research on obesity has revealed that

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More than 1 billion people worldwide are now estimated to have obesity.

The chronic disease affects roughly one-eighth of the global population

The global prevalence of obesity has soared over the last 30 years. A new analysis suggests that more than 1 billion people worldwide now live with the chronic disease.

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By McKenzie Prillaman

February 29, 2024 at 6:30 pm

It’s no secret that global obesity rates have been rising over the past few decades. But a new analysis quantifies the upsurge.

More than 1 billion people worldwide were living with obesity as of 2022, researchers report February 29 in the Lancet . That’s about one-eighth of the global population ( SN: 11/15/22 ). For comparison, nearly 800 million people had obesity in 2016 , according to the World Health Organization, or WHO.

Obesity is “defined by the presence of excess body fat that impairs health,” says obesity expert Arya Sharma of the University of Alberta in Edmonton, Canada, who was not involved in the study. The chronic disease can raise the risk for conditions like heart disease and type 2 diabetes, vulnerability to diseases like COVID-19 , and can also limit mobility and negatively affect mental health ( SN: 4/22/20 ).

Global health researcher Majid Ezzati and colleagues examined more than 3,600 population-based studies published over the last several decades encompassing 222 million participants across nearly 200 countries and territories. The researchers divided each participant’s reported weight by their height squared to find their body mass index, or BMI.

Analyzing the trends suggested that in 2022, almost 900 million adults worldwide had a BMI of 30 or above, classifying them as having obesity. In children and adolescents ages 5 to 19, nearly 160 million were estimated to have the chronic disease, defined as BMI above a certain point on the WHO’s growth reference curves , which account for age and sex.

From 1990 to 2022, the prevalence of obesity roughly doubled in women, tripled in men and quadrupled in children and adolescents . At the same time, global rates of those who were underweight fell. “We shouldn’t be thinking about [underweight and obesity] as two separate things, because the transition from one to the other has been very rapid,” says Ezzati, of Imperial College London.

The estimated obesity rates should raise alarms, he says. “Governments and societies need to deal with this” through prevention and medical care. Despite new anti-obesity medications like Wegovy showing incredible results, Ezzati adds, their high costs and lack of incorporation in worldwide medical guidance will make them inaccessible to most people for the near future ( SN: 12/13/23 ).

Ezzati notes that one of the biggest driving factors of obesity’s increased prevalence is limited access to and the unaffordability of healthy foods. Sharma adds that societal-level lifestyle changes — such as getting less sleep , increased stress levels and spending less time at home — can also lead to eating more processed foods and overconsumption ( SN: 12/21/18 ; SN: 5/16/19 ).

“When you look at appetite, there’s a complex biology behind it,” Sharma says. “And that biology is affected by environmental changes.”

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Large-scale genetic study identifies genes that increase risk of obesity while protecting against other metabolic diseases

To determine whether genetics may play a role, a team of researchers analyzed data from hundreds of thousands of people, mainly of European descent, who had previously been assessed for body fat and disease risk markers. They identified 62 regions of the genome that have a seemingly paradoxical association of increased risk of obesity and favorable effects on cardiometabolic outcomes. Genes identified within these regions point to both known and novel ways in which excess body fat can become uncoupled from cardiometabolic diseases. For example, some of these body fat-increasing genes are associated with storage of the excess fat beneath the skin, as opposed to storage around the internal organs where fat is metabolically harmful. Further analyses identified genes that are functionally implicated in improved blood glucose levels, insulin signaling, regulation and development of fat cells, and energy (calorie) expenditure. Moreover, genes were identified that are linked to both increased body fat and changes in the nature of some of the fat tissue, from calorie-storing “white” fat to a form called “brown” or “beige” fat, a process that can increase calorie burning and promote healthy metabolism. These results are helping to clarify the complex genetic underpinnings of obesity, and the genes identified may represent targets for new therapies to reduce cardiometabolic risk associated with excess body fat.

Huang LO, Rauch A, Mazzaferro E,…Loos RJF. Genome-wide discovery of genetic loci that uncouple excess adiposity from its comorbidities . Nat Metab 3: 228-243, 2021.

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Obesity Research

Language switcher.

Over the years, NHLBI-supported research on overweight and obesity has led to the development of evidence-based prevention and treatment guidelines for healthcare providers. NHLBI research has also led to guidance on how to choose a behavioral weight loss program.

Studies show that the skills learned and support offered by these programs can help most people make the necessary lifestyle changes for weight loss and reduce their risk of serious health conditions such as heart disease and diabetes.

Our research has also evaluated new community-based programs for various demographics, addressing the health disparities in overweight and obesity.

NHLBI research that really made a difference

• In 1991, the NHLBI developed an Obesity Education Initiative to educate the public and health professionals about obesity as an independent risk factor for cardiovascular disease and its relationship to other risk factors, such as high blood pressure and high blood cholesterol. The initiative led to the development of clinical guidelines for treating overweight and obesity.
• The NHLBI and other NIH Institutes funded the Obesity-Related Behavioral Intervention Trials (ORBIT) projects , which led to the ORBIT model for developing behavioral treatments to prevent or manage chronic diseases. These studies included families and a variety of demographic groups. A key finding from one study focuses on the importance of targeting psychological factors in obesity treatment.

Current research funded by the NHLBI

The Division of Cardiovascular Sciences , which includes the Clinical Applications and Prevention Branch, funds research to understand how obesity relates to heart disease. The Center for Translation Research and Implementation Science supports the translation and implementation of research, including obesity research, into clinical practice. The Division of Lung Diseases and its National Center on Sleep Disorders Research fund research on the impact of obesity on sleep-disordered breathing.

Find funding opportunities and program contacts for research related to obesity and its complications.

Current research on obesity and health disparities

Health disparities happen when members of a group experience negative impacts on their health because of where they live, their racial or ethnic background, how much money they make, or how much education they received. NHLBI-supported research aims to discover the factors that contribute to health disparities and test ways to eliminate them.

• NHLBI-funded researchers behind the RURAL: Risk Underlying Rural Areas Longitudinal Cohort Study want to discover why people in poor rural communities in the South have shorter, unhealthier lives on average. The study includes 4,000 diverse participants (ages 35–64 years, 50% women, 44% whites, 45% Blacks, 10% Hispanic) from 10 of the poorest rural counties in Kentucky, Alabama, Mississippi, and Louisiana. Their results will support future interventions and disease prevention efforts.
• The Hispanic Community Health Study/Study of Latinos (HCHS/SOL) is looking at what factors contribute to the higher-than-expected numbers of Hispanics/Latinos who suffer from metabolic diseases such as obesity and diabetes. The study includes more than 16,000 Hispanic/Latino adults across the nation.

Find more NHLBI-funded studies on obesity and health disparities at NIH RePORTER.

Read how African Americans are learning to transform soul food into healthy, delicious meals to prevent cardiovascular disease: Vegan soul food: Will it help fight heart disease, obesity?

