Psychology of Major Depressive Disorder and Obesity: Biological, Cognitive, and Cultural Perspectives

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Last updated 8:08 AM on 7/5/26
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292 Terms

1
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What is the heritability basis of Major Depressive Disorder (MDD)?

MDD has a partially heritable biological basis, meaning inherited genes can increase vulnerability to developing the disorder.

2
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Which neurotransmitter systems are influenced by genes in relation to MDD?

Genes influence the regulation of serotonin and dopamine pathways, which control mood regulation.

3
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What role does the HPA axis play in MDD?

The HPA axis is responsible for cortisol release and stress response, which is frequently dysregulated in MDD patients.

4
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How do specific gene variants affect depression triggers?

Inherited gene variants can lead to less efficient functioning of neurotransmitter systems, lowering the threshold for depression to be triggered.

5
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What do twin studies reveal about the heritability of MDD?

Twin studies estimate heritability by comparing concordance rates between MZ twins (100% shared DNA) and DZ twins (50% shared DNA), with higher MZ concordance suggesting a genetic contribution.

6
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What does a concordance rate of less than 100% in MZ twins indicate?

It suggests that genetics alone cannot fully explain MDD, pointing toward a gene-environment interaction.

7
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What did Kendler et al. (2006) find regarding the heritability of MDD?

Kendler found heritability of MDD at approximately 38-44%, with MZ twins showing significantly higher concordance than DZ twins.

8
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What is the relationship between genetic inheritance and causality in MDD?

Genetic inheritance increases vulnerability to MDD but does not directly cause it; causality is complex and multidirectional.

9
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What is the monoamine hypothesis in relation to MDD?

The monoamine hypothesis suggests that low levels of serotonin, dopamine, and norepinephrine are associated with depressive symptoms.

10
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What role does the serotonin transporter gene (5-HTT) play in MDD?

The 5-HTT gene controls the efficiency of serotonin reabsorption; the short allele variant reduces this efficiency, disrupting serotonin signaling.

11
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How do SSRIs work in the treatment of MDD?

SSRIs block the reabsorption of serotonin, increasing its availability in the synapse, which supports the neurotransmission model of MDD.

12
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What did Caspi et al. (2003) demonstrate about the 5-HTT gene?

Caspi found that individuals with the short allele of the 5-HTT gene were more likely to develop MDD following stressful life events.

13
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What is the DSM-5 and its role in diagnosing MDD?

The DSM-5 is the primary classification system used to diagnose MDD, requiring patients to display 5 or more symptoms for at least 2 weeks.

14
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What are the 9 symptoms used to diagnose MDD according to DSM-5?

Symptoms include depressed mood, anhedonia, significant weight change, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue, feelings of worthlessness or guilt, difficulty concentrating, and recurrent thoughts of death or suicide.

15
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What key change was made from DSM-IV to DSM-5 regarding bereavement?

The bereavement exclusion was removed, allowing for diagnosis of MDD even if symptoms follow the death of a loved one.

16
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What cultural limitations exist in the DSM-5 criteria for MDD?

The criteria were largely developed from Western populations, potentially leading to underdiagnosis or misdiagnosis in cultures with different symptom presentations.

17
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What does the Diathesis Stress Model propose about MDD?

It proposes that MDD develops through the interaction of a biological or psychological predisposition (diathesis) and environmental stressors.

18
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What does 'diathesis' refer to in the context of the Diathesis Stress Model?

Diathesis refers to an underlying vulnerability, which can be genetic, neurobiological, or psychological.

19
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What types of environmental triggers are considered stress in the Diathesis Stress Model?

Environmental triggers include trauma, loss, chronic adversity, or significant life events.

20
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How does the Diathesis Stress Model explain why not everyone with genetic risk develops MDD?

It suggests that both diathesis and stress must be present and interact; individuals with higher diathesis require less stress to develop MDD.

21
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What empirical support did Caspi et al. (2003) provide for the Diathesis Stress Model?

Caspi's study showed that individuals with the short allele of the 5-HTT gene who experienced stress were significantly more likely to develop MDD.

22
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What is the causality of Major Depressive Disorder (MDD)?

MDD arises from the interaction of predisposition and stress, not from either factor alone; causality is interactive and threshold-based.

23
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How does the perspective of MDD integrate different fields?

The model integrates biological and environmental perspectives, providing a more complete explanation than either alone.

24
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What does research suggest about reducing environmental stressors in MDD?

Reducing environmental stressors can prevent MDD even in vulnerable individuals, showing behavior and outcomes are modifiable.

25
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What are common animal models used in MDD research?

Common models include Chronic Mild Stress (CMS), Learned Helplessness, and the Forced Swim Test.

26
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What does the Learned Helplessness model demonstrate?

Animals exposed to inescapable shocks later fail to escape when escape becomes possible, mimicking hopelessness seen in human depression.

27
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What biological markers are examined in animal models of MDD?

Changes in hippocampal neurogenesis, HPA axis dysregulation, serotonin and dopamine pathway disruption, and cortisol levels.

28
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What is a key limitation of animal models in MDD research?

