AN- One biological explanation Flashcards
What did Kipman et al discover the concordance rates in twins were for AN?
MZ- 46.2%
DZ-7.1%
What did Woodside et al discover in his family study related to AN?
Found that first degree relatives are more likely to share having anorexia than 3rd degree relatives.
First degree relatives share more genetics than 3rd.
What specific genes could be related to anorexia ?
- EPHX2
- ITPR3
- DAT1
5-HTR2 (seretonin)
What role does the EPHX2 gene play?
• This gene produces an enzyme that
helps regulate cholesterol metabolism.
• Cholesterol metabolism is connected
to serotonin, a chemical linked to
anxiety and depression.
• The gene also influences parts of the
brain involved in eating and hunger
(the hypothalamus) and the fear
response (amygdala).
What problem does a problem to the EPHX2 gene mean?
Problems with this gene’s expression
may cause fear, and low mood around
food due to its impact on both hunger, regulation and fear response
What does the ITPR-3 gene code for?
This gene codes
for a protein
involved in
detecting the taste
of food, such as
bitter and sweet
What happens if there is a fault to the ITPR-3 gene?
If this gene is
faulty in those with
AN it could mean
they are unable to
use taste as a
motivator to eat.
What does the DAT-1 gene code for?
DAT1 is a specific gene
linked to the function of
dopamine on the reward
system.
What happens if there’s a fault to the DAT-1 gene?
• If the gene is mutated
this can mean dopamine
activity is disrupted,
resulting in lack of
motivation and
satisfaction others would
normally get after
eating.
What is a weakness of explaining AN solely by a single gene?
No one gene can explain the physical, cognitive and behavioural symptoms of AN.
Oversimplification
What is the equal environments assumption (EEA) and how does it affect twin studies?
EEA assumes MZ and DZ twins are raised in equally similar environments. If MZ twins are treated more similarly, higher concordance may reflect shared environment, not genetics.
How did Jay Joseph (2002) critique the validity of twin studies on AN?
He argued that MZ twins often experience more similar environments than DZ twins (e.g. parental treatment, appearance), which could inflate heritability estimates.
Why is the genetic explanation of AN considered overly simplistic by some researchers?
AN is polygenic—many genes contribute in small ways to different symptoms. A single-gene explanation cannot account for the complexity of physical, cognitive, and behavioural symptoms.
What is a practical strength of understanding the genetic basis of AN?
It could lead to better prevention and treatment, such as early intervention based on genetic risk and the development of targeted drug therapies.
