psyc 337 post midterm 2 content ( EDs and Schizophrenia)

Eating disorders

Diagnosed categorically in DSM

Dietary restriction

Actual reduction in overall caloric intake (ex; sipping meals, delaying eating)

Cognitive restraint

The intention and or attempt to restrict caloric intake

Binge eating

The consumption of an objectively large amount of food, sense of loss of control over one's eating, occurs within a discrete period (approx 2 hours)

Compensatory behaviours

Methods to compensate for caloric intake/food eaten

Purging

Self-induced vomiting, laxatives, diuretics

Compensatory exercise

Exercise to compensate for caloric intake

Weight and shape concerns

High levels of body dissatisfaction, preoccupation with weight/shape, significant role in evaluating oneself, extreme fear of gaining weight

Anorexia nervosa

Significant low weight (BMI below 17.5), intense fear of weight gain, overevaluation of weight and shape

Subtypes of anorexia nervosa

Restricting, binge eating/purging type

Avoidant restrictive food intake disorder (ARFID)

Eating or feeding disturbance associated with significant weight loss/failure of weight gain, nutritional deficiency, dependence on feeding through tube, marked interference with psychosocial functioning

Exclusion criteria for ARFID

No overvaluation of weight or shape

Bulimia nervosa

Recurrent binge eating (once a week for past 3 months), recurrent compensatory behaviours, overevaluation of shape and weight

Binge eating disorder (BED)

Recurrent binge eating with 3/5 accompanying features, marked distress, not associated with inappropriate compensatory behaviours

Other specified feeding or eating disorders

More prevalent than other eating disorders

Atypical anorexia nervosa

All criteria for AN are met but weight within normal range

Purging disorder

Recurrent purging behaviour to influence weight or shape in the absence of binge eating

Night eating syndrome

Recurrent episode of night eating after falling asleep/evening meal

AN 1 year prevalence

0.0 - 0.05 %

ARFID 1 year prevalence

1.98 %

BN 1 year prevalence

0.14% to 0.3 %

BED 1 year prevalence

0.44%- 1.2 %

OSFED 1 year prevalence

1.66 %

ARFID age of onset

Approx. 8 years

AN/BN age of onset

Adolescence/young adulthood

BED age of onset

Late adolescence, early adulthood

Comorbidity of EDs

Rates range from 87% - 94% (ex: mood disorders, anxiety disorders, SUD)

Health consequences of EDs

Cardiovascular disease, higher risk for attempted suicide and non-suicidal self-injury, metabolic disorders

Heritability of eating disorders

Mean heritability is about 50 % for AN, BN, BED; 0 % genetic contribution before puberty

Cognitive behavioural model (EDs)

Evaluation based on weight, shape, eating habits, and control over these things; maintenance of disorder caused by dysfunctional system in terms of evaluating self-worth

Dietary restraint model

Physiological and cognitive deprivation from dietary restriction leads to loss of control eating and further attempts of restrictions

Thin ideal internalization

Extent to which an individual buys into socially defined ideals of attractiveness, leading to body dissatisfaction

Familial influence on disordered eating

Appearance-focused culture within family increases disordered eating and body dissatisfaction

Parental fat talk

76 % directed towards themselves, 51 % towards other people, 43.6 % directed towards child

Parental self fat talk

Associated with parental pathology

Parental fat lack towards child

Associated with child eating pathology

Danger of weight stigma

Stigmatizing experiences associated with unhealthy eating patterns

Fiji study (Becker et al)

Assessed impact of novel prolonged exposure to TV on disordered eating attitudes of girls living in Fiji

Fiji's ED prevalence

Low prevalence rates of EDs and lack of exposure to TV in the 90s

GLP-1 agonist

Used in BED → reduction of binge episodes and weight

GLP-1 agonist mechanism

Works by modulating hunger/satiety and emotional responses to food

Schizophrenia

Characterized by disorganization of thought process and split from reality

Dementia Praecox

Something that looks like early onset dementia, characterized by progressive deterioration

Emile Kraepelin

First to propose grouping of psychotic syndromes

Eugen Bleuler

Introduced term schizophrenia (split-mind)

Schizophrenia onset

Often strikes in adolescence or young adulthood

Six major signs/symptoms of schizophrenia

Disturbances in perception, content of thought, form of thought, affect, psychomotor, disorder of relating

Disturbances in perception

Hallucinations can occur in all sensory modalities

Delusions

False belief based on incorrect inference despite contradictory evidence

Types of delusions

Controlled by external force, grandiose, jealousy, nihilistic, persecutory, delusion of references, somatic delusion