Current research on obesity in pregnancy and childhood

• The NHLBI-supported Fragile Families Cardiovascular Health Follow-Up Study continues a study that began in 2000 with 5,000 American children born in large cities. The cohort was racially and ethnically diverse, with approximately 40% of the children living in poverty. Researchers collected socioeconomic, demographic, neighborhood, genetic, and developmental data from the participants. In this next phase, researchers will continue to collect similar data from the participants, who are now young adults.
• The NHLBI is supporting national adoption of the Bright Bodies program through Dissemination and Implementation of the Bright Bodies Intervention for Childhood Obesity . Bright Bodies is a high-intensity, family-based intervention for childhood obesity. In 2017, a U.S. Preventive Services Task Force found that Bright Bodies lowered children’s body mass index (BMI) more than other interventions did.
• The NHLBI supports the continuation of the nuMoM2b Heart Health Study , which has followed a diverse cohort of 4,475 women during their first pregnancy. The women provided data and specimens for up to 7 years after the birth of their children. Researchers are now conducting a follow-up study on the relationship between problems during pregnancy and future cardiovascular disease. Women who are pregnant and have obesity are at greater risk than other pregnant women for health problems that can affect mother and baby during pregnancy, at birth, and later in life.

Find more NHLBI-funded studies on obesity in pregnancy and childhood at NIH RePORTER.

Learn about the largest public health nonprofit for Black and African American women and girls in the United States: Empowering Women to Get Healthy, One Step at a Time .

Current research on obesity and sleep

• An NHLBI-funded study is looking at whether energy balance and obesity affect sleep in the same way that a lack of good-quality sleep affects obesity. The researchers are recruiting equal numbers of men and women to include sex differences in their study of how obesity affects sleep quality and circadian rhythms.
• NHLBI-funded researchers are studying metabolism and obstructive sleep apnea . Many people with obesity have sleep apnea. The researchers will look at the measurable metabolic changes in participants from a previous study. These participants were randomized to one of three treatments for sleep apnea: weight loss alone, positive airway pressure (PAP) alone, or combined weight loss and PAP. Researchers hope that the results of the study will allow a more personalized approach to diagnosing and treating sleep apnea.
• The NHLBI-funded Lipidomics Biomarkers Link Sleep Restriction to Adiposity Phenotype, Diabetes, and Cardiovascular Risk study explores the relationship between disrupted sleep patterns and diabetes. It uses data from the long-running Multiethnic Cohort Study, which has recruited more than 210,000 participants from five ethnic groups. Researchers are searching for a cellular-level change that can be measured and can predict the onset of diabetes in people who are chronically sleep deprived. Obesity is a common symptom that people with sleep issues have during the onset of diabetes.

Find more NHLBI-funded studies on obesity and sleep at NIH RePORTER.

Learn about a recent study that supports the need for healthy sleep habits from birth: Study finds link between sleep habits and weight gain in newborns .

Obesity research labs at the NHLBI

The Cardiovascular Branch and its Laboratory of Inflammation and Cardiometabolic Diseases conducts studies to understand the links between inflammation, atherosclerosis, and metabolic diseases.

NHLBI’s Division of Intramural Research , including its Laboratory of Obesity and Aging Research , seeks to understand how obesity induces metabolic disorders. The lab studies the “obesity-aging” paradox: how the average American gains more weight as they get older, even when food intake decreases.

Related obesity programs and guidelines

• Aim for a Healthy Weight is a self-guided weight-loss program led by the NHLBI that is based on the psychology of change. It includes tested strategies for eating right and moving more.
• The NHLBI developed the We Can! ® (Ways to Enhance Children’s Activity & Nutrition) program to help support parents in developing healthy habits for their children.
• The Accumulating Data to Optimally Predict obesity Treatment (ADOPT) Core Measures Project standardizes data collected from the various studies of obesity treatments so the data can be analyzed together. The bigger the dataset, the more confidence can be placed in the conclusions. The main goal of this project is to understand the individual differences between people who experience the same treatment.
• The NHLBI Director co-chairs the NIH Nutrition Research Task Force, which guided the development of the first NIH-wide strategic plan for nutrition research being conducted over the next 10 years. See the 2020–2030 Strategic Plan for NIH Nutrition Research .
• The NHLBI is an active member of the National Collaborative on Childhood Obesity (NCCOR) , which is a public–private partnership to accelerate progress in reducing childhood obesity.
• The NHLBI has been providing guidance to physicians on the diagnosis, prevention, and treatment of obesity since 1977. In 2017, the NHLBI convened a panel of experts to take on some of the pressing questions facing the obesity research community. See their responses: Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents (PDF, 3.69 MB).
• In 2021, the NHLBI held a Long Non-coding (lnc) RNAs Symposium to discuss research opportunities on lnc RNAs, which appear to play a role in the development of metabolic diseases such as obesity.
• The Muscatine Heart Study began enrolling children in 1970. By 1981, more than 11,000 students from Muscatine, Iowa, had taken surveys twice a year. The study is the longest-running study of cardiovascular risk factors in children in the United States. Today, many of the earliest participants and their children are still involved in the study, which has already shown that early habits affect cardiovascular health later in life.
• The Jackson Heart Study is a unique partnership of the NHLBI, three colleges and universities, and the Jackson, Miss., community. Its mission is to discover what factors contribute to the high prevalence of cardiovascular disease among African Americans. Researchers aim to test new approaches for reducing this health disparity. The study incudes more than 5,000 individuals. Among the study’s findings to date is a gene variant in African Americans that doubles the risk of heart disease.

Explore more NHLBI research on overweight and obesity

The sections above provide you with the highlights of NHLBI-supported research on overweight and obesity . You can explore the full list of NHLBI-funded studies on the NIH RePORTER .

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Obesity and overweight

• In 2022, 1 in 8 people in the world were living with obesity. 
• Worldwide adult obesity has more than doubled since 1990, and adolescent obesity has quadrupled.
• In 2022, 2.5 billion adults (18 years and older) were overweight. Of these, 890 million were living with obesity.
• In 2022, 43% of adults aged 18 years and over were overweight and 16% were living with obesity.
• In 2022, 37 million children under the age of 5 were overweight.
• Over 390 million children and adolescents aged 5–19 years were overweight in 2022, including 160 million who were living with obesity.

Overweight is a condition of excessive fat deposits.

Obesity is a chronic complex disease defined by excessive fat deposits that can impair health. Obesity can lead to increased risk of type 2 diabetes and heart disease, it can affect bone health and reproduction, it increases the risk of certain cancers. Obesity influences the quality of living, such as sleeping or moving.

The diagnosis of overweight and obesity is made by measuring people’s weight and height and by calculating the body mass index (BMI): weight (kg)/height² (m²). The body mass index is a surrogate marker of fatness and additional measurements, such as the waist circumference, can help the diagnosis of obesity.

The BMI categories for defining obesity vary by age and gender in infants, children and adolescents.

For adults, WHO defines overweight and obesity as follows:

• overweight is a BMI greater than or equal to 25; and
• obesity is a BMI greater than or equal to 30.

For children, age needs to be considered when defining overweight and obesity.

Children under 5 years of age

For children under 5 years of age:

• overweight is weight-for-height greater than 2 standard deviations above WHO Child Growth Standards median; and
• obesity is weight-for-height greater than 3 standard deviations above the WHO Child Growth Standards median.

Charts and tables: WHO child growth standards for children aged under 5 years

Children aged between 5–19 years

Overweight and obesity are defined as follows for children aged between 5–19 years:

• overweight is BMI-for-age greater than 1 standard deviation above the WHO Growth Reference median; and
• obesity is greater than 2 standard deviations above the WHO Growth Reference median.

Charts and tables: WHO growth reference for children aged between 5–19 years

Facts about overweight and obesity

In 2022, 2.5 billion adults aged 18 years and older were overweight, including over 890 million adults who were living with obesity. This corresponds to 43% of adults aged 18 years and over (43% of men and 44% of women) who were overweight; an increase from 1990, when 25% of adults aged 18 years and over were overweight. Prevalence of overweight varied by region, from 31% in the WHO South-East Asia Region and the African Region to 67% in the Region of the Americas.

