The only way to define depression is to outline the clinical symptoms of this disorder. The hallmark symptoms of depression are sustained negative affect and difficulties experiencing positive affect. Depression can be defined as a combination of clinical symptoms in affective-cognitive (depressed mood), neurovegetative (poor sleep, energy) and behavioral (loss of interest) domains.
For patients is important to understand the warning signs of depression. Research has shown that abnormalities in neural activity are related to common depression symptoms. The diagnosis is based on clinical signs and symptoms of depression, syndromes and disease course.
Depression can be difficult to diagnose because it takes so many different forms. Common depression symptoms include:
- persistent sadness and despair, perceived loss , hopelessness, feeling guilty,
- feelings of anxiety,
- loss of interest or pleasure in life, low positive affect (reduced pleasurable engagement)
- neglect of personal responsibilities or personal care, self-depreciation, feeling worthless
- changes in eating habits, weight loss, decreased appetite,
- changes in sleeping patterns, early morning waking, insomnia, hypersomnia
- fatigue, loss of energy, psychomotor retardation,
- loss of libido,
- thoughts of death, wanting to die, suicidal ideation,
- retardation, slowed thinking, poor concentration
1. Insomnia and other sleep complaints – the most prevalent depression symptoms
Sleeping problems are some of the earliest and most commonly reported symptoms of depression. Sleep complaints include:
- non-restorative sleep
- early morning awakening
- difficulty falling asleep
- frequent nocturnal awakenings
- decreased or increased total sleep
- disturbing dreams
Insomnia, hypersomnia, or both are reported by approximately 75% of adults with major depression. Disruptions of normal sleep patterns are a core diagnostic criterion of mood episodes reflecting their importance and prevalence in the presentation of these disorders.
Insomnia often precedes the onset of a first episode of major depression. The degree and duration of insomnia were positively correlated with more severe or recurrent major depression, or both.
Sleep problems are extremely common in the general population (more than 35% of the adult population is affected) and are often associated with psychiatric comorbidity: 14% to 20% of persons with significant complaints of insomnia and about 10% of those with hypersomnia showed evidence of major depression.
Sleep changes remain a predictor of recurrent mood episodes in patients who have had a previous episode of depression or mania, and their persistence is associated with a more severe course. Insomnia and fatigue were the most commonly reported symptoms preceding a recurrent major depression.
Women with more disrupted sleep also had more depression both before and after giving birth. Hence, the presence of initial insomnia seemed to be the most relevant screening question for identifying women at risk for postpartum depression.
Although insomnia can improve with remission from major depression, it also often persists and it is the most commonly reported residual symptom during remission of major depression. Unfortunately, the persistence of sleep disturbances has been shown to predict increased severity and recurrence of major depression.
Sleep has been studied more extensively in patients with depression than with any other psychiatric disorder. In addition to the subjective reports, there are objective and specific changes in sleep architecture that can relate to the underlying neurobiology of depression.
Polysomnographic studies have shown that the majority of patients with major depressive disorder have objective sleep disturbances. Sleep electroencephalographic (EEG) changes have been evaluated for their potential as biological markers of mood disorders.
Objective sleep abnormalities in depression have been grouped into three general categories:
- disturbance of sleep continuity
- deficits of slow-wave sleep (SWS, non–rapid eye movement [NREM] sleep stage 3) having an abnormal distribution with a decreased ratio of slow-wave activity in the first relative to the second NREM period
- abnormalities of REM sleep (for e.g one of the most robust finding in depression is a decreased REM sleep latency (time from onset of sleep to onset of REM sleep); other REM sleep abnormalities include a prolonged first REM sleep period and increased REM density. Increased percentage of REM sleep has also been observed.
Depressed patients showed prolonged sleep latency, increased wakefulness after sleep onset, and early morning awakening, which results in sleep fragmentation and decreased sleep efficiency. Sleeping pills can be used as an adjunctive therapy for depression. The improvement of insomnia symptoms leads to an improvement in the overall depression symptoms.
