20 lessons about mental health to take us into 2020 (part 1)
guest author Graham Holloway – originally posted to Facebook.
*While this is not directly about sex ed, sexual health and mental health are inextricably linked. There’s some fun and interesting stuff here, and I know lots of you are fellow nerds who eat this science stuff up, so I got Graham’s permission to share it with you – Professor Sex*
Today is the last day of 2019 so here is a list of 20 things I think everyone should know about mental health as we enter 2020.
1. Mental health includes our emotional, psychological, and social well-being. Mental Health affects how we think, feel, and act. It also helps
determine how we handle stress, relate to others, and make choices (U.S Department of Health and Human Services, 2019).
2. A mental disorder is “a syndrome characterized by clinically significant disturbance in an individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the psychological, biological, or development processes underlying mental functioning. Mental disorders are usually associated with significant distress or disability in social, occupational, or other important activities.” (American Psychiatric Association, 2013, P. 20).
3. Just as it’s possible to have poor mental health but no mental illness, it’s entirely possible to have good mental health even with a diagnosis of a mental illness. Mental illnesses (like other health problems) are often episodic, meaning there are times of ill health and times of better or good health (Canadian Mental Health Association, 2015).
4. The biopsychosocial approach systematically considers biological, psychological, and social factors and their complex interactions in understanding health, illness, and health care delivery; this model assumes mental health problems are influenced by multiple domains (Rochester University, 2019).
This example by Dombeck (2019) incorporates the biological aspect, psychological aspect, and the social aspect while discussing depression.
“Someone who is depressed might have become that way because of a medical condition (such as a heart attack), a social condition (such as losing a loved one), or a psychological condition (such as an overly self-critical nature). Further, regardless of the cause of the condition, that person’s depression will likely show physical symptoms (such as slowed speech and lessened appetite), psychological symptoms (such as suicidal thoughts) and social symptoms (such as social withdrawal). Perhaps most importantly, it is possible to treat depression through physical means (anti-depressant medicine, physical exercise), psychological means (cognitive therapy) and also social means (urging the person to get out and interact with other people) regardless of how that depression got started. All of these methods are likely to prove helpful in lifting depressed mood. What is more, they can all be used at once despite their different origins; you aren’t limited to trying one intervention at a time.”
5. Overall, people with mental illnesses are much more likely to be victims of crime, hate, and discrimination than to be the perpetrators (Mental Health Commission of Canada, 2017).
6. The Diathesis stress model views psychological disease as the result of the interaction between a person’s vulnerability for a disorder and
stress and this model seeks to explain how different people may respond differently to the same source of stress. A susceptible individual may never manifest a mental illness until they encounter a type or degree of stress that is enough to trigger it (Barlow, Durband, Hoffman, & Lalumière, 2017, P. 37).
7. Terms such as “committed suicide”, “failed suicide”, and “successful suicide” are avoided because they evoke connotations of criminality, which are inappropriate and potentially stigmatizing to suicidal individuals and those touched by suicide. Changing the language that we use to describe suicide and suicidal behaviour is the first step in addressing the ways in which nurses can sensitively and emphatically begin working with individuals who are suicidal (Freeman, 2015; Halter, Pollard, & Jakubec, 2018, P. 496; Maple, Edwards, Plummer, Minichiello, 2008, P. 241-248; Mishara & Weisstub, 2016, P. 54-74; Sommer-Rotenberg, 1998, P. 239-40).
8. Suicide is not synonymous with mental illness. Suicidal behaviour indicates deep unhappiness but not necessarily mental illness. Many people living with mental illnesses are not affected by suicidal behaviour and many people who die by suicide aren’t affected by mental illness (Halter, Pollard, & Jakubec, 2018, P. 497; WHO, 2014).
9. Asking about suicidal thoughts does not give a person idea’s, rather, it is a professional responsibility. Talking openly leads to a decrease in ideation and can increase problem-solving alternatives for living (Halter, Pollard, & Jakubec, 2018, P. 502).
