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When Obesity Causes Depression

Obesity causes depression and lowers well-being. A new study from the United Kingdom shows both social and physical factors may play a role in the effect.

Obesity causes mood disorders, increases feelings of sadness, and lowers well-being. A new study from the United Kingdom shows both social and physical factors may play a role in the effects.

Obesity has long been known for its role in causing cardiovascular disease, diabetes, and premature death. However, whether this condition affects our mental health has been remained a topic of research.

Both metabolic factors and social issues, such as social stigma, play a role in the connection between obesity and depression.

In 2008, a comprehensive review published in the journal International Journal of Obesity (London) found weak evidence supporting the idea that obesity may increase the incidence of depression outcomes (Atlantis et al., 2008). The study included 24 studies, 4 were prospective cohort studies, 20 cross-sectional studies, 10 of which were from the United States.


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On the other hand, in their review, Luppino and colleagues established a connection linking depression with obesity. In the study, the authors investigated 15 longitudinal studies involving 58,745 participants. They found that the onset of depression was significantly higher among adults aged 20-59 years and > or =60 years but not among the younger population aged <20 years.

Supporting the finding that people with obesity have a higher risk of depression, a report published in the journal American College of Nutrition stated that people with obesity were 32% more likely to have depression than non-obese (Pereira-Miranda et al., 2017).

Several biological reasons have been highlighted as probable causes for obesity-induced depression:

  1. Obesity activates inflammatory pathways, which in turn induces depression.
  2. Obesity causes dysregulation of the hypothalamic-pituitary-adrenal axis (HPA axis). In depression, the involvement of HPA-axis dysregulation is widely known to the scientific community.
  3. Obesity increases the risks of diabetes mellitus and increased insulin resistance, which could induce alterations in the brain, modulating the pathways leading to the increased risk of depression.

A recent study on a larger population provides further evidence that being overweight causes depression and lowers well-being. The study further indicates that biological factors and several social factors play a role in the effect. The study findings are published in the journal Human Molecular Genetics (Casanova et al., 2021).

Globally, an increasing number of people are suffering from this health condition. In the USA, the prevalence of obesity—Body Mass Index (BMI), greater than or equal to 30 kg/m2 —is 42.2%, according to a 2017-18 estimate. The health condition also affects the younger population.

While the danger of being obese is well known, the new study investigated whether obesity affects mental health and whether other biological issues are involved.

The Study

The research team used genetic analysis, known as Mendelian Randomisation, to examine the involvement of psychosocial traits, such as social influences and community humiliation, or biological conditions, such as altered metabolic pathways linked to higher BMI associated with hypertension, diabetes, and cardiovascular disease.

The team collected data from UK Biobank involving 145,000 participants with detailed mental health information. They analyzed genetic changes linked to higher BMI and outcomes from a relevant mental health exam assessing depression, anxiety, and well-being.

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The team used two sets of previously identified genetic variants to investigate the pathways that may involve in causing depression in overweight or obese people.

Both sets of genes are linked with developing higher adiposity, meaning the genes add more fats to the body. However, their biological impacts are different. One set of genes makes people accumulate more fat but metabolically healthier and are less likely to develop metabolic conditions such as high blood pressure and type-2 diabetes, which are linked with higher BMI.

On the other hand, other genes still make people fatter but prone to developing metabolic conditions such as hypertension and diabetes.

Our research provides additional evidence that being overweight causes depression. Finding ways to support people to lose weight could benefit their mental health as well as their physical health.
Dr. Francesco Casanova
obesity health depression

The team found little difference between the effects of the two sets of gene variants. The estimates for depression and well-being were consistent for both sets of genetic variants, suggesting that the pathway from higher BMI to adverse mental health is not purely metabolic and, to some extent, may be driven by other factors.


“Our research suggests that being overweight leads to a higher risk of depression, regardless of the role of metabolic health.” said author Jess O’Loughlin, at the University of Exeter Medical School. “This suggests that both metabolic factors and social issues, such as social stigma, play a role in the connection between obesity and depression.”

“This is a robust study, made possible by the quality of UK Biobank data.” said lead author Dr. Francesco Casanova at the University of Exeter Medical School.

“Our research provides additional evidence that being overweight causes depression. Finding ways to support people to lose weight could benefit their mental and physical health.”

Related Publication and Further Readings

Atlantis, E. and M. Baker (2008). “Obesity effects on depression: systematic review of epidemiological studies.” Int J Obes (Lond) 32(6): 881-891.

Casanova, F., J. O’Loughlin, et al. (2021). “Higher adiposity and mental health: Causal inference using Mendelian randomisation.” Human Molecular Genetics.

Pereira-Miranda, E., P. R. F. Costa, et al. (2017). “Overweight and Obesity Associated with Higher Depression Prevalence in Adults: A Systematic Review and Meta-Analysis.” J Am Coll Nutr 36(3): 223-233.



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