Sleep deprivation is also a risk factor for depression in healthy individuals.
2. Constant depression symptoms – mood-congruent processing
Abnormal emotion processing affects the onset and maintenance of depression. Numerous studies have described mood-congruent processing in which individuals are biased toward stimuli that match their moods. Thus, individuals in a negative mood are biased toward negative stimuli, whereas those in a positive mood are biased toward positive stimuli. Depression is characterized by extended periods of negative mood which often causes one of the most pronounced cognitive distortions in depression – a greater sensitivity to negative information. Increased sensitivity to negative, mood-congruent information then leads to deeper and more elaborate processing of this content, which in turn influences interpretations of events , subsequent attitudes and mood states.
Neurobiological basis: the amygdala is central to mood-congruent biases being involved in the early detection of salient information at both conscious and subconscious levels. Therefore it identifies the emotional significance of a stimulus and produces affective states.
The amygdala has numerous connections with other regions that are also important for emotion processing such as the orbitofrontal cortex and the hippocampus. Together, this network modulates neural and behavioral responses to emotional stimuli. Therefore, many of the depression neuroimaging studies examining mood-congruent biases have revealed abnormalities in amygdala activity and connectivity. Depressed patients show amygdala hyperactivity in response to negative stimuli. Importantly, studies have shown that aberrant amygdala connectivity and activity can be normalized after treatment and the amygdala may be centrally involved in successful treatment effects.
3. A subsequent depression symptom – biased attention toward negative stimuli
In addition to overall increased sensitivity to negative stimuli, negative cognitive biases in depression can also be seen in specific cognitive domains such as attention and memory.
Depressed individuals pay more attention to negative stimuli and less attention to positive compared to healthy controls. For example, depression has been associated with a bias to attend to negative words and faces. A more detailed examination of this negative attention bias has shown that patients with depression engage more strongly and maintain attention to angry faces, whereas healthy controls not only direct attention away from but also more rapidly disengage from angry faces. Thus, particular difficulty disengaging from negative stimuli may be a symptom of depression.
Neurobiological basis: amygdala hyperactivity is related to increased reactivity to negative stimuli. Also, aberrations in lateral prefrontal cortices and anterior cingulate cortex regions may lead to difficulty disengaging from negative stimuli and abnormal maintenance of attention on them.
Difficulty inhibiting responses to negative stimuli is related to rostral anterior cingulate cortex activity in depression resulting reaction times longer for sad words in the currently depressed group in comparison to healthy controls. Therefore, studies suggest that individuals with MDD require more cognitive effort to disengage from negative stimuli and this difficulty is reflected in increased rostral anterior cingulate cortex activity.
In summary, patients with depression orient their attention toward negative stimuli and also have particular difficulty disengaging from negative stimuli. Further, there is evidence that depressed individuals spend less time attending to positive material. Attentional avoidance of positive material may underlie difficulties savoring positive or using positive material to regulate negative affect.
Attentional biases are a symptom of depression or a scar of a previous depressive episode. They also play an important role in the vulnerability to depression. Attention biases to sad stimuli were associated with greater impairments in mood recovery in depressesd patients.
Difficulties disengaging from negative stimuli may preclude depressed people from using effective emotion regulation strategies such as distraction when confronted with stressful events and this leads to prolonged negative affect. Attentional biases towards negative material also interferes with a person’s ability to successfully reframe emotion-eliciting events. Being “stuck” in attending to negative aspects of the situation may make it more difficult to shift attention to more positive aspects thus hindering a more balanced appraisal of the emotion-eliciting event.
The inability to disengage attention from mood-congruent stimuli may facilitate prolonged processing of such material which is rumination, thereby hindering the use of an adaptive emotion regulation strategy.
