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Extensive lecture/article summary of pharmacological and biological approaches to clinical and health psychology

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Course
Pharmacological and Biological Approaches to Clinical and Health Psychology (6463PS025Y)

Institution
Universiteit Leiden (UL)

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Uploaded on June 1, 2023
Number of pages 50
Written in 2021/2022
Type Class notes
Professor(s) Dr. a.i.m van laarhoven & dr. p.l.j. putman
Contains All classes

neuroendocrinology
genetics
g x e
pituitary gland
pituitary adrenal axis
gnrh
cortisol
neuroscience
action potentials
neurotransmission
pharmacokinetics
pharm
ionotropic amp metabotropic receptors

Institution
Universiteit Leiden (UL)
Education
Psychologie
Course
Pharmacological and Biological Approaches to Clinical and Health Psychology (6463PS025Y)

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Case Ellen why?:
- Genetic sensitivity for RA & depression
- Neurobiological: functional and structural changes in brain network
- Neuroendocrine system: role serotonin in depression; depression & RA more in females than males
- Immune system: immunological changes due to depression & chronic inflammation in RA
- Interaction between all these psychobiological processes → multidimensional target for
intervention

Interaction psychobiological processes:

Genetics:
- Mechanisms:
*Phenotype = observable outward appearance of a cell or organism (e.g. eye color, organ
structures, blood group, personality traits and behavior)
*Genotype = the genetic make up of a cell or organism
*Nature/heredity = transmission of characteristics of a person is based on genetic material
*Nurture/environment = the surroundings of a person affect the development &
characteristics of the person
- Nature and nurture are inseparable:
*Genes contributing to a certain pathology do not always lead to that disease
*”Sensitivity” genes merely set a threshold for the environmental factors to
cross

Genome: chromosomes, DNA and genes
*Chromosomes: entire set of human DNA = genome
- Autosome = non sex chromosomes
- Consist of DNA, which is winded by histones to fit in the cell’s nucleus
*DNA consists of:
- Sugar-phosphate group
- Bases in pairs (A – T & G – C) (sugar-phosphate group + base = nucleotide)
*Genes encode for proteins:
- Gene = part of DNA encoding for 1 protein
- Gene = specific base pair order is template for proteins: building blocks of body;
starts with promotor region and ends with terminator region
- From gene to protein:
*DNA transcribed into mRNA:
*mRNA translated into protein

,From genotype to phenotype:
- Genetic variation:
*Genotype = individuals genetic constitution, overall or at specific gene
*> 99% of DNA is similar across humans → genes are “fixed”
*< 1% differs across individuals (due to mutations or polymorphisms (inherited))
1. Mutations in DNA cause a permanent change in DNA, for example:
- Base-change
Deletions or duplications of DNA stretch (>
- Deletion of base segments
1000 nucleotides)
- Duplication of base segments
- When DNA is not repaired, it can lead to changes in proteins
2. Polymorphisms: multiple frequent variants of gene in population (transmitted to
subsequent generations without causing major defects in biological functions)
- Variable number of tandem repeats
- Single nucleotide polymorphisms = SNPs
- Mendelian inheritance
*Dominant vs. recessive alleles (= variants of genes)
*Homozygous vs. heterozygous
- Not for every cell all proteins encoded in the DNA are needed
*Protein production is dynamic & continuously influenced by various factors:
1. Interactions of genes (= epistasis)
*Allele at one locus interferes or masks an allele at another locus
2. Regulation of gene expression (= epigenetics)
*A series of biochemical processes through which changes in gene expression
are achieved throughout the lifecycle of an organism without change in DNA sequence
*Genes are switched on or off by environmental factors

Epigenome:
- Is changeable
*During different times in life (development, requires epigenetic memory)
*Constantly throughout the day
*Epigenetic signals come from inside the cell, neighbouring cells and from the exterior (e.g.
queen bee: has same DNA but different diet which makes her more suitable for creating offspring).
*There are risk factors as well as protective factors, they are both as important
- Examples of environmental epigenetic factors: Diet, Season (daylight), Exercise, Diseases exposed
to, Drugs used, Negative life events, e.g., childhood maltreatment, Social support