10. Neurotransmitters engage in wiring transmission by acting on neurons in their own immediate vicinity, generally at a synapse. Neurotransmitters are typically released from an axon terminal and cross the synaptic gap. On the postsynaptic membrane, ion channels open when molecules of neurotransmitter interact with either very fast ionotropic or somewhat slower metabotropic channels. At ionotropic receptors, the neurotransmitter performs rapid communication on a scale of milliseconds. At metabotropic receptors, neurotransmitter effects might last as many as several hours (Freberg, 2018, P. 108).
While there are many different types of neurotransmitters, the one’s discussed throughout this post are Acetylcholine, Dopamine, Epinephrine, GABA, Glutamate, Norepinephrine, and Serotonin.
Acetylcholine is the primary neurotransmitter at the neuromuscular junction, the synapse between a neuron and a muscle fiber, and primarily helps in movement (Freberg, 2018, P. 111) but also aids in learning and memory (Hamm & Yakel, 2017; Hasslmo, 2006; Ridley, Bowes, Baker, Crow, 1984), sustaining attention (Himmelheber, Sarter & Bruno, 2000), and alertness when we wake up (Jones, 2005).
Often mistaken as the chemical that produces pleasure and the chemical that can become addictive, dopamine instead appears to have several roles in learning (Hamid, Pettibone, Mabrouk, et al., 2016, P. 117-126; Wise, 2004, P. 483-494) and anticipating rewards (Schultz, 1998, P. 1-27). Roles include predicting the likelihood of reward and generating emotional responses prior to a potentially rewarding stimulus (Schultz, 2016, P. 183-195). Prefrontal dopamine further appears important for executive processes of control (Ko, Antonelli, Monchi, Ray, Rusjan, Houle, et al., 2013, P. 1591-1604). If you kill off the cells that produce dopamine, the animal is not motivated to pursue a goal. It’ll still enjoy something — like the sucrose solution you squeeze directly into its mouth — because the pleasure systems are fine, but the animal won’t actively seek the solution out.
Epinephrine (also known as adrenaline) is a neurotransmitter in the sense that, within the brain, it helps neurons to communicate with one another. However, because epinephrine is mainly produced by the adrenal glands (located at the top of each kidney) and has functions peripherally (i.e., outside the brain), it can also be considered a hormone (Ellis, Farrington, & Hoskin, 2019, 307-387). Epinephrine has effects on the body such as: Increased heart race, increased blood flow, pupil dilation, and other functions (Khurana, 2008, P. 460).
Glutamate’s derivative, GABA, is the most common inhibitory neurotransmitter and decreases the likelihood of an action potential occurring (Olson & Li, 2012, P. 367-376). Glutamate is the most common excitatory neurotransmitter and increases the likelihood of an action potential occurring. It has been reported to be the transmitter in 40% of all synapses in the brain (Alexander, 2009, P. 885-894). While epinephrine and norepinephrine have similar effects throughout the body, in the brain, norepinephrine plays a role in the sleep-wake cycle, helping you to wake up, in increasing attention and focusing on performing a task, and in memory storage, and emotions (Dimarak, 2019).
Serotonin has been implicated in sleep, feeding, sexual behavior, temperature regulation, pain, and cognition as well as in pathological states including disorders connected to mood, anxiety, psychosis and pain (Chilmonczyk, Bojarski, Pilc, & Sylte, 2015, P. 18474–18506).
Neurobiological research shows that brain structures do change over time due to exposure of psychoactive drugs until they reach a threshold, at which point the primary symptom of dependence occurs, making it difficult to stop excessive drug use. The brain continually attempts to keep the body at (or return the body to) a point of balance or homeostasis and in doing so, will adapt to the prolonged or excessive presence of drugs by making changes in brain cells and neuronal pathways (Halter, Pollard, & Jakubec, 2018, P. 396). These changes are evidenced by common cognitive deficits in core executive functions. For example, substance users have difficulty with planning, working memory, inhibition, and decision making. There are also alterations in selective attention, episodic memory, and difficulties with emotional processing. After 3 months of abstinence, executive functions increase about 30% in people with moderate to severe impairment and increase up to 70% in those with mild impairment (Verdejo-Garcia, 2011).