4. A depression symptom which hinders recovery – memory biases for negative information
Memory bias refers to a biased process of retrieval, consisting on either an enhancement or impairment in the recall of a given type of memories. As a depression symptom, this bias is referred to a higher propensity to retrieve more negative memories.
Selective memory for negative information contributes to the duration and severity of depressive symptoms. Depressed patients have a tendency to recall negatively toned information compared to healthy controls who show an enhancement of memory for positive information . Preferential recall of negative compared to positive material is one of the most robust findings in the depression literature.
A negative mood at the time of encoding is thought to be one of the contributing factors for the negative memory bias in depression.
Memory biases such as increased accessibility of negative autobiographical material interferes with the selection and use of effective emotion regulation strategies. It determines people’s perception of a specific situation, change their appraisals, and guide their attention towards specific aspects of that situation.
Depressed patients are less likely to endorse positive words as self-descriptive and more likely to endorse negative words.
Depression is associated with overgeneral memories and enhanced recall of negative events which are most of them generic memories than specific events. Rumination maintains overgeneral memory in depressed patients. Training dysphoric individuals to be more concrete and less over-general in their thinking led to a significant reduction in depressive symptoms and rumination.
Mood-congruent recall contributes to difficulties using emotion regulation strategies such as reappraisal.
Heightened levels of depression are associated with more frequent and longer fixation on negative information, more negative interpretation of ambiguous information and memory biases. Biases in attention and interpretation are associated with memory biases.
Neurobiological basis: the amygdala bolsters memory for emotional material and is thought to be central to the memory bias effect . Right amygdala activity in response to subsequently remembered negative stimuli is also correlated with depression severity in depressed patients.
The amygdala is also involved in negative memory biases. Hyperactivity in this region causes strong memory biases for negative information and interferes with demanding memory tasks that are not affectively laden.
5. Long-term memory deficits might be a sign of depression
Depressed patients display deficits in specific facets of long-term memory.
Studies of human memory have revealed a distinction between two ways of gaining access to past experiences: recollection and familiarity.
Recollection involves the recognition of a stimulus, including the retrieval of contextual information that accompanied the original encounter.
Familiarity refers to a feeling that a stimulus has been encountered before, without contextual retrieval.
Depression is characterized by a selective deficit in recollection of long-term memory with preserved familiarity. Depressed subjects with several past episodes show a reduction in autobiographical memory specificity which is thought to be part of a broader memory deficit in recollecting specific details about the context in which the memory was acquired.
Neurobiological basis: long-term memory is subserved by the hippocampus. Studies show that changes in hippocampal structure and function are related to the later course of MDD and they do not characterize first-episode depression. Thus, instead of uncovering abnormal hippocampal activity in first-episode depression, studies have identified aberrant amygdala activity. Amygdala activation interacts with hippocampal- dependent memory formation of neutral stimuli.
An increased activity in the left prefrontal cortex during memory recollection has also been identified, which is required in order to maintain similar levels of task performance. Thus, a need for high levels of effort during cognitively demanding tasks such as memory recollection may be involved in memory retrieval problems in MDD.
6. Rumination – one of the most persistent symptom of depression
Rumination is a mode of responding to distress characterized by repetitive thinking and focusing on negative mood states. It refers to repetitive and passive focusing on symptoms of distress and on the possible causes and consequences of these symptoms. This depression symptom has been ascribed to deficient control processes that cannot rid memory of negative information. The most prominent display of rumination is when people are at rest, not when they are engaged in a task. The relationship between negative biases and increased rumination in depression is intuitive. Rumination has been associated with the severity and duration of a depressive episode. Its presence increases the risk of relapse in remitted patients.
Neurobiological basis: rumination involves an inability to modulate amygdala activity in response to negative stimuli. Negative introspection often occurs spontaneously and is unintentional. A network of brain regions called the default-mode network (DMN) underlies passive, self-referential mental activity and consists of an anterior portion that covers the medial prefrontal cortex, including parts of the ACC, and a posterior portion including the PCC, precuneus, inferior parietal cortex, hippocampal area, and lateral temporal cortex. The DMN has been related to emotion regulation, episodic memory, and autobiographical memory.