The validity of extrapolating animal findings to human MDD is limited, as animals cannot replicate the full cognitive, emotional, and social complexity of human depression.

29
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What did Rogers & Kesner (2003) find regarding the hippocampus and MDD?

They found that hippocampal dysfunction produced depressive-like behaviors in rats, supporting the biological basis of MDD.

30
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What does Aaron Beck's Cognitive Model of Depression propose?

MDD is maintained by negative patterns of thinking rather than solely by biological factors.

31
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What is the Cognitive Triad in Beck's model?

It consists of negative views of the self, the world, and the future.

32
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How do cognitive schemas relate to MDD according to Beck?

Cognitive schemas are deep-seated belief structures that filter new information and generate automatic negative thoughts when activated by stress.

33
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What are cognitive distortions in Beck's model?

Systematic errors in thinking such as overgeneralization, catastrophizing, and all-or-nothing thinking that maintain the depressive cycle.

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How is Beck's model linked to Cognitive Behavioral Therapy (CBT)?

CBT identifies and challenges cognitive distortions and restructures negative schemas to break the depressive cycle.

35
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What did Alloy et al. (1999) find in their study on cognitive styles?

Students with negative cognitive styles were significantly more likely to develop MDD, providing evidence that negative cognitive schemas precede depression onset.

36
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What is rumination in the context of MDD?

Rumination is the tendency to repetitively and passively focus on symptoms of distress without moving toward active problem-solving.

37
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What does Nolen-Hoeksema's Response Styles Theory suggest about rumination?

Rumination is a maladaptive cognitive response style that prolongs and intensifies depressive episodes.

38
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How does rumination differ from worry?

Rumination is past-focused, replaying negative events, while worry is future-focused.

39
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What is the impact of rumination on mood and motivation?

It amplifies negative mood, increases access to negative memories, impairs concentration, and reduces motivation for behavioral activation.

40
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What did Nolen-Hoeksema (2000) find regarding rumination and MDD?

Ruminative response style predicted future onset of MDD even in initially non-depressed individuals.

41
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What is the Dual Processing Model proposed by Kahneman?

It suggests human thinking operates through two systems: System 1 (fast, automatic) and System 2 (slow, analytical).

42
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How does MDD affect System 1 and System 2 processing?

In MDD, System 1 is dominated by negative thoughts, while System 2 processing becomes impaired, leading to emotionally-biased decisions.

43
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What are the treatment implications of the Dual Processing Model for MDD?

Cognitive interventions can engage System 2 processing to evaluate and restructure automatic negative cognitions.

44
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What did Alter et al. (2007) find regarding cognitive disfluency?

Inducing cognitive disfluency led participants to think more analytically, reducing reliance on intuitive processing, which can help in MDD treatment.

45
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What is the primary cognitive processing imbalance in MDD?

Dominance of automatic System 1 negative processing over deliberate System 2 thinking.

46
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How does the cognitive perspective frame MDD?

As an information processing imbalance rather than purely a biological disorder.

47
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What role does engaging System 2 deliberate processing play in MDD?

It represents a pathway for cognitive and emotional change in MDD.

48
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What do cultural dimensions refer to in the context of MDD?

Value systems and social norms that influence how psychological disorders like MDD are experienced, expressed, and diagnosed.

49
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How do individualistic cultures typically express depression?

Through emotional and psychological symptoms such as sadness and hopelessness.

50
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How do collectivist cultures typically express depression?

Through somatic symptoms such as fatigue, headaches, and bodily pain.

51
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What is meant by 'idioms of distress'?

Culturally specific ways of communicating psychological suffering that may not align with DSM-5 criteria.

52
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How does stigma around mental health vary across cultures?

In collectivist societies, admitting psychological distress may threaten group harmony and bring shame.

53
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What is the imposed etic problem in diagnosing MDD?

Applying Western diagnostic tools like DSM-5 to non-Western populations risks misidentifying or missing MDD due to culturally different symptom presentations.

54
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What did Parker et al. (1999) find regarding MDD symptom profiles?

Chinese patients were more likely to report somatic symptoms and less likely to report emotional symptoms compared to Australian patients.

55
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What does the Biopsychosocial Model propose about MDD?

MDD arises from the interaction of biological, psychological, and social factors, rather than biological factors alone.

56
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What are some biological factors contributing to MDD?

Genetic predisposition, neurotransmitter dysfunction, HPA axis dysregulation, and neuroplasticity changes.

57
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What psychological factors are associated with MDD?

Negative cognitive schemas, ruminative response styles, low self-efficacy, and history of trauma.

58
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What social factors contribute to MDD?

Lack of social support, poverty, chronic stress, relationship difficulties, and exposure to adverse life events.

59
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How does the Biopsychosocial Model inform treatment approaches for MDD?

It integrates multiple levels of explanation and promotes holistic treatment approaches.

60
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What did Brown & Harris (1978) find regarding the onset of MDD?

The presence of a severe life event combined with vulnerability factors significantly predicted the onset of MDD.

61
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What is the difference between domino causality and cumulative causality?

Domino causality suggests a single identifiable trigger, while cumulative causality indicates that MDD results from the accumulation of multiple risk factors over time.