About 16% of adults aged 18 years and older worldwide were obese in 2022. The worldwide prevalence of obesity more than doubled between 1990 and 2022.

In 2022, an estimated 37 million children under the age of 5 years were overweight. Once considered a high-income country problem, overweight is on the rise in low- and middle-income countries. In Africa, the number of overweight children under 5 years has increased by nearly 23% since 2000. Almost half of the children under 5 years who were overweight or living with obesity in 2022 lived in Asia.

Over 390 million children and adolescents aged 5–19 years were overweight in 2022. The prevalence of overweight (including obesity) among children and adolescents aged 5–19 has risen dramatically from just 8% in 1990 to 20% in 2022. The rise has occurred similarly among both boys and girls: in 2022 19% of girls and 21% of boys were overweight.

While just 2% of children and adolescents aged 5–19 were obese in 1990 (31 million young people), by 2022, 8% of children and adolescents were living with obesity (160 million young people).

Causes of overweight and obesity

Overweight and obesity result from an imbalance of energy intake (diet) and energy expenditure (physical activity).

In most cases obesity is a multifactorial disease due to obesogenic environments, psycho-social factors and genetic variants. In a subgroup of patients, single major etiological factors can be identified (medications, diseases, immobilization, iatrogenic procedures, monogenic disease/genetic syndrome).

The obesogenic environment exacerbating the likelihood of obesity in individuals, populations and in different settings is related to structural factors limiting the availability of healthy sustainable food at locally affordable prices, lack of safe and easy physical mobility into the daily life of all people, and absence of adequate legal and regulatory environment.

At the same time, the lack of an effective health system response to identify excess weight gain and fat deposition in their early stages is aggravating the progression to obesity.

Common health consequences

The health risks caused by overweight and obesity are increasingly well documented and understood.

In 2019, higher-than-optimal BMI caused an estimated 5 million deaths from noncommunicable diseases (NCDs) such as cardiovascular diseases, diabetes, cancers, neurological disorders, chronic respiratory diseases, and digestive disorders (1) . 

Being overweight in childhood and adolescence affects children’s and adolescents’ immediate health and is associated with greater risk and earlier onset of various NCDs, such as type 2 diabetes and cardiovascular disease. Childhood and adolescent obesity have adverse psychosocial consequences; it affects school performance and quality of life, compounded by stigma, discrimination and bullying. Children with obesity are very likely to be adults with obesity and are also at a higher risk of developing NCDs in adulthood.

The economic impacts of the obesity epidemic are also important. If nothing is done, the global costs of overweight and obesity are predicted to reach US$ 3 trillion per year by 2030 and more than US$ 18 trillion by 2060 (2) .

Finally, the rise in obesity rates in low-and middle-income countries, including among lower socio-economic groups, is fast globalizing a problem that was once associated only with high-income countries.

Facing a double burden of malnutrition

Many low- and middle-income countries face a so-called double burden of malnutrition.

While these countries continue to deal with the problems of infectious diseases and undernutrition, they are also experiencing a rapid upsurge in noncommunicable disease risk factors such as obesity and overweight.

It is common to find undernutrition and obesity co-existing within the same country, the same community and the same household.

Children in low- and middle-income countries are more vulnerable to inadequate pre-natal, infant, and young child nutrition. At the same time, these children are exposed to high-fat, high-sugar, high-salt, energy-dense, and micronutrient-poor foods, which tend to be lower in cost but also lower in nutrient quality. These dietary patterns, in conjunction with lower levels of physical activity, result in sharp increases in childhood obesity while undernutrition issues remain unsolved.

Prevention and management

Overweight and obesity, as well as their related noncommunicable diseases, are largely preventable and manageable.

At the individual level, people may be able to reduce their risk by adopting preventive interventions at each step of the life cycle, starting from pre-conception and continuing during the early years. These include:

• ensure appropriate weight gain during pregnancy;
• practice exclusive breastfeeding in the first 6 months after birth and continued breastfeeding until 24 months or beyond;
• support behaviours of children around healthy eating, physical activity, sedentary behaviours and sleep, regardless of current weight status;
• limit screen time;
• limit consumption of sugar sweetened beverages and energy-dense foods and promote other healthy eating behaviours;
• enjoy a healthy life (healthy diet, physical activity, sleep duration and quality, avoid tobacco and alcohol, emotional self-regulation);
• limit energy intake from total fats and sugars and increase consumption of fruit and vegetables, as well as legumes, whole grains and nuts; and
• engage in regular physical activity.

Health practitioners need to

• assess the weight and height of people accessing the health facilities;
• provide counselling on healthy diet and lifestyles;
• when a diagnosis of obesity is established, provide integrated obesity prevention and management health services including on healthy diet, physical activity and medical and surgical measures; and
• monitor other NCD risk factors (blood glucose, lipids and blood pressure) and assess the presence of comorbidities and disability, including mental health disorders.

The dietary and physical activity patterns for individual people are largely the result of environmental and societal conditions that greatly constrain personal choice. Obesity is a societal rather than an individual responsibility, with the solutions to be found through the creation of supportive environments and communities that embed healthy diets and regular physical activity as the most accessible, available and affordable behaviours of daily life.

Stopping the rise in obesity demands multisectoral actions such as food manufacturing, marketing and pricing and others that seek to address the wider determinants of health (such as poverty reduction and urban planning).

Such policies and actions include:

• structural, fiscal and regulatory actions aimed at creating healthy food environments that make healthier food options available, accessible and desirable; and
• health sector responses designed and equipped to identify risk, prevent, treat and manage the disease. These actions need to build upon and be integrated into broader efforts to address NCDs and strengthen health systems through a primary health care approach.

The food industry can play a significant role in promoting healthy diets by:

• reducing the fat, sugar and salt content of processed foods;
• ensuring that healthy and nutritious choices are available and affordable to all consumers;
• restricting marketing of foods high in sugars, salt and fats, especially those foods aimed at children and teenagers; and
• ensuring the availability of healthy food choices and supporting regular physical activity practice in the workplace.

WHO response

WHO has recognized the need to tackle the global obesity crisis in an urgent manner for many years .

The World Health Assembly Global Nutrition Targets aiming to ensure no increase in childhood overweight, and the NCD target to halt the rise of diabetes and obesity by 2025, were endorsed by WHO Member States. They recognized that accelerated global action is needed to address pervasive and corrosive problem of the double burden of malnutrition.

At the 75 th World Health Assembly in 2022, Member States demanded and adopted new recommendations for the prevention and management of obesity and endorsed the WHO Acceleration plan to stop obesity . Since its endorsement, the Acceleration plan has shaped the political environment to generate impetus needed for sustainable change, created a platform to shape, streamline and prioritize policy, support implementation in countries and drive impact and strengthen accountability at national and global level.

1. GBD 2019 Risk Factor Collaborators. “Global Burden of 87 Risk Factors in 204 Countries and Territories, 1990–2019: a systematic analysis for the global burden of disease study 2019”. Lancet. 2020;396:1223–1249.

2. Okunogbe et al., “Economic Impacts of Overweight and Obesity.” 2nd Edition with Estimates for 161 Countries. World Obesity Federation, 2022.

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Adult Obesity Facts

At a glance.