The DMN is most active during rest and is typically examined during resting state or wakeful rest. Activity in the DMN is decreased during demanding cognitive tasks. Aberrant DMN activity is related to rumination in depression.
Hyper-connectivity at rest in the DMN existed when rest periods were joined with task periods, a finding that approximate real-world situations under which people are likely to engage in rumination such as idle moments at work. Ruminative psychological processes and connectivity is mitigated by engaging in a task.
Distraction, responsibility for completing a task can be effective at temporarily relieving rumination and improving mood. When patients with depression engage in a memory task, they displayed attenuated levels of connectivity in rumination- related regions. However, when left to their own thoughts, ruminative processes restarts.
Hyper-connectivities that were found at rest disappeared during the task, and periods of quiescence may provide a neural mechanism of rumination/brooding, a destructive form of mind-wandering.
7. Anhedonia – a typical depression symptom
Pathological losses of pleasure may be a devastating part of depression. Individuals with depression generally rate positively valenced stimuli as being less positive, less arousing, or less able to affect their mood. Anhedonia is a mood-like phenomenon in which individuals exhibit a general tendency to feel unmotivated and have a reduced ability to experience pleasure or interest from previously pleasurable stimuli. It is a core symptom of depression.
Motivational anhedonia can be described, for example, as either a general feeling that it is not worth getting out of bed, or a string of finite choices between staying in bed and some other activity in which a depressed patient consistently chooses the former. As a conclusion, the clinical phenomenon of anhedonia can be seen to emerge from a succession of individual decisions.
Anhedonia can also be described in terms of abnormal reward-based decision-making. One manifestation of anhedonic symptoms results in an impaired ability for normative decision-making.
Decisional anhedonia can be described as the impaired ability to balance costs and benefits when selecting among multiple options and is independent from cognitive or reasoning ability. Decisional anhedonia does not imply making poor choices about complex financial instruments. It rather occurs when reward-based decision-making results in choices that substantially differ from normative decisions about potential cost–benefit choices.
Decisional anhedonia has many key components such as an overestimation of costs associated with gaining different types of rewards which is broadly consistent with a negative response bias in depression, a hypersensitivity to punishment, and a tendency to remember negative information.
The general aspects of anhedonia may lead to distinct decision-making impairments such that individuals overestimate future costs, underestimate future benefits, or simply fail to integrate cost/benefit information in a consistent manner, leading to erratic choice behavior.
Depressed individuals show a deficit in the ability to represent the value of future rewards in a consistent manner and a greater tendency to pick the delayed option, possibly reflecting a diminished sensitivity to reward magnitude of the immediate option.
Anhedonia in mood disorders may be associated with an impaired ability to accurately represent future costs and benefits during decision-making.
Anhedonia is a difficult symptom to treat, as evidence suggests that current first line pharmacotherapies do not adequately address motivational and reward-processing deficits in depression. Additionally, it is a predictor of poor treatment response.
Depression is usually associated with blunted reactivity to both positively and negatively valenced stimuli. At least in part, the decline in hedonic responses may be due to a generalized affective blunting, rather than a specific deficit in experienced pleasure.
A pleasant stimulus is often called a rewarding stimulus. Actual reward lies in active processes of the brain that reacts to a stimulus rather than the stimulus itself. Pleasure is not only a sensation, it always requires the activity of hedonic brain systems to convert the sensation to make it ‘ being liked’. Pleasure is defined as a ‘liking’ reaction to reward. For pleasure feelings, specialized brain mechanisms of conscious elaboration are likely needed to convert an objective ‘liking’ reaction to a hedonic stimulus into a subjectively felt liking experience. Reward is actually a complex process containing several psychological components that correspond to distinguishable neurobiological mechanisms.
