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Depression Incidence and the Risk for Developing a Food Addiction

Alana Todd

PSY 499: Psychology of Addiction

Dr. Dermody

Addiction has primarily been studied on the basis of drugs and alcohol; however, more recent

research has explored the role of addiction in other daily or lifestyle activities including

exercising, gambling, shopping, and eating. Of course, eating is necessary to sustain life;

however, food, specifically highly palatable foods have become the central theme to our culture.

The cyclic relationship between individual liking and wanting of highly palatable foods and the

food industry’s monumental increase in portion sizes and palatability has led to an obesity

epidemic, where many individuals have developed a food addiction. While the environment has

played a large role in promoting food addiction, there are certain individual changes that can be

made to help prevent the development of food addiction and obesity including understanding the

risk factors for addiction. This paper will focus on the link between depression and food

addiction to gain a better understanding of the role of mental and emotional disability as a risk

factor for addiction. It is predicted that the presence of depression will increase the risk for

developing a food addiction.

Depression Incidence and the Risk for Developing a Food Addiction

Obesity and food addiction have become much more prevalent in part due to

environmental factors as well as biological adaptations. The food industries excel at producing

highly palatable foods to increase consumer consumption regardless of the health risks involved.

As a result, the prevalence of further chronic diseases like type 2 diabetes and cardiovascular

diseases have risen, contributing to greater healthcare costs even though these illnesses are

entirely preventable. These environmental factors can have major implications on not just

physical health, but mental health as well.

This paper will focus on the question of whether depression increases the risk of

developing a food addiction. Depression is characterized by negative affect or despondency that

can interfere with daily cognitive, emotional, and behavioral functioning. Food addiction

comprises of a subset of disordered eating patterns and can be defined by preferring highly

palatable foods in addition to presenting addictive behaviors such as withdrawal, tolerance, and

loss of control (Piccini et al., 2015). Disordered eating patterns include emotional eating,

increased food intake in response to emotional distress, restrained eating, deliberately restricting

food intake to aid weight loss, and external eating, which is described as the increase of food

intake in response to sensory food cues rather than internal satiety cues like hormonal response

and the presence of food in the stomach. It is predicted that the presence of depressive symptoms

may lead to addictive eating behaviors due to the alteration of the reward systems in the brain

following the consumption of highly palatable foods. For example, food high in carbohydrates

can act as a physiological stress reliever via the hypothalamic-pituitary adrenal axis and help

individuals cope with psychological stress (Leow et al., 2018). Similar to other substance use
disorders, using food versus a drug as a stress reliever can lead to disordered and addictive eating


Review of Literature

In a study conducted by Sanlier et al. (2016), the relationship between body image, food

addiction, depression, and body mass index (BMI) were examined to better understand the role

of these factors in obesity or the risk for becoming obese. 793 students enrolled in the Health and

Social Sciences Faculty at a university in Ankara, Turkey were surveyed using self-report

measures including a body image scale assessing satisfaction with one’s body and functioning of

one’s body, food addiction symptoms (using the Yale Food Addiction Scale), depression

symptoms (using the Beck Depression Inventory), and BMI measurements. The researchers

found that body image scores were lower for overweight and obese participants compared to

underweight and normal weight individuals. Additionally, there was a positive, but not

statistically significant relationship between depression and food addiction scores and BMI. A

negative relationship was also found between food addiction and body image scores. These

findings indicate that there is a link between the neurobiological and behavioral factors and food

addiction, which are similar to substance abuse behaviors as seen in alcoholism and drug

addiction. Despite the correlation between BMI, body image, depression, and food addiction, the

causality of whether depression causes addiction or addiction causes depression remains unclear.

Subsequent research has attempted to move away from self-report measures to

objectively examine the link between depression and appetite. Specifically, a research article

conducted by Mills et. al. (2019) investigates the relationship between the presence of major

depressive disorder (MDD) and appetite disturbances as measured by serum leptin and ghrelin

levels, which are both appetite hormones. Leptin acts as an appetite suppressor once the body is
fed and ghrelin acts as an appetite enhancer to indicate when the body is hungry. In this study,

120 adults ranging from 18 to 54 years of age were recruited by media and university

advertisements and screened to confirm the presence of major depressive disorder. Depression

symptoms were measured using the Beck Depression Inventory. Food addiction behaviors were

measured using the Yale Food Addiction Scale and assessed withdrawal symptoms, cravings, and

tolerance to increased food intake. The results indicated that disordered eating was higher in

individuals who fit the criteria for MDD. Additionally, leptin levels were positively correlated,

and ghrelin levels were negatively correlated with disordered eating patterns. Higher leptin levels

would typically increase satiety; however, individuals with disordered eating exhibit leptin

resistance due to hormonal adaptation from continuous overeating. Ghrelin levels were

negatively correlated with restrained eating, indicating that lower ghrelin levels are associated

with restrained eating. Higher ghrelin levels are likely to increase hunger, food intake, and a lack

of control over these behaviors. The study mentions that there was little influence of MDD in

leptin levels, but there was a significant correlation between problematic eating behaviors with

both MDD and leptin levels, which may require further investigation. Overall, disordered eating

behaviors correlate strongly with the presence of MDD and leptin levels, but there is little

evidence that MDD alters leptin levels.

