obesity- biological explanations Flashcards

1
Q

how do we know it may run in families

A

There is a substantial genetic component to obesity
Twin studies are some of the best evidence for a genetic component.

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2
Q

who researched it running in families

A

Chaput et al (2014)

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3
Q

who research the twin studies of it

A

Nan (2012)

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4
Q

Chaput et al (2014)

A

Obesity may run in families – 20-50% concordance rate for first-degree relatives

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5
Q

Nan (2012)
good evidence to use

A

[meta analysis :12 twin studies] [8,000 MZ and 10,000 DZ]
Concordance rates ranged from 61% to 80%,
They found this was influential from late childhood through adolescence into adulthood.

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6
Q

polygenetic meaning

A

2 or more different genes

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7
Q

Obesity= polygenic and perhaps different genes may influence different aspects of obesity

A

not a flashcard dawg
carry on going
u wanna go to a good city to go cleerrbb
u got this

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8
Q

obesity slide 5!
who researched this

A

Locke (2015) Polygenic
Watson (2009)

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9
Q

what did Locke (2015) uncover

A
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10
Q

what did Watson (2009) uncover

A
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11
Q

what is the thrifty gene hypothesis

A

suggests that genes promoting fat storage were advantageous for survival in ancestral environments with scarce food but have become maladaptive in modern contexts with food abundance
this is not a useful adaptation

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12
Q

what is a problem with this explanation that we need to be aware of
think our environment and cause and effect ish
if the cause and effect thing isnt right soz pls dont blame jan 2025 you!

A

It is almost impossible to separate shared genetic influences and from shared environmental influences.

We live with our parents and siblings; we might be learning their bad habits. We can’t prove either way

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13
Q

what is a weakness of this explanation

A

Doesn’t explain recent rise in obesity
Genetic explanations cannot adequately explain the upsurge in obesity over the last 20 years. Genes for humans have not changed that much unlike environmental factors such as the variety, availability and affordability of food. This undermines genetic influences and suggests the environment may play a larger role (urbanization reduced the need for physical activity, more screen time etc)

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14
Q

what is the neural explanations (not the hormones)
just like a over view
dont be too hard on yourself if you dont get this first time!

A

Abnormalities in the neural and hormonal mechanisms that control of feeding behaviour led to overeating.
In turn this makes us obese.
Physical damage or malfunctioning in hypothalamic centres.
If the Ventromedial hypothalamus is affected, then appetite is unregulated.

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15
Q

what part in the hypothalamous has involvement in appetite

A

the arc nuclei

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16
Q

what’s the arc nuclei’s role

A

Within the hypothalamus, the arcuate nucleus [arc], has been identified as responsible for appetite and therefore obesity.

Were the arcuate nucleus to be damaged we could overeat and this could cause obesity.

17
Q

whats leptins role

A

Leptin inhibits food intake by acting on leptin receptors in the hypothalamus.
As Leptin has a central role in regulating appetites any deficiency Leptin or be a risk factor in obesity.
some individuals lack leptin due to a gene mutation so do not receive the message in the VMH to stop eating when full

18
Q

what did Coleman 2010 suggest

A

Some people may have a lack of sensitivity to Leptin or may not some produce any at all
Each of which would make them vulnerable to obesity

19
Q

what other 2 hormones may have an effect

A

serotonin and dopamine

20
Q

are high or low levels associated with obesity

21
Q

what’s serotonins involvement

A

Serotonin normally signals to the VMH that a person has eaten to satiety so when low this creates inaccurate satiety signals to the hypothalamus, disinhibiting eating behavior

22
Q

who researched this

A

(Wurtman 1995)

23
Q

what did he conclude

A

Low levels of serotonin have also been linked with cravings for energy-rich foods, such as cake and chocolate that are high in fats and sugars, that cause weight gain through consuming too many calories

24
Q

what’s dopamine’s involvement

A

Dopamine is essential to the brain’s reward and motivation systems, stimulating areas like the hypothalamus and amygdala to produce feelings of pleasure and well-being when we eat. This pleasure response is linked to dopamine activity, which responds to food cues (like smell) by rewarding us.
Low levels of dopamine reduce pleasure in eating, and overeating is an attempt to activate reward centers in the brain by increasing dopamine levels

25
Q

what are the strengths of this

26
Q

who researched this

A

Gene-Jack Wang et al. (2001)

27
Q

what did they uncover

A

found that obese individuals have significantly fewer dopamine D2 receptors in the striatum, a part of the brain involved in reward. Low dopamine levels prevent the usual pleasure response from eating, so some people may overeat to try to increase dopamine levels and activate the brain’s reward centres. This explanation suggests that obesity could result from a neurochemical food addiction similar to other types of addiction.
(pretty similar to a01 idk)

28
Q

what is a strength of the neural explanation

29
Q

what is a weakness of the neural explanation

A

Neural explanations for obesity that examine serotonin and dopamine levels are correlational and so it is not clear whether low neurotransmitter levels are a cause or an effect of being obese- makes us skeptical about the evidence as you cant establish a cause and effect relationship