While many like to think that anything that increases Dopamine can become addicting, that is not the case. Dopamine is necessary for addiction but not sufficient (Prause & Donaghue, 2019). In other words, there’s more to addiction than just the presence of dopamine as dopamine is more about learning and pursuing rather than pleasure.
A comprehensive conceptualization of addiction must include three elements: Psychological, Biological, and Social (Csiernik, 2016).
In contrast to addiction, compulsive behaviours do not have the biological element, only the psychological and social elements so there is no biological risk of withdrawal or overdose (Halter, Pollard, & Jakubec, 2018, P. 392).
The process of addiction occurs in four steps (Halter, Pollard, & Jakubec, 2018, P. 392-394).
- No contact: Prior to a person coming into contact with a psychoactive agent, there is no use and thus no risk. Just as someone can be predisposed to substance use due to biological (genetic), psychological, or social factors, one’s personal disposition or social environment may dissuade the use of certain substances or behaviours.
- Experimentation: Some people may use a substance to enhance an already pleasurable and ongoing experience and therefore consider their use to be a social habit. This integrated use of a substance in a socially and culturally accepted manner has few negative consequences.
- Excessive use: The misuse or excessive use of a substance results in problems for the user and for those associated with them. People who misuse drugs may experience lapses in memory, conflict in their relationships, and engage in acts they would not consider when not under the influence. Treatment intervention becomes appropriate when someone reaches this degree of Psychoactive drug consumption.
- Addiction: At this stage, the person has reached the state where they are physically and psychologically dependent. They have lost their ability to choose to use and the drug becomes the central organizing principle of the person’s life. With regular use, the user develops tolerance and their reaction to a substance decreases with repeated administration of the same dose. If the person attempts to stop, they may also experience withdrawal, which entails cravings for the substance of abuse that is accompanied by decreased physical and emotional health. Withdrawal also produces physiological changes as the blood and tissue concentrations of a drug decrease after heavy and prolonged use.
The complex combination of both substance abuse and a mental health condition is referred to as a concurrent disorder. More than 50% of those engaged in treatment for substance use are also struggling with mental illness, and 15% to 20% of those engaged for treatment for mental illness are struggling with addiction (Halter, Pollard, & Jakubec, 2018, P. 394).
Up to 25% of Canadian will experience an anxiety disorder and 24% of them will also have a substance use disorder. Major depression will affect 15% to 20% of Canadians and among them 27% will experience substance use disorder and while only 1% to 2% of the population suffer from bipolar disorders, a staggering 56% of them will have a substance use disorder (Canadian Institute for Health Information, 2012, 2013; Skinner, O’Grady, Bartha, et al., 2004).
Prevention models in healthcare are classified as primary, secondary, and tertiary (Halter, Pollard, & Jakubec, 2018, P. 418-424).
- Primary prevention focuses on reducing the demand for a substance or behaviour, as well as stopping the occurrence of alcohol or drug use or abuse. Examples include implementing healthy public policy, offering health education related to addiction, taxing and health-related warning labelling of licit products such as cigarettes and alcohol and promoting educational campaigns such as addiction and mental health in the workplace.
- Secondary prevention seeks to limit further health deterioration and social harm from the use of, abuse of, dependence on, and addiction to substances and behaviours. Examples would be programs of early recognition, awareness campaigns, relapse prevention, and harm reduction approaches such as Safe Injection Sites; Needle Exchange programs; Methadone treatment and methadone maintenance; heroin-assisted treatment; controlled drinking; managed alcohol programs; and relapse prevention programs like AA.
- Tertiary prevention is concerned with limiting and reducing complications and dysfunctions related to the experience of addiction. Examples include recovery homes, rehabilitation programs, addiction supportive housing, withdrawal management services, and community-based (outpatient) treatment.