From various human studies, Parylak et al. (2011) compiled an array of evidence to

support the relationship between negative affect and food addiction. One study exhibited higher

rates of major depression, bipolar disorder, anxiety disorders, and alcohol or drug abuse in

individuals with bulimia nervosa or binge eating disorder, which present food addictive

behaviors. Another study found that participants most reported depression and sadness as a

trigger to binge eat. The literature has demonstrated an association between depression and food
addiction thus far, but there has been little research on the neuroadaptations that can occur as a

result of emotional distress or food addiction. Parylak et al. (2011) also discusses the role of

negative reinforcement to provide relief from a negative emotional state that presents in absence

of the substance. In relation to food addiction, the absence of food, particularly highly palatable

food triggers the antireward systems in the brain to amplify a negative emotional state. More

specifically, another research study investigated the neuroadaptations that occur with repeated

overconsumption of highly palatable foods. Participants were instructed to consume a high-fat

diet for 1-month and then instructed to either continue the diet or switch to a low-fat, high-carb

diet. Individuals who switched to the low-fat, high-carb diet reported greater anger and hostility

during the following month than the participants who continued on the high-fat diet. This

negative mood alteration is suggested to have resulted from neuroadaptations to increased dietary

carbohydrates, which is exhibited as a downregulation of dopaminergic modulation. During this

mechanism, there is a reduction in dopamine receptor availability as well as a reduction in

dopamine release, leading to deflated mood. This mechanism is similar to that of drug addiction

withdrawal symptoms. Additionally, some research argues that weight gain itself can cause a

downregulation of dopamine and dopamine receptor activity, which play a role in controlling

behavior. A decrease in dopamine activity inducing depressive symptoms can then cause

impaired inhibitory control, potentially leading to overeating.


This paper aimed to investigate the relationship between the presence of depression and

the risk of developing a food addiction. After reviewing the literature, there is a clear link

between depression and food addiction; however, further investigation may be necessary to

understand the causal relationship between the two. Some evidence indicates that depression
may increase the risk for developing a food addiction while some research suggests that food

addiction might increase the risk of developing depression. In either case, the evidence seems to

show a strong correlation between food addiction coexisting with depression and/or other mental


Limitations to the analyzed studies include population and possible prior treatment for

depression. In the first study, the sample size only included students from one university rather

than various students from different universities, locations, and age groups. Students may have

also been receiving treatment for depression during the study, which may have altered the results.

The study might have also benefited from categorizing each individual by BMI group to compare

and contrast depression severity by standard weight classification. The second study’s limitations

involved a lack of measuring baseline blood samples during both fasting and non-fasting rather

the study did not require participants to fast prior to blood sampling. Researchers also indicate

that prior research has shown that non-fasting leptin levels do not show significant differences to

fasting leptin levels. Confounding variables such as dietary nutrient intake, physical activity, and

menstrual cycles were also not accounted for during this study. Lastly, longitudinal research

should be applied to measure for changes in disordered eating, appetite hormones, and weight

gain in MDD over time.

Future research might explore the causal or cyclic relationship between depression and/or

other mental illness and the risk for developing a food addiction. More specifically, research

could further explore the neuroadaptations that cause both food addiction and depression and

how the two so closely intertwine. Another area of research should include possible interventions

for preventing food addiction from developing as well as treatments for food addiction. Some
studies have investigated the use of antidepressants to aid in reducing depression as well as the

development of food addictive behaviors.

While food addiction is a consequence of many factors including environmental

influence, genetic predisposition, and biological adaptations, there are certainly person-centered

treatments and interventions to help reduce the risk for developing a food addiction or for

helping to alleviate food addiction once it has already advanced. Because food addiction has

many similar characteristics and diagnostic criteria to substance addiction including drugs and

alcohol, treatments and interventions could target the same risk factors and symptoms.

Understanding potential risk factors specific to certain populations and individuals can help to

prevent the development of food addiction. For example, education about presence of depression

and the possible risk for food addiction may allow susceptible individuals to seek help prior to

becoming ill. By also becoming educated on the mechanism for which a food addiction develops,

people might have the ability to find the resources specific to the issue.


The literature has demonstrated a positive correlation between depression and food

addictive behaviors; however, more research should be conducted to better understand the causal

relationship between the two. Does depression cause food addiction, does food addiction cause

depression, or do both occur simultaneously? Some studies have exhibited that depression does

in fact increase the risk for developing a food addiction as seen in neuroadaptations caused by

consuming highly palatable foods to create a withdrawal state. However, these neuroadaptations

may be a result of dietary intake due to environmental factors secondary to depressive

symptoms. These are questions for future studies that may also explore preventative

interventions and/or treatments for depression and food addiction.


Leow, S., Jackson, B., Alderson, J.A., Guelfi, K.J., Dimmock, J.A. (2018). A role of exercise in

attenuating unhealthy food consumption in response to stress. Nutrients, 10(2), 176. doi:


Mills, J.G., Larkin, T.A., Deng, C., Thomas, S.J. (2019). Weight gain in major depressive

disorder: Linking appetite and disordered eating to leptin and ghrelin. Psychiatry

Research, 1781(19), 30196-30199. doi: 10.1016/j.psychres.2019.03.017.

Parylak, S.L., Koob, G.F., Zorrilla, E.P. (2011). The dark side of food addiction. Physiology &

Behavior, 104(1), 149-156. doi: 10.1016/j.physbeh.2011.04.063.

Piccini, A., Marazziti, D., Vanelli, F., Frencheschini, C., Baroni, S., Costanzo, D…Dell’Osso, L.

(2015). Food addiction spectrum: a theoretical model from normality to eating and

overeating disorders. Current Medicinal Chemistry, 22(13), 1161-1638.

Sanlier, N., Türközü, D., Toka, O. (2016). Body image, food addiction, depression, and body

mass index in university students. Ecology of Food and Nutrition, 55(6), 491-507. doi: