Abnormal Psychology: Biological Etiology of MDD

etiology

a set of causes of a disease or condition

(separated into biological, cognitive and sociocultural)

The Falconer Model

assumes that phenotype is comprised of three types of influences: Genetics, Shared environment, Individual Environment

Implications of Sullivan, Neale and Kendler (2000)

established the estimate of heritability of major depression at A = 37%, with a minimal contribution of shared environment (C=0%) and a substantial contribution of unique/individual environmental factors (E =63%)

Aim of Kendler et al (2006)

Aim: To compare genetic effects on MDD first in males and females and second across different generations.

Conclusion of Kendler et al (2006)

Conclusion: Heritability of MDD was significantly higher in women than men

No evidence was found for differences in the roles of genetic and environmental factors across genterm-16erations

phenotype

Observed characteristics such as the presence of symptoms of MDD. Comprised of three types of influence: genetics, shared environment, and individual environment. Can be written in the following form: 1= A+C+E

Gene-environment interaction

occurs when two different genotypes respond to the same environment in different ways

Aim of Silberg et al (1999)

investigated the link between susceptibility to depression and environmental factors (stressful life events)

Conclusion of Silberg et al (1999)

The effect of negative life events on depressive symptoms in adolescent girls was stronger, suggesting that genetic predisposition causes girls at this age to be more vulnerable to negative or stressful events.

Implications of Silberg et al (1999)

Results exemplifies one of the ways in which genes may interact with the environment: environmental factors serve as necessary mediators or triggers for genetic predisposition

Molecular genetics

allows us to identify specific genes influencing complex psychological disorders

Method of Caspi et al (2003)

Longitudinal study on possible role of gene 5-HTT in depression.

Conclusion of Caspi et al (2003)

found that a functional polymorphism in a serotonin transporter gene (5-HTT) moderated the influence of stressful life events on depression.

What was the theory of Chiao and Blizinsky (2010)?

"culture-gene coevolution theory"

"culture -gene coevolution theory"

posits that cultural values buffer genetically susceptible populations from increased prevalence of affective and mood disorders

Gene environment correlation

Genes and environment are important in determining he development of a mental disorder.

Breakdown of phenotype

A=genetics

C=shared environment

E= and individual environment

Gene-Environment Correlation (rGE)

Gene predisposition can influence the environment.

Gene-Environment Interaction IGxE)

Different genotypes will react differently to the same environment. For example: predisposition will make people more vulnerable to stressful events.

Passive gene-environment correlation (passive rGE)

Parents provide a rearing environment. Genes and environment are correlated. Ex. Parents might pass a genetic predisposition to depression and provide a high-demanding stressful environment.

Strengths of Genetic argument for MDD

Twin studies are highly reliable, large samples now have revealed a lot of genetic variation. Modern research sees interaction between environment and biology.

Limitations of Genetic Argument for MDD

Correlational studies do not establish cause and effect. Twin studies lead to validity issues. It is impossible to isolate and control all variables. Genetics DO NOT explain symptomology differences.

Selective Serotonin Reuptake Inhibitors (SSRIs)

classification of drugs that present the reuptake of serotonin. Class of drugs that are used as antidepressants for the treatment of MDD and anxiety disorders.

"Treatment etiology fallacy"

the mistaken belief that the effectiveness of a form of treatment indicates the cause of a disorder.

Aim of Chiao and Blizinsky (2010)

examine the association between cultural values of individualism-collectivism and the frequency of allele variations of the serotonin transporter gene 5-HTT relating to global variation in the prevalence of affective disorders

Bidirectional ambiguity

An uncertainty in whether or not x causes y, or if they are simply correlated.

For example, serotonin hypothesis

neurogenesis theory of depression

an explanation of depression that proposes that neurogenesis, the growth of new neurons, in the hippocampus stops during depression, and when it resumes, the depression lifts

niche-picking

tendency to actively choose environments that complement our heredity

Falconer model

assumes phenotype is made of influences such as genetics, shared environment and individual environment. This is made up of 3 influences: Genetic inheritance, shared common environment, and individual environment. (I=A+C+E)

. Hasler (2010)

argues against a single hypothesis of depression; he suggests that depression is a complex disorder that involves the interaction of a number of factors.

ABC'S of MDD

Affective symptoms: feelings of guilt and sadness; lack of enjoyment or pleasure in familiar activities or company;

Behavioural symptoms: passivity; lack of initiative;

Cognitive symptoms: frequent negative thoughts; low self-esteem; suicidal thoughts; irrational hopelessness; may also experience difficulties in concentration and inability to make decisions;

Somatic: loss of energy, insomnia, or hypersomnia; weight loss/gain; diminished libido.

How long must a person show symptoms of depression before they can diagnosed?

2 Weeks

Sullivan et al. (2000)

concluded that there is not a single gene that leads to depression, but rather that depression is the result of several genes that act together to produce a vulnerability to depression when other risk factors are present.

Cai et al (2015),

- found genetic sequences that seemed to be linked to depression

-gene which is important for energy-producing cell structures called mitochondria.

neurogenesis theory of depression

an explanation of depression that proposes that neurogenesis, the growth of new neurons, in the hippocampus stops during depression, and when it resumes, the depression lifts

HPA-axis hyperactivity

one of the most consistent biological findings in anxiety- and depression-related disorders.

-results in the over-secretion of cortisol.

Result of over secretion of cortisol

leads to reduced serotonin and other neurotransmitters in the brain, including dopamine, which has been linked to depression.

Malberg et al (2000)

treatments increased neurogenesis in the hippocampus and proposed that this increase is a mechanism to fight depression

Videbech and Ravnkilde (2004)

A hippocampal reduction could explain the common symptom of memory problems in patients with depression.

How many genes may be linked to depression?

Eleven genes - but we are not sure exactly the role they play.

What is the key advantage of using GWAS (genome wide association studies) as in the study by Cai et al (2015)?

Large sample size

Which of the following is evidence in support of the neurogenesis theory of depression?

Depressed patients have smaller hippocampi than the general population.

Cortisol and Depression

increased MAO-A Enzyme which breaks down serotonin

Cortisol impacts prefrtonal cortex and hippocampus