Harm reduction refers to a range of programs, policies, and interventions designed to reduce or minimize the adverse consequences of associated with drug use such as overdose, infection, and spread of communicable diseases (Halter, Pollard, & Jakubec, 2018, P. 418).
Safe Injection Sites (SISs) offer a safe place that drug-dependent individuals can access to inject drugs under the supervision of trained multidisciplinary health and social services staff who can provide education in regard to safer practices and to help in the event of an overdose. SISs allows individuals to have their privacy while also offering the comfort of knowing that trained medical staff is there to help in case of emergency. SISs do not allow the sharing of drugs or equipment and prohibit assisted Injection. SISs have been shown to decrease new HIV and HCV infections and reduce the number of overdose-related deaths while providing access to primary and emergency healthcare for a traditionally oppressed population (Halter, Pollard, & Jakubec, 2018, P. 419). A systematic literature review of 75 studies showed that SISs fulfilled their harm-reduction objectives and were not found to increase drug use or crime (Potier, Laprevote, Dubois-Arber, Cottencin, & Rolland, 2014, P. 48-68). SISs have also been found to increase referrals to and uptake of programs such as detoxification and opiate substitution therapy (OST) (Kennedy, Karamouzian, & Kerr, 2017, P. 161-183).
Uptake of OST can reduce or eliminate injection drug use and has been shown to reduce injection risk behaviors and HIV rates among people who inject drugs (MacArthur, Minozzi, Martin, et al., 2012). Research also shows that SISs use is associated with a greater likelihood of accessing medical care when needed and that SISs provides opportunities to access other services located on or off-site, such as nursing, counseling, HIV testing, mental health care, and support for basic needs (Kennedy, Karamouzian, & Kerr, 2017, P. 161-183). Research also shows that SISs are effective at reducing public drug use and discarded injection equipment and they do not contribute to increases in drug-related crime in the areas surrounding SISs (Kennedy, Karamouzian, & Kerr, 2017, P. 161-183; Potier, Laprevote, Dubois-Arber, Cottencin, & Rolland, 2014, P. 48-68).
In the brains of people with Alzheimer’s, there are signs that neuronal degeneration begins in the hippocampus and then spreads into the cerebral cortex. There are two processes that contribute to cell death. The first is the accumulation of the protein amyloid outside the neurons,
which interfere with the synapses. The second is an accumulation of the protein Tau inside the neurons, which forms tangles that block the flow of nutrients (Halter, Pollard, & Jakubec, 2018, P. 373). However, some people who have these brain changes do not develop Alzheimer’s (Alzheimer’s association, 2014).
There are three known genetic mutations that guarantee that a person will develop Alzheimer’s. A susceptibility gene has been identified for late onset Alzheimer’s. It is a gene that makes the protein Apolipoprotein E (APOE), which supports lipid transport and injury repair in the brain (Halter, Pollard, & Jakubec, 2018, P. 373). Individuals carrying the e4 allele are at an increased risk for developing Alzheimer’s compared to those carrying the more common e3 allele whereas carrying the e2 allele deceases the risk (Liu, Kanekiyo, Xu, et al., 2013). Head injuries and traumatic brain injuries (TBIs) are associated with a greater risk for developing Alzheimer’s and other dementias (Halter, Pollard, & Jakubec, 2018, P. 375). There is also suggestion of a greater risk for those who suffer brain injuries and who carry the gene APOE 4 (Alzheimer’s Association, 2014).
Excitotoxicity has also been implicated in Alzheimer’s (Lewerenz, & Maher, 2015). When Glutamate bonds to NMDA receptors in a healthy brain, it opens calcium channels and calcium flows into the neurons. Excessive stimulation of these receptors by high concentrations of glutamate can lead to excitotoxicity. This is a phenomenon where too much calcium enters a neuron and may lead to neuronal damage and even death (Halter, Pollard, & Jakubec, 2018, P. 195) as the cell undergoes apoptosis (programmed cell death) (Dong, Wang, & Qin, 2009, P. 379-387; Mattson, 2000, P. 120-130).
Deficits in Acetylcholine also appear to play a role in Alzheimer’s (Francis, 2005).
VACCINES DO NOT CAUSE AUTISM!!!!!
According to the DSM-5, Autism is characterized by deficits in two behavioral domains: social communication and interaction and restricted, repetitive patterns of behavior, interests, or activities (APA, 2013). A study by the Autism and Developmental Disabilities Monitoring (ADDM) Network and funded by the Centers for Disease Control and Prevention (CDC) determined the prevalence of ASD in the United States to be about 11.3 per 1,000 (1 in 88) children (CDC, 2012b). It occurs about 4.5 times more often in boys than in girls. Onset of the disorder occurs in early childhood, and in most cases it runs a chronic course, with symptoms persisting into adulthood (APA, 2013).
Neurological imaging studies have revealed a number of alterations in major brain structures of individuals with ASD. In one study, the investigators found a disproportionate enlargement in temporal lobe white matter and an increase in surface area in the temporal, frontal, and parieto-occipital lobes (Hazlett et al., 2011). Other imaging studies have revealed an overall impairment in brain connectivity networks associated with attention, consciousness, and self-awareness (Black & Andreasen, 2011). Genetics Research has revealed strong evidence that genetic factors play a significant role in the etiology of Autism. Studies have shown that parents who have one child with Autism are at increased risk for having more than one child with the disorder. Other studies with both monozygotic and dizygotic twins also have provided evidence of a genetic involvement. A number of linkage studies have implicated areas on several chromosomes in the development of the disorder, most notably chromosomes 2, 7, 15, 16, and 17 (Brkanac, Raskind, & King, 2008; Shriber, 2012; Ursano et al., 2008). The results of a study by the Autism Genome Project Consortium, which was funded by the U.S. National Institutes of Health, have implicated a region on chromosome 11 and aberrations in a brain development gene called neurexin 1 (Autism Genome Project Consortium, 2007) but more research into this area is needed.
In regard to research for neurotransmitters, serotonin has been studied the most in terms of research efforts and investigations (Eissa et al., 2018). Serotonin signaling facilitates many neural processes including that of neurogenesis, cell migration and survival, synaptogenesis, and synaptic plasticity (Eissa et al., 2018). It was noted that 45% of individuals with autism who were tested contained high levels of serotonin in their blood (Eissa et al., 2018).
14. Bipolar Disorder:
Bipolar disorders have been described as a “bridge” between the psychotic disorders, such as schizophrenia, and depressive disorders in respect to their symptoms, family histories, and genetics (APA, 2013, p. 123). Bipolar disorder is characterized by at least one lifetime episode of mania, which is often preceded or followed by a period of depression. Mania consists of a distinct period of abnormally and persistently elevated, expansive, or irritable mood, abnormally and persistently increased goal-directed activity or energy, lasting at least one week and present most of the day, nearly every day (or any duration if hospitalization is necessary) (APA, 2013, P. 124). Further symptoms include inflated self-esteem, decreased need for sleep, higher-than-normal verbal output, flight of ideas, distractibility, increased goal-directed activity, and excessive involvement in activities that have a high potential for negative consequences (such as buying sprees or risky sexual encounters) (APA, 2013). Many people with bipolar disorder experience depression as well as mania, although depression is no longer required for a diagnosis of bipolar disorder. In cases in which depression does occur, the symptoms are the same as those found in major depressive disorder (APA, 2013)
Bipolar disorder affects approximately 5.7 million American adults, or about 2.6 percent of the U.S. population age 18 and older in a given year (National Institute of Mental Health [NIMH], 2013). In terms of gender, the incidence of bipolar disorder is roughly equal, with a ratio of women to men of about 1.2 to 1. The average age of onset for bipolar disorder is the early 20s, and following the first manic episode, the disorder tends to be recurrent (Townsend, 2015, P. 499). As with depression, bipolar disorder appears to be more common in unmarried than in married persons (Joska & Stein, 2008). Unlike depressive disorders, bipolar disorder appears to occur more frequently among the higher socioeconomic classes (Sadock & Sadock, 2007). Bipolar disorder is the sixth leading cause of disability in the middle age group, and the loss of earnings and productivity attributable to mood disorders (depression and bipolar disorder) may amount to about $33 billion per year in the United States (Joska & Stein, 2008).
