Biological explanations for obesity
Genetic
Some proposed genes make one more likely to develop obesity, such as DRD2, associated
with impulsivity and addictive behaviour.
The Thrifty gene is proposed as an evolutionary explanation, suggests we are
programmed to store food when we have enough to continue eating, and use it
when we have a lack of food. In developed countries where food is plentiful, this
gene is now maladaptive (instead of adaptive) and leads to obesity.
Twin studies into BMI generally suggests a greater genetical component. Nan (2012)
conducted Meta-analysis, found concordance rate to be 61%-80%, suggests strong
genetical component in obesity from childhood through to adulthood.
Neural
Research shows Damage/lesions to the ventromedial hypothalamus causes ‘hyperphagia’
which is overeating, stimulation of Lateral hypothalamus could be responsible for cravings.
Serotonin: Obesity is associated with low levels of this, or its main metabolite 5-HIAA.
Normal levels of serotonin regulate feeding behaviour by inhibiting the activity by
the ventromedial hypothalamus, it signals we have reached fullness (satiety).
Dysfunctions of the serotonin system can occur due to stress/depression.
Low levels send inaccurate satiety signals and leads to excessive cravings of energy
Dense foods.
Dopamine: Normal levels stimulate brain areas such as the hypothalamus and
amygdala, providing reward feelings of pleasure. This can be explained through the
pleasure that comes from eating and smelling food. Research links obesity with a
dysfunctional dopamine system and metabolite HVA.
Wang (2001) found that obese individuals had significantly fewer dopamine D2
receptors than ‘normal weight’ control group.
Because levels are low, the dopamine needed to provide feelings of pleasure are
much higher, this leads to overeating in attempt to activate reward centres.
Evaluation +/- of genetic explanation to obesity
One limitation is contradictory findings challenging the role of genes in obesity. Parachinni (2005) conducted a meta-analysis
on 25 studies researching genes thought to be involved with leptin (hormone concerned with weight regulation) and found no
evidence of a link between these genes and obesity, this raises doubt about the validity of genetic explanations for obesity as
findings are not consistent.
One limitation of the biological/ genetic approach to obesity is that it represents hard biological determinism. Although
genes make a significant contribution to the likelihood of obesity, this approach leaves little room for free will explanation e.g.,
the conscious choice on the amount of food one chooses to eat, similarly it does not explain the influence of the environment.
Factors such as bereavement, exams may trigger the ‘diathesis’ whereby people overeat to cope with the anxiety/depression
od certain stressors, this can explain how one’s environment is equally likely to aid obesity. (Developed) This also suggests that
if these stressors were to be controlled e.g., seeking help for depression through counselling or therapies, the overeating is less
likely to occur and therefore obesity is controlled.
Genetic
Some proposed genes make one more likely to develop obesity, such as DRD2, associated
with impulsivity and addictive behaviour.
The Thrifty gene is proposed as an evolutionary explanation, suggests we are
programmed to store food when we have enough to continue eating, and use it
when we have a lack of food. In developed countries where food is plentiful, this
gene is now maladaptive (instead of adaptive) and leads to obesity.
Twin studies into BMI generally suggests a greater genetical component. Nan (2012)
conducted Meta-analysis, found concordance rate to be 61%-80%, suggests strong
genetical component in obesity from childhood through to adulthood.
Neural
Research shows Damage/lesions to the ventromedial hypothalamus causes ‘hyperphagia’
which is overeating, stimulation of Lateral hypothalamus could be responsible for cravings.
Serotonin: Obesity is associated with low levels of this, or its main metabolite 5-HIAA.
Normal levels of serotonin regulate feeding behaviour by inhibiting the activity by
the ventromedial hypothalamus, it signals we have reached fullness (satiety).
Dysfunctions of the serotonin system can occur due to stress/depression.
Low levels send inaccurate satiety signals and leads to excessive cravings of energy
Dense foods.
Dopamine: Normal levels stimulate brain areas such as the hypothalamus and
amygdala, providing reward feelings of pleasure. This can be explained through the
pleasure that comes from eating and smelling food. Research links obesity with a
dysfunctional dopamine system and metabolite HVA.
Wang (2001) found that obese individuals had significantly fewer dopamine D2
receptors than ‘normal weight’ control group.
Because levels are low, the dopamine needed to provide feelings of pleasure are
much higher, this leads to overeating in attempt to activate reward centres.
Evaluation +/- of genetic explanation to obesity
One limitation is contradictory findings challenging the role of genes in obesity. Parachinni (2005) conducted a meta-analysis
on 25 studies researching genes thought to be involved with leptin (hormone concerned with weight regulation) and found no
evidence of a link between these genes and obesity, this raises doubt about the validity of genetic explanations for obesity as
findings are not consistent.
One limitation of the biological/ genetic approach to obesity is that it represents hard biological determinism. Although
genes make a significant contribution to the likelihood of obesity, this approach leaves little room for free will explanation e.g.,
the conscious choice on the amount of food one chooses to eat, similarly it does not explain the influence of the environment.
Factors such as bereavement, exams may trigger the ‘diathesis’ whereby people overeat to cope with the anxiety/depression
od certain stressors, this can explain how one’s environment is equally likely to aid obesity. (Developed) This also suggests that
if these stressors were to be controlled e.g., seeking help for depression through counselling or therapies, the overeating is less
likely to occur and therefore obesity is controlled.