• Obesity is a serious, common, and costly chronic disease. More than 2 in 5 U.S. adults have obesity.
• Obesity affects some groups more than others, including non-Hispanic Black adults and adults with less education.
• Many adults with obesity have other serious chronic diseases, including diabetes and heart disease.
• Obesity accounts for nearly $173 billion in medical expenditures in 2019 dollars.

Many U.S. adults have obesity

The prevalence of obesity among U.S. adults 20 and over was 41.9% during 2017–March 2020. 1 During the same time, the prevalence of severe obesity among U.S. adults was 9.2%. This means that more than 100 million adults have obesity, and more than 22 million adults have severe obesity.

The prevalence of obesity increased from 30.5% in 1999-2000 2 to 41.9% in 2017–March 2020. During the same time, the prevalence of severe obesity increased from 4.7% to 9.2%.

Note: Obesity is defined as having a body mass index (BMI) of 30.0 or higher. Severe obesity is defined as having a BMI of 40.0 or higher.

Obesity Prevalence Maps‎

Obesity affects some groups more than others, race and ethnicity.

In 2017–March 2020, non-Hispanic Black adults had the highest obesity prevalence (49.9%) followed by Hispanic (45.6%), non-Hispanic White (41.4%), and non-Hispanic Asian (16.1%) adults. 1

In 2017–March 2020, obesity prevalence was highest among U.S. adults with a high school diploma or some college education (46.4%) followed by those with less than a high school diploma (40.1%) and those with a college degree or above (34.2%). 1

In 2017–March 2020, differences by age group were not statistically significant. Obesity prevalence was 39.8% among U.S. adults aged 20–39 years, 44.3% among adults aged 40–59 years, and 41.5% among adults aged 60 years and older. . 1

Obesity is serious and expensive

Many adults with obesity have other serious chronic diseases. For example, 58% of U.S. adults with obesity have high blood pressure, a risk factor for heart disease. Also, approximately 23% of U.S. adults with obesity have diabetes. 1

Health care for obesity is expensive for patients and the health care system. In 2019 dollars, annual medical costs for adults with obesity were $1,861 higher per person than adults with healthy weight. For adults with severe obesity, the excess costs were $3,097 per person. This accounts for nearly $173 billion in medical expenditures in 2019 dollars. 2

Related information

Risk Factors for Obesity

Determinants of health, health behaviors, and other factors that are associated with obesity.

What body mass index is, how it is used, and how it is interpreted.

Adult BMI Calculator

Calculate BMI and the corresponding BMI category for adults 20 years and older.

Child Obesity Facts

Information about obesity among children in the U.S.

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Tools to help remove barriers to health and achieve health equity.

Person-First Language‎

• Stierman B, Afful J, Carroll MD, et al. National Health and Nutrition Examination Survey 2017–March 2020 prepandemic data files development of files and prevalence estimates for selected health outcomes . Natl Health Stat Report . 2021;158.
• Ward ZJ, Bleich S, Long MW, Gortmaker SL. Association of body mass index with health care expenditures in the United States by age and sex. PLoS One . 2021;16(3):e0247307. doi: 10.1371/journal.pone.0247307
• Division of Nutrition, Physical Activity, and Obesity , National Center for Chronic Disease Prevention and Health Promotion
• Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among U.S. adults, 1999-2000. JAMA . 2002;288(14):1723–7. doi: 10.1001/jama.288.14.1723

CDC's obesity prevention efforts focus on policy and environmental strategies to make healthy eating and active living accessible for everyone.

For Everyone

Health care providers, public health.

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Nature Reviews Disease Primers volume  3 , Article number:  17034 ( 2017 ) Cite this article

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• Bariatric surgery
• Metabolic syndrome
• Type 2 diabetes
• Weight management

Excessive fat deposition in obesity has a multifactorial aetiology, but is widely considered the result of disequilibrium between energy intake and expenditure. Despite specific public health policies and individual treatment efforts to combat the obesity epidemic, >2 billion people worldwide are overweight or obese. The central nervous system circuitry, fuel turnover and metabolism as well as adipose tissue homeostasis are important to comprehend excessive weight gain and associated comorbidities. Obesity has a profound impact on quality of life, even in seemingly healthy individuals. Diet, physical activity or exercise and lifestyle changes are the cornerstones of obesity treatment, but medical treatment and bariatric surgery are becoming important. Family history, food environment, cultural preferences, adverse reactions to food, perinatal nutrition, previous or current diseases and physical activity patterns are relevant aspects for the health care professional to consider when treating the individual with obesity. Clinicians and other health care professionals are often ill-equipped to address the important environmental and socioeconomic drivers of the current obesity epidemic. Finally, understanding the epigenetic and genetic factors as well as metabolic pathways that take advantage of ‘omics’ technologies could play a very relevant part in combating obesity within a precision approach.

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The authors thank the Spanish Government Carlos III Health Institute Centre of Biomedical Research Network (CIBERobn Physiopathology of Obesity and Nutrition) for support and funding.

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Introduction (P.G.-M. and J.A.M.); Epidemiology (F.B.H. and M.-A.M.-G.); Mechanisms/pathophysiology (J.-P.D., Y.M. and R.J.F.L.); Diagnosis, screening and prevention (L.A.M.); Management (G.A.B.); Quality of life (M.-A.M.-G.); Outlook (P.G.-M. and J.A.M.); Overview of the Primer (J.A.M.).

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González-Muniesa, P., Mártinez-González, MA., Hu, F. et al. Obesity. Nat Rev Dis Primers 3 , 17034 (2017). https://doi.org/10.1038/nrdp.2017.34

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Novel secreted regulators of glucose and lipid metabolism in the development of metabolic diseases

• Published: 24 August 2024

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• Lianna W. Wat 1 , 2 , 3 &
• Katrin J. Svensson 1 , 2 , 3  

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The tight regulation of glucose and lipid metabolism is crucial for maintaining metabolic health. Dysregulation of these processes can lead to the development of metabolic diseases. Secreted factors, or hormones, play an essential role in the regulation of glucose and lipid metabolism, thus also playing an important role in the development of metabolic diseases such as type 2 diabetes and obesity. Given the important roles of secreted factors, there has been significant interest in identifying new secreted factors and new functions for existing secreted factors that control glucose and lipid metabolism. In this review, we evaluate novel secreted factors or novel functions of existing factors that regulate glucose and lipid metabolism discovered in the last decade, including secreted isoform of endoplasmic reticulum membrane complex subunit 10, vimentin, cartilage intermediate layer protein 2, isthmin-1, lipocalin-2, neuregulin-1 and neuregulin-4. We discuss their discovery, tissues of origin, mechanisms of action and sex differences, emphasising their potential to regulate metabolic processes central to diabetes. Additionally, we discuss the translational barriers, particularly the absence of identified receptors, that hamper their functional characterisation and further therapeutic development. Ultimately, the identification of new secreted factors may give insights into previously unidentified pathways of disease progression and mechanisms of glucose and lipid homeostasis.

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Metrnl: a secreted protein with new emerging functions

Involvement of the secreted protein Metrnl in human diseases

Fibroblast Growth Factor Binding Protein 3 (FGFBP3) impacts carbohydrate and lipid metabolism

Abbreviations.