Anhedonia can be clasified as motivational and consummatory anhedonia.
Consummatory anhedonia refers to deficits in the hedonic response to rewards and motivational anhedonia is a diminished motivation to pursue them.
Neurobiological basis: the cortical-basal ganglia reward network is anchored in the VS, ventral tegmental area, substantia nigra (VTA/SN), OFC, and the ACC, including the ventromedial prefrontal cortex. Using positive words and images as well as monetary rewards, a number of studies have demonstrated reduced activity in MDD in subcortical regions such as the VS, caudate, and putamen that are within the cortical-basal ganglia reward network.
Reduced responsivity in the brain’s cortical-basal ganglia reward network in depression shows that anhedonia is related to abnormalities in reward processing. Reduced connectivity within the reward network has also been related to anhedonia. Individuals with depressive symptoms fail to develop a response bias towards rewarded stimuli.
The dopamine system is one aspect of the reward circuit involved in motivation. Depression is associated with compromised dopamine function. Manipulations of the dopamine system contribute to the actions of antidepressants. Alterations of dopamine function are often a downstream consequence of genetic and environmental risk factors, such as exposure to stress.
8. Depression leads to deficits in cognitive controls
Cognitive control refers to top–down support for task relevant processes. It is needed to overcome habitual errors or to direct attention from task irrelevant to task relevant stimuli.
Depressed individuals have considerable difficulty with cognitive control when processing emotion stimuli, competing responses that have to be inhibited or new information is selected.
Overriding prepotent responses and inhibiting the processing of irrelevant material that captures attention are core abilities that allow us to respond flexibly and to adjust behavior and emotional responses to changing situations. Cognitive control is related to the functioning of executive control processes such as inhibition, disengagement and updating in attention and working memory.
Difficulties inhibiting salient but irrelevant thoughts and memories would also discourage the use of more effective emotion regulation strategies, such as reappraisal. Effective reappraisal may depend on a person’s ability to override (automatic) attention and interpretation biases that lead to unwanted appraisals of the emotion eliciting cues. Replacing automatic appraisals with alternative evaluations of the situation requires cognitive control.
Deficits in the inhibition of mood-congruent material are one of the most common depression symptoms.
Depression involves difficulties keeping irrelevant emotional information from entering working memory. It is associated with difficulties removing previously relevant negative material from working memory (updating). Difficulties inhibiting the processing of negative material that was, but is no longer relevant explains why people respond to negative mood states and negative life events with recurring, uncontrollable, and unintentional negative thoughts.
Depression and rumination are associated with difficulties removing negative irrelevant material from working memory.
People who ruminate exhibit deficits in executive control. This is related to sustained processing of negative material which in turn maintains the negative mood state and hinders recovery from negative affect.
Poorer performance on an executive control task is related to an increased tendency to ruminate following exposure to stressful life events.
Deficits in cognitive control make it difficult to employ attention flexibly and impair the ability to reinterpret the situation in a more adaptive way interfering with the use of adaptive strategies (reappraisal) and predispose to increased use of maladaptive strategies (rumination).
Inappropriate responding to positive affect plays an important role in emotion regulation difficulties in depression as shown by the inability to use positive memories to repair negative affect.
9. Depression is characterized by difficulties in the self-regulation of affect after experiencing negative life events
Depressed patients exhibit more frequent use of inappropriate strategies when regulating affect and show difficulties effectively implementing adaptive strategies.
Cognitive biases and deficits associated with depression are linked to difficulties in the self regulation of emotion. Emotions also influence cognitions. Emotional states facilitate the activation of mood congruent cognitions in memory and also can be considered a disposition to make certain types of appraisals thereby increasing the probability that people will experience specific emotions.
The experience of stressful life events plays a critical role in the onset of depression symptoms. Failures in self-regulation when faced with negative affect resulting from the experience of a negative event may be an important factor in the development of depressive symptoms.