Formal thought disorder

Includes derailment, word salad, alogia, neologism, blocking, illogical thinking

Affect in schizophrenia

Includes blunted/flat affect, inappropriate affect, problems perceiving others' emotions

Catatonia

Behavior not contingent to what is happening in the environment

Positive symptoms

Presence of symptoms that shouldn't be there (e.g., hallucinations)

Negative symptoms

Absence of something that should be there (e.g., blunted affect, alogia)

DSM-5 criteria for schizophrenia

Need at least two symptoms present for 1 month, signs dating 6 months

Schizoaffective disorders

People with schizophrenic features and severe mood disorder

Lifetime prevalence of schizophrenia

0.7-1%, M 1.4: 1 F

Estrogen and schizophrenia

May be protective of schizophrenia, second wave of increase postmenopausal

Late onset of schizophrenia

More common in women than men.

Onset of schizophrenia for men

Highest risk between 18 - 24 years.

Onset of schizophrenia for women

Second bump postmenopausal.

Schizophrenia under age 13

Rare, more common in boys, characterized by early speech and language problems.

Course of schizophrenia

Only 20 - 30% can live independently.

Schizophrenia recovery study

Only 40% had one or more periods of recovery.

Life expectancy in schizophrenia

People with schizophrenia die 20 years younger than the general population.

Good prognostic indicators of schizophrenia

Good premorbid adjustment, acute onset, main depressive symptoms.

Bad prognostic indicators of schizophrenia

Poor premorbid adjustment, insidious onset, negative symptoms.

Comorbidity in schizophrenia

Substance abuse is common, especially alcohol and nicotine.

Suicide risk in schizophrenia

20% will attempt suicide, 5% will die.

Schizophrenia and violence

Slight increase in risk for aggressive behavior, but most are victims.

Genetic risk factors in schizophrenia

Risk increases with genetic relatedness to proband.

Twin studies in schizophrenia

Higher concordance for MZ twins (28%) than DZ twins (6%).

Perinatal complications

Increase genetic risk factors for schizophrenia.

Endophenotype

Intermediate step between genes and experiential phenotype.

Eye tracker abnormalities

Seen in 50% of people with schizophrenia → possible endophenotypes

Social causation theory

Low SES is proposed to cause schizophrenia.

Social selection/downward drift theory

Becoming ill makes you descend the economic ladder.

Advanced paternal age

Increases risk for schizophrenia in offspring ( novo mutations in sperm cells)

Birth complications

Patients more likely to have experienced complications like hypoxia.

Prenatal exposure to viral infections

Increases risk of schizophrenia later in life.

Season of birth risk factor

Increased rates for those born in late winter and early spring.

Malnutrition in pregnancy

Higher rates of schizophrenia in children born during the Dutch hunger winter.

Neurodevelopment in 2nd trimester

Disruptions can affect neural connectivity and migration.

Schizophrenia brain volume

Decreased brain volume and progressive loss of gray matter over time.

Gray matter deficits in twins

Evident in discordant MZ twins of people with schizophrenia.

Dopamine hypothesis

Antipsychotic drugs work on DA system by blocking D2 receptors.

Cocaine and amphetamines

Boost DA reactivity → psychosis, paranoia, distorted sense of reality.

Excess DA transmission

Excess DA transmission in striatum, reduced DA transmission in frontal lobes.

Aberrant salience

Increased DA may cause patients to attend more to irrelevant stimuli making it difficult to make sense of everyday life.

Movement abnormalities

Oral facial, upper limb dyskinesias.

DLPFC activity

DLPFC activity (important for working memory) heavily regulated by DA - cognitive deficits consistent in schizophrenia.

Working memory deficits in schizophrenia study

People with schizophrenia are much worse at remembering where the target was after distractor (unique to schizophrenia; people with bipolar did not have same deficits).

Deficits evident

Deficits evident when ill and healthy, including college students with schizotypal symptoms, 1st degree relative.

Cannabis use and schizophrenia

People with schizophrenia 2 times more likely to consume marijuana.

Dose response relationship

More frequent use of higher potency cannabis associated with greater risk of schizophrenia.

Cannabis associated with earlier onset

Use of cannabis associated with earlier onset.

Brain volume changes study

Patients with schizophrenia not using cannabis show reduction but is much more pronounced in those using cannabis at baseline.

Cannabis natural experiment

91,106 individuals (0.7%) developed schizophrenia in general population without CUD vs 10,583 (8.9%) of those with CUD.

PARF

Population attributable risk fraction — proportion of disease cases in population that can be attributed to specific risk factor.