterations associated with PTSD include hyper-arousal of the sympathetic nervous system, increased sensitivity of the startle reflex, and sleep abnormalities (Bonomo, Cella, Gagliano, Galimberti, Giunta, Guaita, Muller, and Rigamonti, 2005).
People with PTSD tend to have abnormal levels of key hormones involved in the body’s response to stress. Thyroid function also seems to be enhanced in people with PTSD. Some studies have shown that cortisol levels in those with PTSD are lower than normal and epinephrine and norepinephrine levels are higher than normal. People with PTSD also continue to produce higher than normal levels of natural opiates after the trauma has passed. An important finding is that the neuro-hormonal changes seen in PTSD are distinct from, and actually opposite to, those seen in major depression. The distinctive profile associated with PTSD is also seen in individuals who have both PTSD and depression (Bonomo et al, 2005).
Mood disorders
There is wide array of mental illnesses. Depression, bipolar disorder, schizophrenia and obsessive-compulsive disorder are all mood disorders. They are among the U.S.’s top 10 leading causes of disability. Approximately 20.9 million American adults, or about 9.5 % of the U.S. population age 18 and older, in a given year, have a mood disorder. The median age of onset is 30 years. Mood disorders include major depressive disorder, dysthymic disorder, and bipolar disorder (Chiu et al, 2005). Depression. Major Depressive Disorder is a type of mood disorder. It is the leading cause of disability in the U.S. for ages 15-44. Depressive disorders often co-occur with anxiety disorders and substance abuse. Major depressive disorder affects approximately 14.8 million American adults, or about 6.7 percent of the U.S. population age 18 and older in a given year. While major depressive disorder can develop at any age, the median age at onset is 32 and is more prevalent in women than in men. More than twice as many women (6.7 million) as men (3.2 million) suffer from major depressive disorder each year. All ethnic, racial and socioeconomic groups suffer from depression. About three-fourths of those who experience a first episode of depression will have at least one other episode in their lives. Some individuals may have several episodes in the course of a year (Kessler, Berglund, Demler, Jin, Koretz, Merikangas, Rush, Walters, & Wang, 2005).
The symptoms of major depression characteristically represent a significant change from how a person functioned before the illness.. Social, occupational, educational or other important functioning must also be negatively impaired by the change in mood. A person who has missed work or school because of their depression for instance, or has stopped attending classes or usual social engagements altogether may suffer from major depressive disorder. A depressed mood caused by substances, such as drugs, alcohol, or medications, is not considered a major depressive disorder, nor is one which is caused by a general medical conditioner (Kessler et al, 2005).
Typically the diagnosis of major depression is also not made if the person is grieving over a significant loss in their lives. Symptoms also include pronounced changes in sleep, appetite, and energy, difficulty thinking, concentrating, and remembering, physical slowing or agitation, lack of interest in or pleasure from activities that were once enjoyed, feelings of guilt, worthlessness, hopelessness, and emptiness, and persistent physical symptoms that do not respond to treatment, such as headaches, digestive disorders, and chronic pain (Kessler et al, 2005). There is no single cause of major depression. Psychological, biological, and environmental factors may all contribute to its development. Whatever the specific causes of depression, scientific research has firmly established that major depression is a biological brain disorder. Norepinephrine, serotonin, and dopamine are three neurotransmitters (chemical messengers that transmit electrical signals between brain cells) thought to be involved with major depression. Scientists believe that if there is a chemical imbalance in these neurotransmitters, then clinical states of depression result. Antidepressant medications work by increasing the availability of neurotransmitters or by changing the sensitivity of the receptors for these chemical messengers (Kessler et al, 2005).
Scientists have also found evidence of a genetic predisposition to major depression. There is an increased risk for developing depression when there is a family history of the illness. Not everyone with a genetic predisposition develops depression, but some people probably have a biological make-up that leaves them particularly vulnerable to developing depression. Life events, such as the death of a loved one, a major loss or change, chronic stress, and alcohol and drug abuse, may trigger episodes of depression (Kessler et al, 2005).
Bipolar disorder. Bipolar disorder causes dramatic mood swings, from overly “high” and/or irritable to sad and hopeless, and then back again, often with periods of normal mood in between. Severe changes in energy and behavior go along with these changes in mood. The periods of highs and lows are called episodes of mania and depression (Berglun, Demler, Jin, Kessler & Walters, 2005).
Signs and symptoms of mania, or a manic episode, include increased energy, activity, and restlessness, Excessively “high,” overly good, euphoric mood, Extreme irritability, Racing thoughts and talking very fast, jumping from one idea to another, Distractibility, can’t concentrate well, Little sleep needed, Unrealistic beliefs in one’s abilities and powers, Poor judgment, Spending sprees, A lasting period of behavior that is different from usual, Increased sexual drive, Abuse of drugs, particularly cocaine, alcohol, and sleeping medications, Provocative, intrusive, or aggressive behavior, and/or Denial that there is anything wrong (Berglun, et al, 2005).
Scientists are learning about the possible causes of bipolar disorder through several kinds of studies. Most scientists now agree that there is no single cause for bipolar disorder, rather, many factors act together to produce the illness. Because bipolar disorder tends to run in families, researchers have been searching for specific genes passed down through generations that may increase a person’s chance of developing the illness (Berglun et al, 2005).
Studies of identical twins, who share all the same genes, indicate that both genes and other factors play a role in bipolar disorder. If bipolar disorder were caused entirely by genes, then the identical twin of someone with the illness would always develop the illness, and research has shown that this is not the case. However, if one twin has bipolar disorder, the other twin is more likely to develop the illness than is another sibling (Berglun et al, 2005).