Emotion regulation can take many different forms. Difficulties recovering from negative affect after experiencing negative life events may be due to the use of emotion regulation strategies that incur additional costs such as heightened physiological arousal or cognitive demand.
Depressed people are more likely to respond to the experience of negative affect with rumination. Rumination is considered a detrimental response to negative affect and has been shown to exacerbate sad mood and predict future depressive episodes. Rumination is defined as repetitive thinking that focuses one’s attention on the implications, causes, and meanings of depressive symptoms.
Rumination has not been shown to improve mood. It occurs as a more automatic response to experiencing negative affect which may be difficult to control and to terminate even if unwanted. However, depressed individuals perceive many benefits of rumination such as feelings of increased self-awareness and understanding and an enhanced sense of insightfulness and thus may use it as a strategy to respond to and change their affective state. But, considerable evidence has linked higher trait rumination with the onset and maintenance of depression.
Rumination is usually contrasted with distraction, another emotion regulation strategy. Compared with distraction, rumination leads to increased negative cognitions and overgeneral autobiographical memory, sustained negative mood, and decreased effective problem solving.
Rumination plays an important role in onset of psychological symptoms following stressors.
What characterizes rumination and differentiates it from negative automatic thoughts is that it is a style of thought rather than just negative content. It is defined by the process of recurring thoughts described as a “recycling” of thoughts, and not necessarily by the content of these recurring thoughts.
Depression is associated with increased dampening of positive affect which is related to anhedonia symptoms.
Depression is not only associated with suppression of negative but also of positive emotion which is related to increased symptom severity.
Dysphoria is associated with apprehension about experiencing intense emotions.
10. Decreased reappraisal use is a symptom of depression or indeed a risk factor
Reappraisal involves changing a situation’s meaning to alter one’s emotional response to the situation. It has been shown to reduce negative affect at the same time avoiding additional costs such as heightened arousal.
Reappraisal is associated with reduced physiological activation in response to negative emotion.
Less frequent habitual use of reappraisal is tied to greater depression severity.
Reappraisal was associated with a reduced impact of emotional reactivity on depressive symptoms.
11. Depressed individuals avoid distraction
Distraction is an effective strategy. Patients with depressive symptoms engaged in rumination reported less willingness to engage in pleasant, distracting activities. They may avoid distraction because it may interfere with their efforts to gain insight into their problems.
Depression is associated with an inability to offset negative affect, to focus on positive material, which may be an important automatic mood repair mechanism.
Depression is associated with reduced savoring of positive experiences and positive affect.
Patients with depressive symptoms show a more frequent use of maladaptive (rumination, suppression) and less frequent use of adaptive emotion regulation strategies (distraction, reappraisal).
Depressed people can implement strategies like reappraisal successfully if they are instructed to use it but fail to do so spontaneously.
12. Biases in interpretation and appraisal – a core symptom of depression
Most situations that evoke emotions are ambiguous. How cues in these situations are initially interpreted and appraised determines the emotional response and determines whether this response is appropriate in this situation or not.
Reinterpretation or reappraisal allows flexible emotional responding without changing the situation and without ignoring the emotion-eliciting cues. Biases in interpretation, especially when they are automatic, can make it difficult to use reappraisal and can lead to inflexible and inappropriate responding. Negative interpretation biases mostly result in rigid, automatic mood-congruent interpretations of emotion-eliciting events. They also make it difficult to see the situation from a different perspective or to entertain alternative interpretations.
Changes in interpretation biases can lead to changes in emotional responding and decrease negative mood.
Studies reported an effect of interpretive bias training in depressed participants on depressive symptoms and also observed reductions in self-reported negative thinking, improvement in memory and on physiological stress responding when confronted with a stressor.
13. Lower self-esteem
Self-esteem is the affective and evaluative component of the self-concept and signifies how people feel about themselves. It refers to a person’s general sense of worth.