- Bipolar I: The Bipolar I disorder is the diagnosis given to an individual who is experiencing a manic episode or has a history of one or more manic episodes that last at least seven days (most of the day, nearly every day) or when manic symptoms are so severe that hospital care is needed. Usually, separate depressive episodes occur as well, typically lasting at least two weeks. The client may also have experienced episodes of depression. This diagnosis is further specified by the current or most recent behavioral episode experienced. For example, the specifier might be single manic episode (to describe individuals having a first episode of mania) or the specifier may be identified as current (or most recent) episode manic, hypomanic, mixed, or depressed (to describe individuals who have had recurrent mood episodes). Psychotic or catatonic features may also be noted (Townsend, 2015, P. 501).
- Bipolar II: The Bipolar II disorder diagnostic category is characterized by recurrent bouts of major depression with episodic occurrence of hypomania. The individual who is assigned this diagnosis may present with symptoms (or history) of depression or hypomania. The client has never experienced a full manic episode. The diagnosis may specify whether the current or most recent episode is hypomanic, depressed, or with mixed features. If the current syndrome is a major depressive episode, psychotic or catatonic features may be noted (Townsend, 2015, P. 501).
- Cyclothymic Disorder: The essential feature of cyclothymic disorder is a chronic mood disturbance of at least 2 years’ duration, involving numerous periods of elevated mood that do not meet the criteria for a hypomanic episode and numerous periods of depressed mood of insufficient severity or duration to meet the criteria for major depressive episode. The individual is never without the symptoms for more than 2 months (Townsend, 2015, P. 501).
Neurotransmitters implicated in Bipolar disorder include an increase in Dopamine (Lahera & Freund, 2013, P. 45-51; Salvadore et al., 2010, P. 1488-1501), an increase in Glutamate (Michael, Erfurth, & Ohrmann, 2003, P. 344–346, and an increase in GABA (Benes & Berretta, 2001, P. 1-27).
15. Eating Disorders:
Anorexia nervosa is characterized by a morbid fear of obesity. Symptoms include gross distortion of body image, preoccupation with food, and
refusal to eat while Bulimia nervosa is an episodic, uncontrolled, compulsive, rapid ingestion of large quantities of food over a short period of time (binging), followed by inappropriate compensatory behaviors to rid the body of the excess calories (Townsend, 2015, P. 648).
A hereditary predisposition to eating disorders has been hypothesized on the basis of family histories and an apparent association with other disorders for which the likelihood of genetic influences exists. In their study of monozygotic and dizygotic twins, Bulik and associates (2006) concluded that genetic factors account for 56 percent of the risk for developing anorexia nervosa. Other genetic studies have suggested possible linkage sites for anorexia nervosa on chromosomes 1, 2, and 13 (Halmi, 2008). Anorexia nervosa is more common among sisters and mothers of those with the disorder than among the general population (Townsend, 2015, P. 649). Several studies have reported a higher than expected frequency of mood and substance use disorders among first-degree biological relatives of individuals with eating disorders (Puri & Treasaden, 2011). Some speculation has occurred regarding a primary hypothalamic dysfunction in anorexia nervosa. Studies consistent with this theory have revealed elevated cerebrospinal fluid cortisol levels and a possible impairment of dopaminergic regulation in individuals with anorexia nervosa (Halmi, 2008). Research demonstrates that altered brain serotonin and function contributes to the dysregulation of appetite, mood, and impulse control (Kaye, Wierenga, Bailer, Simmons, & Bischoff-Grethe, 2013). This hypothesis has been supported by the positive response these individuals have shown to therapy with the selective serotonin reuptake inhibitors (SSRIs). Some studies have found high levels of endogenous opioids in the spinal fluid of clients with anorexia nervosa, promoting the speculation that these chemicals may contribute to denial of hunger (Sadock & Sadock, 2007).