In addition, findings from gene research suggest that bipolar disorder, like other mental illnesses, does not occur because of a single gene. It appears likely that many different genes act together, and in combination with other factors of the person or the person’s environment, to cause bipolar disorder. Brain-imaging studies are helping scientists learn what goes wrong in the brain to produce bipolar disorder and other mental illnesses. New brain-imaging techniques allow researchers to take pictures of the living brain at work, to examine its structure and activity, without the need for surgery or other invasive procedures (Berglum et al, 2005).
These techniques include magnetic resonance imaging (MRI), positron emission tomography (PET), and functional magnetic resonance imaging (MRI). There is evidence from imaging studies that the brains of people with bipolar disorder may differ from the brains of healthy individuals (Berglum et al, 2005).
Late adulthood (65 years to death)
Anxiety
PTSD. PTSD can have its onset in late adulthood. Some older veterans, who report a lifetime of only mild symptoms, experience significant increases in symptoms following retirement, severe medical illness in themselves or their spouses, or reminders of their military service such as reunions or media broadcasts of the anniversaries of war events. Those who experience greater stressor magnitude and intensity. Those with prior vulnerability factors such as genetics, early age of onset and longer-lasting childhood trauma, lack of functional social support, and concurrent stressful life events, and those with a social environment that produces shame, guilt, stigmatization, or self-hatred are most likely to develop posttraumatic stress disorder (Fairbank et al, 2005).
Cognitive disorder
Alzheimer’s disease. Alzheimer’s (AD) disease affects an estimated 4.5 million Americans. The number of Americans with AD has more than doubled since 1980. AD is the most common cause of dementia among people age 65 and older. Increasing age is the greatest risk factor for Alzheimer’s. In most people with AD, symptoms first appear after age 65. One in 10 individuals over 65 and nearly half of those over 85 are affected. Rare, inherited forms of Alzheimer’s disease can strike individuals as early as their 30s and 40s. From the time of diagnosis, people with AD survive about half as long as those of similar age without dementia (National Institute on Aging, 2005).
Incidence and prevalence of AD is higher in postmenopausal women than in age-matched men. Since at menopause the endocrine system and other biological paradigms undergo substantial changes. Studies show that the balance between some biological parameters related to estrogen and others related to glucocorticoid (naturally produced steroid hormones) vary during lifespan in either sex in either normalcy or neurodegenerative disorders (National Institute on Aging, 2005).
Conclusion
The field of behavioral genetics has made great strides in cracking the genetic code as it pertains to psychological disorders. Behavioral genetics is the study of the effects of heredity on behavior and psychological characteristics. The role of genetics serves to produce a tendency towards the potential to develop a specific disorder. Three other factors increase the likelihood for the development of the disability. They are structural abnormalities in the brain, biochemical imbalance, and environmental influences of parenting and other socializing factors.
There are inherent barriers to the research efforts of behavioral genetics. Often, persons with mental disabilities are nonadherent to medications. Outcomes of samples are affected by frequent non-compliant medication behavior. Secondly, disabilities tend to comorbid with other disabilities, complicating research outcomes for a specific disability. Finally, the impact of all etiological factors vary significantly on a continuum from weak to severe and change over the developmental life span. As the child ages, the environmental influence of the parent lessens and genetic traits manifest.
Epidemiological studies of mental health problems in the first years of life are few. More studies are needed to examine infancy predictors of psychopathology in the first years of life.
The mental health of young children is affected by parents’ negative expectations of the child because of an unwanted pregnancy. This behavior toward the child as recorded in the first months of the child’s life becomes significant predictors of relationship disturbances at 1(1/2) years.
The lack of understanding of the pathogenesis of many disabilities has hindered the development of effective interventions. Particularly amongst illnesses that need effective interventions are AN and Bipolar disorder. AN has the highest death rate of any psychiatric disorder. Bipolar has a high rate of suicide. Ongoing research is needed to develop these interventions.
Dementia is a cognitive neurodegenerative disorder that most fear as they approach late adulthood. Menopausal transition is a critical phase of women’s life where the occurrence of an unfavorable biological milieu would predispose to an increased risk of neurodegeneration, making the incidence of Alzheimer’s disorder much higher in women than women. Research should continue to lessen the incidence and onset of this disorder.
As technological advances continue, researches will continue to identify the biological differences in the brain of individuals with specific mental disability and a “normal” brain. When the differences are more clearly identified and defined through research, scientists will gain a better understanding of the underlying causes of the illness, and eventually may be able to predict which types of treatment will work most effectively. The author’s belief is that scientist will be able to identify genes and prevent the occurrence of disabilities.
In summary, this paper examined the disorders that significantly affect a given life stage: anxiety, cognitive, communication, disruptive behavior, eating, mood and psychosis. The author gave a general description of several of the most prevalent mental disabilities that occur throughout the life span; organized the disabilities by onset as it relates to stages of development over the life span; and examined research that discussed causes for each disability. The author attempted to answer the question for each disability, “nature or nurture?”
How much of a behavior is due to nature and how much is due to nurture is a challenging question. Nature refers to traits inherited from one’s parents and any factor produced by predetermined genetic information. Nurture refers to the environmental influences that shape behavior. They include biological factors such as a mother’s drug use. Other environmental factors are social such as a parent’s parenting style or socioeconomic circumstances. Although one’s genetic disposition orients toward particular behaviors, those behaviors will not occur without an appropriate environment. The two sides of the nature versus nurture issue are at opposite ends of the continuum. There are no absolutes. The behaviors will always fall somewhere along the continuum based on the circumstantial influences of genetics, biology, brain chemistry, and social environment.
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