62
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Why is cumulative causality more supported in MDD research?

Individuals rarely develop MDD from a single event; it typically results from multiple overlapping risk factors.

63
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What does the reductionism perspective in psychology entail?

Explaining complex behavior by breaking it down to its simplest components, such as biological mechanisms.

64
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What does the holism perspective argue regarding MDD?

MDD cannot be understood by examining components in isolation; biological, psychological, and social factors must be considered together.

65
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What are the implications of reductionist approaches in understanding MDD?

They provide precise explanations but risk oversimplifying the disorder by ignoring cognitive and sociocultural contributions.

66
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What are holistic approaches to MDD treatment?

Integrating biological, cognitive-behavioral, and social support interventions.

67
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What is the tension between reductionism and holism in psychology?

It reflects the debate between the scientific precision of biological research and the ecological validity of integrative models.

68
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What do Caspi's Diathesis Stress findings and Brown & Harris's model demonstrate about Major Depressive Disorder (MDD)?

They show that MDD emerges through the interaction of multiple factors across biological, psychological, and social domains.

69
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How do reductionist and holistic perspectives differ in understanding MDD?

Reductionist perspectives isolate biological variables, while holistic perspectives integrate multiple domains.

70
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What does reductionism imply about causality in mental health?

Reductionism implies linear single-cause explanations.

71
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What is the risk of relying solely on reductionist biological explanations in treatment?

It risks incomplete treatment; clinicians must consider the whole person.

72
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What is Cognitive Behavioral Therapy (CBT)?

CBT is a structured, evidence-based psychological treatment for MDD developed by Aaron Beck.

73
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What premise does CBT operate on regarding depressive symptoms?

CBT operates on the premise that negative cognitive schemas and automatic distorted thoughts maintain depressive symptoms.

74
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What are the two core components of CBT?

Cognitive restructuring and behavioral activation.

75
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How does cognitive restructuring work in CBT?

It involves identifying and challenging automatic negative thoughts and cognitive distortions.

76
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What role does Socratic questioning play in CBT?

It helps patients examine the evidence for and against their automatic negative thoughts.

77
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How long is CBT typically delivered?

Over 12-20 structured sessions.

78
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What is the effectiveness of CBT compared to antidepressant medication?

CBT is as effective as antidepressant medication for mild to moderate MDD and superior in preventing relapse.

79
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What did Beck et al. (1979) establish about CBT?

They established CBT as an effective treatment for MDD, showing significant reductions in depressive symptoms.

80
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How is obesity clinically defined?

Obesity is defined as excessive body fat accumulation, clinically measured using Body Mass Index (BMI) of 30 or above.

81
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What hormones are key in regulating energy homeostasis related to obesity?

Leptin and ghrelin.

82
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What happens in obesity regarding leptin signaling?

Leptin resistance develops, meaning the brain no longer responds to fullness signals.

83
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What role does the hypothalamus play in obesity?

The hypothalamus regulates appetite and energy expenditure; disruption leads to overconsumption.

84
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What is the heritability percentage of obesity?

Approximately 40-70%.

85
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What environmental factors contribute to obesity?

High availability of calorie-dense processed foods, sedentary lifestyles, and food marketing.

86
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How do psychosocial factors influence obesity?

Stress, emotional eating, socioeconomic status, and cultural norms contribute to obesity.

87
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What does the WHO report about global obesity trends?

Global obesity has nearly tripled since 1975, with over 650 million adults classified as obese.

88
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What is Social Learning Theory in relation to obesity?

It proposes that behavior is learned through observation, imitation, and reinforcement from social models.

89
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What is the most significant social learning mechanism in childhood obesity?

Parental modeling.

90
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How does vicarious reinforcement affect children's eating behaviors?

Children develop positive associations with foods they see peers rewarded for consuming.

91
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What role does self-efficacy play in healthy eating?

Individuals with low self-efficacy for healthy eating are less likely to initiate or maintain behavior change.

92
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What interventions can reshape food-related behaviors according to Social Learning Theory?

Interventions using positive role models, peer support, and media literacy.

93
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What did Brown & Ogden (2004) find regarding parental and child eating behavior?

They found significant correlations, particularly in snack food consumption and body dissatisfaction.

94
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What did Aghasi et al. (2020) discover about digital food environments?

Greater exposure to digital food environments was significantly associated with increased consumption of unhealthy foods.

95
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What factors contribute to eating behaviors that lead to obesity?

Social models, media exposure, and vicarious reinforcement.

96
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How does the sociocultural perspective explain obesity?

It highlights how social learning environments shape food behavior, complementing biological explanations.

97
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What is a pathway for behavior change in obesity prevention?

Modifying social models, peer environments, and digital food exposure.

98
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How do cultural dimensions influence obesity prevalence?

They shape attitudes toward body weight, food consumption, physical activity, and healthcare-seeking behavior.

99
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In collectivist cultures, how is larger body size perceived?

As associated with prosperity, health, and social status, which can normalize obesity.

100
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What is the difference between individualistic and collectivist cultures regarding health responsibility?

Individualistic cultures emphasize personal responsibility, while collectivist cultures view eating as communal and celebratory.