High self-esteem predicts success in life domains such as relationships, work, and health. Self-esteem is related to positive psychological outcomes such as psychological adjustment, positive emotion and prosocial behavior.
The enhanced self-esteem acts as a cushion for people against feelings of anxiety. It also enhances coping, and promotes physical and mental health. Individuals with low self-esteem experience every negative emotion more often than those with high self-esteem.
Thoughts must be identified as mental processes rather than facts. One must notice that thoughts and feelings are events in the mind and not self-evident truths or aspects of the self. This fact might reduce the tendency to develop strong emotions as a consequence of cognitions related to low self-esteem.
Low self-esteem is a symptom of depression and also shows vulnerability for depression.
Negative self-evaluations play a major role in the onset and maintenance of depression by leading individuals to select and remember information congruent with their perception of themselves.
Depressed individuals report lower levels of global self-esteem, with a lower endorsement of positive qualities and a higher endorsement of negative qualities about themselves. They also report higher recall of negative information and less recall of positive self-referent information compared to never-depressed individuals.
Within the self-esteem construct, a further distinction is made between implicit self-esteem and explicit self-esteem. Implicit self-esteem is based on automatic and possibly unconscious processes and associations with the self. It is thought to be more primitive and to develop earlier in life.
Explicit self-esteem is based on conscious verbal self-evaluations.
Individuals are generally aware of their explicit self-esteem and only scarcely aware of their implicit self-esteem.
Low explicit self-esteem is a key feature of affective disorders. Depressed patients usually report lower explicit self-esteem compared to never-depressed individuals. Low explicit self-esteem does not only result from the experience of a depression, but it also contributes to the onset of subsequent depressive episodes.
Thoughts and interpretations of information about oneself plays a significant role in maintaining residual depressive symptoms.
Explicit self-esteem is associated with past and present depressive symptoms. Implicit self-esteem is superior in predicting future depressive symptoms.
Future studies are necessary to determine whether interventions that modify self-esteem might help to reduce the incidence and recurrence of depression by enhancing both explicit and implicit self-esteem.
Perfectionism is thought to increase vulnerability to depression.
There are two dimensions of perfectionism that encompass the diverse conceptualizations of this construct:
1. personal standards perfectionism: involves setting and striving for excessively high goals and standards for the self. It is often unrelated to depressive symptoms.
2. self-critical perfectionism: involves constant and harsh self-scrutiny and critical self-evaluation of one’s own behavior, and continuous worry about others’ approval, criticism, and rejection. It exhibits a strong relation with depressive symptoms.
Self-critical evaluations of the self maintain the perceived gap between an individual’s ideal self and their actual self which leads to experiences of low self-esteem.
Self-critical perfectionism differs conceptually from low self-esteem. It involves a harsh and critical self-evaluation relating to feelings of failure to live up to one’s own or others’ expectations. These characteristics may serve as motivation for individuals to avoid feelings or situations of failure and disappointment. Accordingly, experiential avoidance is a mediating mechanism that explains the relation between self-critical perfectionism and depressive symptoms. Experiential avoidance is defined as an individuals’ unwillingness to remain in contact with uncomfortable internal experiences (distressing thoughts, feelings, sensations) and involves attempts to avoid these situations that produce them. Individuals with self-critical perfectionism may engage in experiential avoidance in order to regulate feelings of low self-esteem.
The desire to escape from unpleasant emotional states that are associated with self-critical views of the self contributes to a greater use of experiential avoidance to escape from negative self-awareness. Individuals with self-critical perfectionism usually adopt a helplessness orientation when faced with obstacles. This contributes to their tendency to engage in avoidant types of coping.
Experiential avoidance is related to negative outcomes such as depression. Emotional avoiders have a greater tendency toward experiences of depressive symptoms, particularly when they engage in thought suppression. Usually, attempts to avoid or control internal experiences may increase these unwanted feelings and thoughts. Individuals with self-critical perfectionism have a tendency toward avoidance, which can maintain and increase their depressive symptoms. The persistent use of experiential avoidance is ineffective and harmful in the long-term, leading to greater experiences of depressive symptoms and demonstrating that what we resist, persists.