16. Generalized Anxiety Disorder:
Generalized anxiety disorder (GAD) is characterized by persistent, unrealistic, and excessive anxiety and worry, which have occurred more days than not for at least 6 months, and cannot be attributed to specific organic factors, such as caffeine intoxication or hyperthyroidism. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Townsend, 2015, P. 532).
Anxiety can be considered apprehension, tension, or uneasiness from anticipation of danger, the source of which is largely unknown or unrecognized. Anxiety may be regarded as pathological when it interferes with social and occupational functioning, achievement of desired goals, or emotional comfort (Black & Andreasen, 2011, p. 590-591). Anxiety disorders are the most common of all psychiatric illnesses and result in considerable functional impairment and distress (Hollander & Simeon, 2008). Statistics vary widely, but most agree that anxiety disorders are more common in women than in men by at least 2 to 1. Prevalence rates for anxiety disorders within the general population have been given at 3 to 5 percent for generalized anxiety disorder and panic disorder, 13 percent for social anxiety disorder, and 25 percent for phobias. Obsessive-compulsive disorders account for 2 to 3 percent (Rowney, Hermida, & Malone, 2010).
Although many neurotransmitters have been implicated in the pathophysiology of anxiety disorders, disturbances in serotonin, glutamate, norepinephrine, and gamma-aminobutyric acid (GABA) appear to be most significant. Serotonin is thought to be decreased in anxiety disorders, Norepinephrine is thought to be increased in anxiety disorders, and GABA is thought to be decreased in anxiety disorders (Taylor, Fricker, Devi, & Gomes, 2005; Townsend, 2015, P. 530) while glutamate is thought to also be increased (Vardanyan & Hruby, 2016, P. 77-86).
17. Major Depressive Disorder:
Clinical depression (otherwise known as Major Depressive Disorder) is a complex mood disorder caused by various factors, including genetic predisposition, personality, stress, and brain chemistry (CAMH, 2019). In order to be diagnosed with MDD, the individual is required to have at least a depressed mood or a loss of interest or pleasure as one of the symptoms. The other symptoms can include: Affected sleep (sleeping too much or too little), feelings of worthlessness or excessive or inappropriate guilt, fatigue or loss of energy, diminished ability to think or concentrate or indecisiveness, significant change in weight or appetite (undereating or overeating), psychomotor agitation (movement that is without purpose or meaning) that is observable by others (e.g. pacing around the room, tapping of fingers or toes, fidgeting, fast talking), and suicidal ideation (APA, 2013, P. 160-161).
In regard to biological factors, it has been hypothesized that depression may be related to a deficiency of the neurotransmitters norepinephrine, serotonin, and dopamine, at functionally important receptor sites in the brain (Slattery, Hudson, & Nutt, 2004). The catecholamine norepinephrine has been identified as a key component in the mobilization of the body to deal with stressful situations. Neurons that contain serotonin are critically involved in the regulation of many psychobiological functions, such as mood, anxiety, arousal, vigilance, irritability, thinking, cognition, appetite, aggression, and circadian rhythm (Dubovsky, Davies, & Dubovsky, 2003).
Tryptophan, the amino acid precursor of serotonin, has been shown to enhance the efficacy of antidepressant medications and, on occasion, to be effective as an antidepressant itself (Townsend, 2015, P. 464).
The level of dopamine in the mesolimbic system of the brain is thought to exert a strong influence over human mood and behavior. A diminished supply of these biogenic amines inhibits the transmission of impulses from one neuronal fiber to another, causing a failure of the cells to fire or become charged (Townsend, 2011, P. 362). Research also suggests that individuals with depression have
lower levels of hippocampal neuro-genesis compared to individuals who do not have depression (Wilner, Scheel-Kruger, & Belzung, 2013).
For the rest of the list, head to Part 2.