Adeno-associated virus

Adipose triglyceride lipase

Brown adipose tissue

Cartilage intermediate layer protein 2

Endoplasmic reticulum membrane complex subunit 10

Endoplasmic reticulum

Erb-b2 receptor tyrosine kinase

Glucose-stimulated insulin secretion

High-fat diet

Human scEMC10

IGF-1 receptor

Lipocalin-2

Metabolic dysfunction-associated steatotic liver disease

Membrane-bound EMC10

Fusion protein of human Nrg1 and the Fc domain of human IgG1

Oxidised LDL

Phosphoinositide 3-kinase

Protein kinase A

Peroxisome proliferator-activated receptor γ

Secreted isoform of EMC10

Sterol regulatory element-binding protein 1

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Wat, L.W., Svensson, K.J. Novel secreted regulators of glucose and lipid metabolism in the development of metabolic diseases. Diabetologia (2024). https://doi.org/10.1007/s00125-024-06253-x

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Why Cynics Are Less Likely to Succeed

Three ways to stop cynicism from holding you and your organization back.

New research in behavioral science has revealed that cynical thinking stands in the way of success in the workplace. Cynics, it turns out, earn less money, report lower job satisfaction, and are less likely to be elevated to leadership positions. That’s because success is not the winner-take-all battle that cynics believe it to be. Cynicism, in fact, can bleed workplaces of creativity, openness, and morale, and the bottom line — whereas the people who succeed at work tend to so by building trusting connections and alliances. As a research psychologist, the author has worked with organizations and leaders to help them fight cynicism and bring the cooperative advantage to their teams, and in this article he lays out some effective approaches for doing so.

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• Jamil Zaki is a professor of psychology at Stanford University and the author of  Hope for Cynics: The Surprising Science of Human Goodness .

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Diet, Obesity, and Depression: A Systematic Review

Olivia patsalos.

1 Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King’s College London, London SE5 8AF, UK; [email protected] (O.P.); [email protected] (J.K.); [email protected] (U.S.); [email protected] (A.H.Y.)

Johanna Keeler

Ulrike schmidt.

2 South London and Maudsley NHS Foundation Trust, London SE5 8AZ, UK

Brenda W. J. H. Penninx

3 Department of Psychiatry, Amsterdam Public Health Research Institute, Amsterdam UMC, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands; [email protected]

Allan H. Young

Hubertus himmerich, associated data.

Not applicable.

Background: Obesity and depression co-occur in a significant proportion of the population. Mechanisms linking the two disorders include the immune and the endocrine system, psychological and social mechanisms. The aim of this systematic review was to ascertain whether weight loss through dietary interventions has the additional effect of ameliorating depressive symptoms in obese patients. Methods: We systematically searched three databases (Pubmed, Medline, Embase) for longitudinal clinical trials testing a dietary intervention in people with obesity and depression or symptoms of depression. Results: Twenty-four longitudinal clinical studies met the eligibility criteria with a total of 3244 included patients. Seventeen studies examined the effects of calorie-restricted diets and eight studies examined dietary supplements (two studies examined both). Only three studies examined people with a diagnosis of both obesity and depression. The majority of studies showed that interventions using a calorie-restricted diet resulted in decreases in depression scores, with effect sizes between ≈0.2 and ≈0.6. The results were less clear for dietary supplements. Conclusions: People with obesity and depression appear to be a specific subgroup of depressed patients in which calorie-restricted diets might constitute a promising personalized treatment approach. The reduction of depressive symptoms may be related to immunoendocrine and psychosocial mechanisms.

1. Introduction

Both depression and obesity are major public health concerns [ 1 , 2 ] with high worldwide prevalence and associated increased cardiovascular risks [ 3 , 4 ]. Research has revealed an association between depression and obesity, with the prevalence of depression in obese individuals being twice as high as in those of normal weight [ 5 ]. The relationship between depression and obesity, although established and confirmed by numerous epidemiological studies and meta-analyses, has not yet been fully clarified. The association has been repeatedly examined with some authors asserting that depression results in weight gain and obesity and others claiming that obesity leads to depression, implying a bidirectional causality [ 6 ]. It has been suggested that both depression and obesity are due to dysregulation of stress responses, principally involving the hypothalamic–pituitary–adrenal (HPA) axis [ 7 ]. Additional mechanisms linking the two disorders are inflammation, oxidative stress, and other endocrine dysfunctions [ 8 ], as well as psychological mechanisms such as rumination, stigmatization and ostracism that contribute to and maintain the bidirectional relationship [ 9 , 10 ].

1.1. Diet and Depression

The typical diets of western societies have high amounts of saturated fats and refined sugars, as well as high amounts of red and processed meats, with concurrent low levels of fruit, vegetable and fiber intake. This results in a diet that is energy-dense and nutrient-poor with profound consequences for both our physical and mental health. The relationship between diet and obesity is clear; individuals consuming more calories than the recommended daily allowance, combined with consuming high amounts of foods high in fat and sugar content, are more likely to develop obesity. More recently, the impact of diet on mental health has also been revealed to be significant; for example, a recent meta-analysis found that adults following a healthy dietary pattern have fewer depressive symptoms and lower risk of developing depressive symptoms [ 11 ].

The precise etiology of depression is unknown, but many psychological, social, and biological underpinnings are thought to contribute to its development [ 12 ]. The latter includes genetic, hormonal, immunological, biochemical, and neurodegenerative factors. Concurrently, research has shown that these physiological aspects can be modulated by diet and nutrition. For example, in the case of genes, vitamin E has been shown to modulate several genes involved in neural signal transduction, inflammation and cell proliferation among others, while omega-3 polyunsaturated fatty acids (n-3 PUFAs) [ 13 ] have been shown to interact with genes that code for cytokines, cholesterol metabolizing enzymes, and growth factors [ 14 ].

1.2. Depression and Obesity

Many authors posit that depression is a heterogenous assortment of symptoms that can be divided into subtypes based on the accompanying presenting symptoms beyond low mood. Most recently, it has been subdivided into two main subtypes: type 1, which is characterized by loss of appetite and body weight, insomnia, and suicidal ideation, and type 2, also known as atypical depression, which presents with increased appetite and weight gain, leaden paralysis, hypersomnia, and a persistently poor metabolic profile [ 15 ]. Several factors are thought to moderate the relationship between obesity and depression. Stunkard et al. have reviewed the literature pertaining to what those moderators and mediators could be, and they have identified several including the severity of obesity, the severity of depression, and stress [ 16 ].

Correlations between both disorders involve disturbance of appetite regulation, changes in metabolic, hormonal and immunological parameters, and behavioral problems such as reduced physical activity [ 9 , 10 , 17 , 18 , 19 , 20 ]. More specifically, obesity has been shown to induce important physical, psychological, and behavioral changes in vulnerable patients, such as changes in the hormone and cytokine systems [ 18 , 21 ], changes in thought processes such as rumination [ 9 ], and behavioral changes such as reduced physical activity [ 20 ]. These changes are known risk factors of depression [ 17 , 20 ]. Thus, in obese patients, depression can be seen as a health consequence of obesity. If obesity contributes to the development and maintenance of depression, we can hypothesize that weight loss might help those depressed patients who are obese. Indeed, recent studies indicate that weight loss due to caloric restriction or gastric bypass surgery improves depressive symptoms among obese patients with depression [ 22 , 23 , 24 , 25 ]. Therefore, we sought to review and collate the existing research literature on the effects of diet modifications on depressive symptoms in overweight or obese individuals enrolled in dietary weight loss programs. The underlying idea was that in people with obesity and depression, depression occurs as a consequence of obesity, and therefore weight loss could not only help with regard to obesity but could also reduce depressive symptoms.

2. Materials and Methods

We conducted this systematic review according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines [ 26 ].