Perfectionistic individuals who perceive a discrepancy between their ideal and actual self develop lower self-esteem.
Individuals with self-critical perfectionism develop a pattern of avoidance, of aversive self-awareness in order to diminish the impact of self-critical thoughts and concerns about negative perceptions by others.
14. Signs of depression – maladaptive thinking and negative appraisals of life circumstances
Maladaptive thinking is believed to contribute to the onset of depression in the context of stressful life circumstances.
There are three main models of thinking involved in the maintenance of depression:
1. depressive self-schemas which represent the way humans come to identify, interpret, categorize, and evaluate their experiences. Usually previous experience influence the processing of new information. The self-schemas of individuals who are vulnerable to depression embody a dysfunctional attitudes that lead to negative perspectives about oneself, the world, and the future.
Depressive self-schemas usually develop during early childhood. They remain latent until activated by adverse circumstances such as stressful life events (a failure or rejection experience). An individual who is vulnerable to depression may engage in information processing biases and experience negative thoughts that center on themes of loss, failure, worthlessness, defectiveness, incompetence and inadequacy.
Example of disfunctional attitudes:
- failing partially is equivalent to complete failure
- if-then ” statements: “If I am not approved by everyone, then I am not worthwhile ”
- self-worth or happiness depends on the approval of others
- personal rules and compensatory strategies for coping with negative core beliefs (“ I must succeed in everything I do ”)
2. maladaptive beliefs
3. negative automatic thoughts
Negative thinking related to interpersonal themes (defining self-worth on the basis of interpersonal approval and acceptance) confers a particular risk factor for depression.
Examples of negative appraisal of life circumstances:
1.to see things in terms of two mutually exclusive categories with no “ shades of gray ” in between (e.g. believing that one is either a success or a failure and that anything short of a perfect performance is a total failure)
2. to overgeneralize a specific event. To see it as being characteristic of life in general rather than as being one event among many. (e.g concluding that an inconsiderate response from one’s spouse shows that she doesn’t care despite her having showed consideration on other occasion).
3. to ignore other relevant aspects of a complex situation and focus only on one thing(e.g. focusing on the one negative comment in a performance evaluation received at work and overlooking a number of positive comments).
4. to disqualify the positive. Positive experiences that would conflict with the individual’s negative views are discounted by declaring that they “ don’t count. ” (e.g. disbelieving positive feedback from friends and colleagues and thinking “ they’re only saying that to be nice. ”).
5. mind reading- to assume that others are reacting negatively without evidence that this is the case. (e.g. thinking, “ I just know he thought I was an idiot! ”, despite the other person’s having behaved politely).
6. to react as though negative expectations about future events are established facts (e.g. thinking, “He’s leaving me, I just know it! ”, and acting as though this is definitely true).
7. to catastrophize. Negative events that might occur are treated as intolerable catastrophes rather than being seen in perspective (e.g. thinking “ Oh my God, what if I faint! ” without considering that, whereas fainting may be unpleasant and embarrassing, it is not terribly dangerous).
8. to assume that emotional reactions necessarily reflect the true situation (e.g. deciding that because one feels hopeless, the situation must really be hopeless).
9. “ Should ” statements: the use of should and have-to statements to provide motivation or control behavior (e.g. thinking, “ I shouldn’t feel aggravated. She’s my mother, I have to listen to her. ”)
10. to attache a global label to yourself rather than referring to specific events or actions (e.g. thinking, “ I’m a failure! ”, rather than “ Boy, I blew that one! ”)
11. to assume that one is the cause of a particular external event when, in fact, other factors are responsible(e.g. assuming that a supervisor’s lack of friendliness is a reflection of her feelings about the client rather than realizing that she is upset).