Epigenetic gene regulation:
- Example of baby rats and maternal care:
*Offspring of caring mother rats show different expression of cortisol receptor and
decreased stress response than offspring of mother rats caring less
*Humans: maltreatment decreased glucocorticoid receptor expression and increased stress
response
- Environment → chemical modifications (epigenetic factors) to histones or DNA → changes
accessibility to DNA transcription machinery
*Gene modification: e.g. tags on promotor region (start of gene)
*Histone modification (affecting a stretch of DNA)
- Thus, phenotype (observable characteristics) is dependent on genetic constitution and the
expression of genes (phenotype = G x E, nature + nurture)

,Studying G x E:
- Comparing cases and controls in:
*Pedigree (family) studies
- Particularly good for rare diseases caused by rare mutationF
*Twin studies:
- Similar genes (monozygotic twins)
- Different epigenomes due to different environment
*Population studies
- Genetic association studies → 2 approaches:
*Candidate-gene association study: testing a priori hypothesis that specific genes (also with
low allele frequencies) are associated with disease, e.g. based on biological mechanisms
*Genome-wide association study: test over 1 billion genetic variants that are frequent in the
population (SNPs). Requires very large sample size to indicate small contribution of frequent alleles.

Genetics & psychobiology: applications
- GxE in:
*Medical diseases:
- allergy
*Psychopathology:
- Major depressive disorder
- Schizophrenia
*Clinical applications
- Gene environment interaction (G x E):
*The importance of G & E varies across medical diseases:

- 1 gene (/chromosome): down’s syndrome 100%, for example explained by trisomy
rd
21 (3 copy of chromosome 21- copy number variation)
- Multiple genes and environmental factors: interact and their expression may differ
= the case for most diseases
- G x E models to explain the interaction (see slide 54)
*Biological interaction: dependence of the effect of one factor at cellular or molecular level
on the presence or absence of the other

Allergy: indication for G x E
- Why:
*hay fever, asthma, eczema or food allergy
*Early manifestation of immune dysregulation
*Considered ‘classic psychosomatic disorder’: good example of G x E:
- Complex interactions
- Better understood than psychopathologies (clearer environmental factor?)
*Socially relevant: high prevalence (30% of Western population) & dramatically increasing
- Genes: higher allergy rate within families and twins (ca. 35-75% explained genetically)
- Environment:

, *Incidence increase too rapidly to be explained genetically
*More allergies in developed countries (hygiene hypothesis = better hygiene → allergy)
*Influence of psychological factors, e.g. psychosocial stress increasing incidence, probability
of symptom exacerbation and severity of condition
- G x E: allergy – complexity:
*Heterogenous disease: multiple genes and multiple environmental factors (&interactions)
*Time window of exposure of environmental risk factors
*Not all environmental factors usually measured

Complex G x E: psychopathology
- Based on twin studies
*Heritability gap: twin studies seem to overestimate genetic component → twins also share
environment
- G x E major depression:
*Mainly based on candidate-gene association studies: indications for higher risk of
depression:
-Short allele of serotonin transporter x stressful life events or childhood
maltreatment
→ Role of monoamines (including serotonin) in depression according to the
revised monoamine hypothesis
→ Antidepressants increase levels of monoamines
- Discrepancies between studies:
-Findings from candidate-gene association studies are not always replicated by GWAS:
*Candidate-gene studies often underpowered (too small sample size)
*Biological hypothesis difficult to formulate
*Multiple genes play role (polygenic)
*Environmental factors
*Differential susceptibility averages out the impact of genes (see slides 72)

G X E in major depression: based on GWAS & candidate gene association studies:
- Polygenic: > 100 loci involved
- Evidence for interaction with: childhood, trauma, socioeconomic adversity, social support and
physical activity

G X E: Schizophrenia
- Candidate gene studies: risk of schizophrenia COMT-gene (polymorphism determines efficiency of
dopamine metabolizing enzyme) x active cannabis use during adolescence
*Hypothesis of schizophrenia: cannabis triggers dopamine release
*Antipsychotic drugs suppress dopamine receptor
*Individuals with specific genotypes: suggested to avoid/limit cannabis use
- GWAS meta-analysis confirms role of dopamine

G x E: psychopathology in progress
- Because psychopathologies are polygenic & involve many environmental factors, there is a need
for:
*Systematic & replication of GWAS incorporating G x E: genome wide gene-environment
interaction studies (GWEIS) → though larger n required due to more statistical tests
*Careful assessment of environmental factors:
- Prenatal – adulthood

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