2.1. Literature Search

Three electronic databases (PubMed, Medline, and EMBASE) were systematically searched from inception until 5 October 2020 using the following search terms: diet in combination with depression , in combination with obesity . Reference lists of potentially relevant papers and reviews were also scanned for potentially eligible papers.

2.2. Eligibility Criteria

Searches were limited to abstracts, studies with adult human participants, and studies written in English. Any study which assessed the effect of any dietary intervention or dietary supplementation on depressive symptoms in the context of obesity (BMI ≥ 30 kg/m 2 ) at baseline and at least at one follow-up point was eligible for inclusion. To be eligible, at least a subgroup of study participants had to be obese. However, we did not exclude studies, when in addition to people with obesity, other study participants were overweight or of normal body weight (used as controls).

Studies were excluded if they (a) were not longitudinal clinical studies, (b) did not comment on weight/BMI change after intervention, (c) did not discuss change of depressive symptoms after intervention, or (d) were association or observational studies without a dietary intervention. Review articles, meta-analyses, case studies, conference proceedings/abstracts, book chapters, and unpublished theses were not included.

2.3. Study Selection

Figure 1 depicts the study selection and screening flowchart. Titles and abstracts of publications resulting from the search were imported into Mendeley and duplicates were removed. Two independent reviewers (O. P. and J. K.) performed all stages of the search, screening, and evaluation. Titles and abstracts were screened, and irrelevant articles were disregarded. Articles whose abstracts passed the first screen were read in full and assessed for eligibility based on our prespecified inclusion criteria, described above. Study quality assessment was performed using a quality assessment tool for pre-post studies from the National Heart, Lung and Blood Institute [ 27 ].

PRISMA flow diagram.

3.1. Characteristics of Included Studies

Individual study characteristics are described in Table 1 . Twenty-four longitudinal clinical trials met the inclusion criteria. A total of 3244 patients participated in trials investigating the impact of diet, dietary supplements, or behavioral modification/counselling on weight and depression scores. All study participants were overweight or obese aside from some of the participants in the Breymeyer et al. [ 28 ] study which included a group of nonobese participants used as healthy controls.

Characteristics of included studies.

Abbreviations: AED = almond-enriched diet, AIT = aerobic interval training, BDI = Beck’s depression inventory, BDI-II = Beck’s Depression Inventory-2, BWL = behavioral weight loss, CES-D = center for epidemiologic studies depression scale, CRT-O = cognitive remediation therapy for obesity, DASS-21 = depression anxiety stress scale 21 items, EBT = emotional brain training, FRBA = food-related behavioral activation, HADS = hospital anxiety and depression scale, HCLF = high carbohydrate and low fat diet, HDRS = Hamilton depression rating scale, HGL = high glycemic index, HP = high protein diet, HPLC = high protein, low carbohydrate diet, LCD = low calorie diet, LCHF = low carbohydrate, high fat diet, LED = low energy diet, LF = low fat diet, LGL = low glycemic index, LPHC = low protein, high carbohydrate diet, MHP = moderately high protein diet, MINI = mini international neuropsychiatric interview, N/A = not applicable, NF = nut-free diet, PHQ-9 = patient health questionnaire, POMS = profile of mood states, SD = standard deviation, VLCD = very low calorie diet.

The sample sizes of included studies ranged between n = 25 [ 29 ] and n = 1025 [ 30 ] participants, and adherence and completion rates varied between ≈60% [ 31 ] and 100% [ 28 , 32 , 33 , 34 , 35 , 36 , 37 , 38 ] (see Table 1 ). Mean age of patients was reported in 19 studies, with a combined mean of 47.1 years. Gender was reported in 21 studies with a total of 2041 females and 863 males. The mean BMI was reported in 15 studies and pooling those means gave a mean of 33.9 kg/m 2 . The shortest intervention duration was 28 days [ 28 ] whilst the longest was 52 weeks [ 31 , 39 , 40 , 41 ]. One study did not explicitly state the data collection end point [ 35 ].

The most frequently used depression scale was Beck’s Depression Inventory (BDI) used by 11 studies [ 25 , 31 , 32 , 33 , 35 , 39 , 40 , 42 , 43 , 44 , 45 ], followed by the Profile of Mood States (POMS) used in six [ 28 , 31 , 39 , 41 , 44 , 46 ], and the Centre for Epidemiologic Studies Depression Scale (CES-D) [ 28 , 36 , 38 ] and the Hospital Anxiety and Depression Scale (HADS) used in three [ 29 , 47 , 48 ]. Two studies used the 21-item Depression Anxiety Stress Scale (DASS-21) [ 34 , 49 ] A further seven scales were used by some studies, either in conjunction with the aforementioned, or on their own (see Table 1 ). The majority of studies compared different dieting therapy groups to each other, with only three studies comparing an energy-restricted dieting group to a nondieting control group [ 43 , 47 , 50 ].

3.2. Study Findings

A summary of the findings of each of the included studies can be found in Table 2 . Not all studies provided all values for every outcome measure but all of them commented on the desired outcomes, i.e., the effects of diet interventions on depressive symptoms in obese or overweight participants. Overall, the majority of studies concluded that weight loss, whether through calorie restriction, dietary supplements, or behavioral training, resulted in a reduction of depressive symptoms, with reported values of effect sizes on depression and depressive symptoms varying between a Cohen’s d of 0.16 [ 42 ] and 0.64 [ 49 ], while effect sizes of weight change ranged from a Cohen’s d of 0.0 [ 31 ] to 0.45 [ 39 ].

Findings of included studies.

Abbreviations: AED = almond-enriched diet, BD = balanced diet, BDI = Beck’s depression inventory, BDI-II = Beck’s Depression Inventory-2, BWL = behavioral weight loss, C = control, CES-D = center for epidemiologic studies depression scale, CRT-O = cognitive remediation therapy for obesity, D = diet, EBT = emotional brain training, FRBA = food-related behavioral activation, HCLF = high carbohydrate and low fat diet, HDRS = Hamilton depression rating scale, HE = H. erinaceus supplement, HGL = high glycemic index, HP = high protein diet, HPLC = high protein, low carbohydrate diet, I = intervention group, LCHF = low carbohydrate, high fat diet, LED = low energy diet, LGL = low glycemic index, LPHC = low protein, high carbohydrate diet, NF = nut-free diet, P = placebo, Pro = probiotic group, POMS = profile of mood states, S = supplements, Su = sumac supplement group, SD = standard deviation, SF-36 = short form health status survey, VLCD = very low calorie diet.

As we obtained studies in people with obesity and diagnosed depression and with obesity and depressive symptoms without the clinical diagnosis of depression, we will report on these two types of studies in separate sections. In people with obesity and depressive symptoms, but no diagnosis of depression, authors used different treatment approaches: energy restricted diets, energy restricted diets plus pre/probiotic supplementation, diet combined with an exercise intervention, and counselling. Thus, we dedicated one paragraph to each of these approaches. However, as these are not disjointed categories, some studies fell into multiple categories.

3.2.1. Effects of Diet Interventions on Obesity and Clinically Diagnosed Depression

Of the included studies only three were conducted in participants with concurrent obesity and clinically established depressive disorder. Participants in these three studies were on an energy restricted diet plus an additional supplement or placebo. Hariri et al. reported all relevant values for weight, BMI, and depression scores and demonstrated a decrease in weight and depression scores for both groups (sumac vs. placebo) [ 33 ]. Vaghef-Mehrabany et al. [ 25 ] and Vigna et al. [ 37 ] did not provide values for all groups at all time points but nonetheless commented on the outcomes. Vaghef-Mahrabany et al. did not find any difference between the group receiving supplementation and the placebo group, however, they did note that regardless of group classification, participants that lost more than 1.9 kg of weight showed significantly improved depression scores. In contrast, Vigna et al. reported significant reductions in depression scores for the group receiving the H. erinaceus supplement.

