Anorexia: Biological Explanation - Genetics Flashcards

(30 cards)

1
Q

What is a gene?

A

A sequence of DNA that codes certain information.

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2
Q

What is a genome?

A

All genes in a cell.

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3
Q

How many pairs of chromosomes do we have?

A

23

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4
Q

What is a dominant gene?

A

A gene that only needs 1 chromosome for an observable characteristic (phenotype) to show.

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5
Q

What is a recessive gene?

A

A gene that needs 2 of the same chromosome for an observable characteristic (phenotype) to show.

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6
Q

How are genetics studied in psychology?

A

Twin/adoption studies.

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7
Q

What are the two types of twins?

A
  • Monozygotic

- Dyzygotic

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8
Q

What are monozygotic twins and so how much DNA do they share?

A

Identical - 100%

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9
Q

What are dyzygotic twins and so how much DNA do they share?

A

Non-identical - 50%

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10
Q

Briefly explain what measure determines if a behaviour is genetic in twin studies.

A

Concordance rates, the higher the rate the more likely the behaviour is to be genetic.

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11
Q

List 3 strengths of twin studies.

A
  • High reliability- Uses scientific methods such as DNA sequencing which provides objective quant data
  • High validity- MZ and DZ twins are naturally occurring variables so low researcher bias
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12
Q

List 3 weaknesses of twin studies.

A
  • Low generalisability- MZ twins may not be representative of other twins in a different environment
  • Low reliability- Environmental differences between MZ and DZ twins may be hard to compare due to differences
  • Low validity- One twin of an MZ pair may be exposed to different environmental triggers for one gene
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13
Q

What would anorexia being a cause of genes imply in regards to twins?

A

That frequency is higher in MZ than DZ twins.

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14
Q

Define ‘heritability estimate’.

A

The percentage that a characteristic is due to genes.

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15
Q

How is a heritability estimate often calculated?

A

Looking for similarities between families and twins in relation to that characteristic.

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16
Q

Identify 3 supporting pieces of evidence for anorexia being a cause of genes.

A

1) Kipman et al (1999)
2) Holland et al (1988)
3) Scott-Van Zealand et al (2013)

17
Q

What did Kipman et al (1999) find in regards to the cause for anorexia.

A

Kipman et al (1999) supports the genetic cause of anorexia. Kipman looked at many twin studies involving anorexia, and produced a heritability estimate of 71%- given that 46.2% of 106 MZ twins involved were concordant for the disorder, and 7.1% of the DZ twins was concordant. This therefore demonstrates that anorexia has genetic components

18
Q

What did Holland et al (1988) find in regards to the cause for anorexia.

A

Holland, Sicotte and Treasure can be used to support the genetic basis of AN, through studying AN in MZ and DZ twins. In each case, at least one of the twins in each pair had a diagnosis of AN, and over a period of time, interviews were carried out to check the incidence of AN in the other twin. A significant difference of a much higher concordance rate of AN in MZ twins (56%) than DZ (7%). This therefore supports the idea that AN can be genetically inherited and there may be a biological predisposition to developing it.

19
Q

What did Scott-Van Zealand et al (2013) find in regards to the cause for anorexia.

A

Scott van Zealand can be used to support a genetic basis for AN. He looked at genetic variants associated with development of AN, and compared 261 AN twins wuth 73 twins, and compared this to a data base of 500 twins with and without AN. Scott van Zealand found that not one gene variant worked in isolation to explain the cause of AN- (ITPR-3 and EPHX-2). Overall, he concluded that genes may increase the risk of anorexia, but are not a direct cause of it (use as evidence for biological determinism)

20
Q

Evidence in family studies about the genetic basis of AN .

A

Grice et al (2007) supports the idea of a genetic basis for AN. The study followed 192 families where one member had received a diagnosis and then at least one other also had received a diagnosis. Grice then focused on a subgroup of 37 families where at least two relatives had been diagnosed with a restrictive type AN, and found a genetic link on chromosome 1 in family members of the individual with AN. Grice concluded that an individual who is a first degree relative of someone who has had or currently has an eating disorder is 7-12x more likely to have one themselves- thus suggesting there is a biological component found in genetic inheritance to the development of AN.

21
Q

What did Garner and Fairburn (1988) find in regards to the cause for anorexia.

A

However, Garner and Fairburn (1988) rejects the genetic cause of anorexia. They argued that the increase in eating disorders of 15 in 1979 to over 140 in 1986 cannot be genetic due to no major genetic changes in the past 3 decades. Therefore there must be other factors involved such as the environment that is experienced, so social leaning theory is a better explanation, as this can explain how the rise in social media has contributed to the rise in eating disorders.

22
Q

Using the acronym ‘GRV’, evaluate a low ‘generalisability’ point for research into anorexia being genetic.

A

A weakness of supporting evidence from ….. is that it has low generalisability. This is because sample sizes are often small and unrepresentative as twins only make up 1.5% of the population. This therefore cannot be generalised to people who don’t have a twin, reducing its usefulness as an explanation for the cause of AN.

23
Q

Criticism of theory (concordance).

A

However, a weakness of this theory is that it lacks credibility. There is never a 100% concordance rate for anorexia being genetic in twins- despite sharing 100% of DNA in MZ twins. Therefore there must be other factors such as the environment affecting whether or not someone develops anorexia with different interactions stimulating different genes, so stress-diathesis model is a better explanation.

24
Q

Suggest an alternative explanation for the development of anorexia.

A

Social Learning Theory can be used as an alternative explanation. Someone may idolise a role model who they pay attention to being praised for being skinny by the media. By constantly seeing this person in magazines and on their social media feed, they are able to form mental images and retain the behaviour which they complete of exercise regimens and their diet plan, and so they may reproduce this behaviour by starving themselves to be as skinny as them, receiving motivation through external reinforcement of praise for weight loss from friends. This therefore demonstrates that anorexia may instead be a disorder caused by the environment, not by biology.

25
Describe a conclusion to the argument of anorexia being biological.
Anorexia may not be completely genetic. The interactionist theory of diathesis-stress model states that someone may be predisposed to developing anorexia but environmental stressors trigger the disorder instead of the genes themselves.
26
Name 4 genes which can be linked to the development of AN
* ITPR-3 * EPHX-2 * DAT-1 * Taq-1 allele
27
Describe the ITPR-3 gene and how it is linked to AN
* codes for a protein involved in detecting the taste of food, such as bitter and sweet. * if this gene is faulty, it could mean that they are unable to use pleasant taste as a motivator to eat * hence predisposition to AN
28
Describe and explain how EPHX-2 is related to the development of AN
* has links to the thalamus- which regulates hunger levels and regulates cholesterol metabolism * if this gene has faults with coding it could mean that the thalamus may not be able to regulate hunger levels efficiently, so explains why those with AN have less of a desire to eat * also codes for an enzyme which regulates metabolism * also has links to the amygdala which regulates the fear response * faults within coding can affect the regulation oof the amygdala- explaining the fear around food/gaining weight
29
Describe and explain the link between DAT-1 allele and the development of AN
* specific gene linked to reward when eating food deemed as desirable * releases dopamine when eating a pleasurable food * motivates a person (if coded correctly) to eat again * if there are faults within coding, dopamine activity is disrupted and becomes disregulated * this causes a lack of motivation to keep repeating eating food that others may get * so predisposition to AN
30
Describe and explain how the Taq-1 allele is linked to the development of AN
* gene that is linked to addiction. * often mutated in those with AN * this could explain the obsessive behaviour over diet/exercise regimes or even body appearance * can explain addiction to monitoring calorie intake