3.2.2. Effects of Diet Interventions on Obesity and Depressive Symptoms

Studies of energy restricted diets.

The majority of studies ( n = 16) investigated the effects of specific calorie restricted diets on weight and depressive symptoms in overweight or obese participants without an established current clinical diagnosis of depression. None of the studies included here reported full datasets with values at each time point and corresponding significance values. Most authors reported a decrease in depressive symptoms following a calorie restricted diet, aside from one study [ 48 ] that reported no change in depression scores. Three studies compared a calorie restricted diet with a noncalorie restricted control group, and all three found a reduction in both weight and depression scores in the intervention group [ 40 , 43 , 50 ]. However, most studies compared different calorie reduced diets with each other, i.e., four studies compared a low carbohydrate, high fat (LCHF) diet with a high fat, low carbohydrate (HCLF) diet [ 29 , 31 , 39 , 44 ], one study compared a high protein diet with a high carbohydrate diet [ 41 ], one study compared a high protein diet with low fat diet [ 32 ], one compared a very low calorie diet with an energy reduced balanced diet [ 42 ], and one study compared the traditional Brazilian diet with olive oil supplementation [ 47 ]. The remaining studies on energy restricted diets included the use of dietary supplements and will thus be discussed separately in the next section.

Studies on Energy Restricted Diets Plus Pre/Probiotic Supplementation

Three studies reported on the impact of calorie restriction with additional pre/probiotic supplementation [ 25 , 45 , 49 ]. Hadi et al. [ 49 ] and Sanchez et al. [ 45 ] found a significant decrease in depression scores for the groups receiving pro/prebiotics whereas Vaghef-Mehrabany et al. [ 25 ] reported a decrease in depression scores for participants who achieved a weight loss greater than 1.9kg regardless of prebiotic supplementation.

Studies on Diet Combined with Exercise Intervention

Four studies investigated the impact of diet and exercise/lifestyle interventions on depressive symptoms [ 35 , 39 , 40 , 48 ]. Three of them reported significant reductions in depression scores accompanying reductions in weight, except from Pedersen et al. [ 48 ] who reported no differences in depression scores between the two groups (aerobic interval training (AIT) vs. low energy diet (LED)) even though the LED group achieved a 10.4% decrease in body weight.

Studies on Counselling (Not Explicitly Calorie Restricted)

We found seven studies that reported on the effects of supplements without calorie restriction [ 46 ] or on the effects of behavioral modifications/counselling on depression scores [ 28 , 30 , 34 , 35 , 36 , 38 ]. These studies were not specifically prescribing calorie restricted diets but were rather providing additional supplements and/or counselling on healthy lifestyle modifications, such as dietary and exercise recommendations. The exception to this was the Breymeyer et al. study, which did not include any training or calorie restriction but was comparing the effects of a high glycemic (HG) diet (vs. a low glycemic (LG) diet) on depression scores [ 28 ]. The authors concluded that mood disturbance was higher for the group on the HG diet, with higher depression scores associated with higher glycemic load. Coates et al. investigated the effects of an almond-enriched diet compared to a nut-free diet and found no differences in depression scores between the two groups [ 46 ]. Three studies [ 35 , 36 , 38 ] investigated what effect counselling or behavioral training has on depression scores and all three found improvements in depressive symptoms following the intervention. One study investigated the effects of multinutrient supplementation and/or food-related behavioral activation therapy (in a 2 × 2 design) on depressive symptoms and did not find any significant effect of either on depression scores [ 30 ]. Lastly, one study compared the effect of behavioral weight loss with or without cognitive remediation therapy on body weight and depression scores and found no changes in depression scores between the two groups [ 34 ].

4. Discussion

4.1. summary of the main findings.

This systematic review summarizes the existing data on the effects of diet on depressive symptoms in overweight or obese patients. Findings from the included studies were mixed, with the majority of studies reporting significant improvements in depression scores after diet and weight loss, and the remaining studies reporting no differences between depression scores between pre- and postintervention [ 34 , 46 , 48 ]. No studies reported deterioration of depressive symptoms aside from one that reported increased mood disturbance in participants on a high glycemic load diet [ 28 ]. Importantly, the majority of authors reported high adherence to the intervention, whether those were hypocaloric diets or supplements. The trend of obese individuals experiencing an improvement in their depressive symptoms after diet and weight loss is in line with previous research. Dietary interventions using a calorie-restricted diet (e.g., [ 25 , 29 , 44 ]) resulted in decreases in depressive symptoms. However, the results are less clear for dietary supplements (e.g., [ 33 , 37 , 46 ]). Overall, the dietary approaches were heterogenous in that the diets investigated were calorie reduced, traditional, high/low in protein, high/low in carbohydrates, with/or without pre-/probiotic, vitamins, or naturopathic supplements.

4.2. Possible Mechanisms for Improved Mood after Weight Loss

It is well established that depression and obesity co-occur to a high degree [ 5 , 6 , 51 , 52 , 53 , 54 ], however the relationship between the two disorders is complex and currently of ambiguous directionality. Stunkard et al. presented a summary on the existing data using a moderator/mediator framework in which they classified eating and physical activity as an important mediator of obesity and comorbid depression [ 16 ]. Some authors consider depression as a consequence of obesity resulting from societal stigmatization, dissatisfaction with one’s appearance, and low self-esteem [ 55 , 56 , 57 ]. Others consider obesity as resulting from decreased physical activity, excessive ‘comfort’ eating, and antidepressant medication use that often accompanies depression [ 58 , 59 , 60 , 61 , 62 ].

Several epidemiological studies have found associations between mood and diet. Particularly, a western-style diet high in processed foods and sugar content and low in fruits and vegetables, is associated with worsening of mood states. Indeed, one of our included studies found increases in depression scores in participants on a high glycemic load diet [ 28 ]. Diets that are high in carbohydrates but low in fat and protein have also been associated with lower mood scores in cross-sectional studies [ 63 , 64 ], whereas an abundance of research extols the beneficial effects of Mediterranean-style diets [ 65 ] which are high in fruit, vegetables, nuts, pulses and wholegrains, low in fat and carbohydrate, with very little processed foods. The differences in mood scores between these two types of diets are thought to be partly due to the increased systemic inflammation and oxidative processes that often accompanies a western-style diet [ 66 , 67 , 68 , 69 ].

4.2.1. Physiological Mechanisms

Research has exposed metabolic and inflammatory dysregulation as a common denominator in depression and obesity [ 70 , 71 ]. Additionally, both depressed and obese patients exhibit dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis [ 72 , 73 ] and consequently chronic elevations in cortisol [ 74 , 75 ]. Increases in cortisol levels have been reported as having a causal role in depression, as well as leading to weight gain, specifically in abdominal adiposity. Recently, white adipose tissue (WAT) has been conceptualized as an endocrine organ, as opposed to how it was previously thought of—as an inert storage tissue—due to its ability to produce cytokines and other related molecules. Among these are interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α [ 76 , 77 , 78 ], which are known proinflammatory cytokines, as well as chemokines, including monocyte chemoattractant protein (MCP)-1 [ 79 , 80 ]. The ensuing signaling cascade leads to immune activation and white blood cell accumulation, and an overall increased inflammatory response. This immune activation has various downstream effects. For example, IL-2 reduces tryptophan plasma levels [ 81 ], possibly by activating tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO). Tryptophan is an essential amino acid necessary for 5-HT synthesis. Low levels of tryptophan could lead to lower levels of serotonin and thus affect mood. Another example is the accumulation of peripheral monocytes in the brain as a result of systemic inflammation [ 82 ], and specifically the increased production of MCP-1 in hypothalamic neurons. This monocyte migration has been associated with increased anxiety and depression [ 83 ]. Minimization of accumulated adipose tissue through weight loss could attenuate this inflammatory process, leading to improved mood.

Another molecule implicated in both obesity and depression is leptin. Leptin is a peptide hormone released by adipocytes and crosses the blood–brain barrier via a saturable transport mechanism. Low plasma levels of leptin have been observed in depressed patients [ 84 , 85 ]. In the case of obesity however, plasma leptin levels have been found to be elevated [ 86 , 87 ]. This contradictory finding can be explained by leptin resistance (as in the case of type 2 diabetic patients being resistant to insulin) and could be a result of impaired transport across the blood–brain barrier, of reduced function of the leptin receptor, or errors in signal transduction [ 88 , 89 ]. Similar to cortisol and inflammatory molecules described previously, leptin modulates HPA axis function [ 90 , 91 ]. Leptin also interacts with monoamines and although its effect on monoamine neurotransmission remains unclear, there is evidence for leptin’s involvement in the 5-HT system [ 92 ] and in the activation of STAT3 in dopamine neurons of the ventral tegmental area (VTA) [ 93 ]. Reducing the amount of adipose tissue through diet and subsequent weight loss could ameliorate leptin resistance, reinstate leptin function, and relieve low mood.

4.2.2. Psychosocial Mechanisms

It should be borne in mind that psychosocial attributes may affect physiology, and the distinction between the two mechanisms here is for ease of discussion. A good example of this environment x biology interaction is the finding that weight discrimination, often experienced by obese individuals, increases cortisol levels [ 94 ]. Additionally, repeated discrimination can lead to lower self-esteem and increased negative affect [ 95 ]. Many studies have reported on the negative attitudes of employers, peers, and even clinicians towards obese persons [ 96 , 97 ]. Continued maltreatment can impact obese persons’ mood and self-concept, both of which can contribute to depression.

Even if obese individuals do not experience weight discrimination or stigma by others, their self-esteem could be impacted by their own body image dissatisfaction (BID). Some research has found correlations between BID and depressive symptoms and suggested that obesity confers risk for developing depression through increased BID [ 98 , 99 ]. Therefore, it is possible that losing weight improves body image satisfaction and low mood. For a more thorough discussion see Markowitz et al. [ 100 ].

It is important to note that some researchers posit that while obese individuals experiencing weight loss also experience an improvement in mood, this improvement does not seem to be mediated by the weight loss itself but is rather related to active participation in treatment [ 101 , 102 , 103 , 104 ].

4.3. Clinical Implications

Given the high prevalence of obesity and depression and the strain exerted on healthcare systems it would be of great value if prescribing dietary modifications for the amelioration of obesity had the additional consequence of improving depressive symptoms. Our findings suggest that dietary interventions leading to weight loss improve mood scores in both clinically and subclinically depressed obese individuals. Importantly, adherence to intervention seemed to be high in our included studies, which provides clinicians reason for optimism.

People with obesity and depression or depressive symptoms are a particularly vulnerable group who are at risk of worsening of depressive symptoms (e.g., [ 105 ]), switching from depression to mania (e.g., [ 106 ]), and of the appearance of eating disorder symptoms (e.g., [ 107 ]). Thus, further studies in obese and depressed patients should focus on the safety of diets regarding the reoccurrence of depressive symptoms, the switch from depression to mania, and the appearance of eating disorder symptoms.

4.4. Strengths and Limitations

This is the first review to systematically collate research on the effects of dietary interventions on depression and depressive symptoms in overweight/obese patients. Our strict inclusion of longitudinal clinical trials strengthens the validity of our findings. Additionally, the quality of most of the studies was good, and only one was deemed fair (see Table 1 ). However, the respective study quality was deemed good according to each study’s specific research question which is not the same as being of good quality to answer the research question of this review. Therefore, our finding of weight loss ameliorating depression scores in obese individuals is based on limited and heterogeneous data.

Furthermore, even though a meta-analytic approach would have provided more quantifiable evidence, such an approach would have been inappropriate based on the heterogeneity of the studies. This heterogeneity emerged from both the plethora of dietary approaches investigated as well as the varied comparison groups, and the lack of data. However, future meta-analytic research could investigate well-defined dietary categories by being less stringent with inclusion criteria, for example by including all studies in depressed patients regardless of the weight status.

A further limitation of our review is the inclusion of only three studies that compared the depression scores of participants in an energy-restricted diet group to a non-dieting control group. The lack of well-defined randomized controlled trials (RCTs) with this specific research question limits the validity and generalizability of our conclusion. Further RCTs are necessary to confirm the trend we have noted in this review.

Our study focused on the use of diet in people with both, obesity and depression. We did not include studies if obesity was not an important aspect of the study design, e.g., the SMILES trial [ 108 ] and the HELFIMED study [ 109 ], both of which showed that dietary improvement is associated with a reduction in depression scores. However, this systematic review focused on people with both, obesity and depression, because we wanted to investigate whether dietary modifications would help people who suffer from both disorders.

5. Conclusions

The findings of the current review provide preliminary evidence for the importance of weight loss in obese individuals experiencing low mood. The majority of studies included showed decreases in depression scores following dietary interventions, specifically through calorie-restricted diets. This is in line with a large body of research reporting amelioration of depressive symptoms in obese patients after weight loss. It is plausible that pursuing dietary interventions for obese patients with comorbid depression could have the additional benefit of relieving some of their depressive symptoms as well as improving their metabolic profile and cardiovascular risk. Therefore, a restricted diet might specifically help people with type 2 depression which is characterized by an increased appetite and weight gain, leaden paralysis, hypersomnia, and a persistently poor metabolic profile [ 13 ].

In summary, people with obesity and depression appear to be a specific subgroup of depressed patients. In this subgroup, calorie-restricted diets could constitute a promising personalized treatment approach which might lead to a reduction of depressive symptoms. The underlying mechanisms at play may be related to the immune and endocrine systems and to psychosocial aspects obesity.

Author Contributions

Original idea by H.H.; H.H., A.H.Y., U.S. and B.W.J.H.P. developed the scientific concept of the manuscript; O.P. and J.K. performed the systematic review; O.P. drafted the manuscript, and all authors provided feedback; all authors have read and agreed to the published version of the manuscript.

O.P., U.S., H.H., and A.H.Y. received salary support from the National Institute for Health Research (NIHR) Biomedical Research Centre for Mental Health, South London and Maudsley NHS Foundation Trust, and Institute of Psychiatry, Psychology and Neuroscience, KCL. U.S. and A.H.Y. are also supported by NIHR Senior Investigator Awards. The views expressed in this publication are those of the authors and not necessarily those of the National Health Service, the NIHR, or the UK Department of Health.

Institutional Review Board Statement

Informed consent statement, data availability statement, conflicts of interest.

The authors declare no conflict of interest.

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