obesity summary essay

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Essay on Obesity

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Obesity is a chronic health condition in which the body fat reaches abnormal level. Obesity occurs when we consume much more amount of food than our body really needs on a daily basis. In other words, when the intake of calories is greater than the calories we burn out, it gives rise to obesity.

Audience: The below given essays are exclusively written for school students (Class 5, 6, 7, 8, 9, 10, 11 and 12 Standard), college, science and medical students.

Introduction:

Obesity means being excessively fat. A person would be said to be obese if his or her body mass index is beyond 30. Such a person has a body fat rate that is disproportionate to his body mass.

Obesity and the Body Mass Index:

The body mass index is calculated considering the weight and height of a person. Thus, it is a scientific way of determining the appropriate weight of any person. When the body mass index of a person indicates that he or she is obese, it exposes the person to make health risk.

Stopping Obesity:

There are two major ways to get the body mass index of a person to a moderate rate. The first is to maintain a strict diet. The second is to engage in regular physical exercise. These two approaches are aimed at reducing the amount of fat in the body.

Conclusion:

Obesity can lead to sudden death, heart attack, diabetes and may unwanted illnesses. Stop it by making healthy choices.

Obesity has become a big concern for the youth of today’s generation. Obesity is defined as a medical condition in which an individual gains excessive body fat. When the Body Mass Index (BMI) of a person is over 30, he/ she is termed as obese.

Obesity can be a genetic problem or a disorder that is caused due to unhealthy lifestyle habits of a person. Physical inactivity and the environment in which an individual lives, are also the factors that leads to obesity. It is also seen that when some individuals are in stress or depression, they start cultivating unhealthy eating habits which eventually leads to obesity. Medications like steroids is yet another reason for obesity.

Obesity has several serious health issues associated with it. Some of the impacts of obesity are diabetes, increase of cholesterol level, high blood pressure, etc. Social impacts of obesity includes loss of confidence in an individual, lowering of self-esteem, etc.

The risks of obesity needs to be prevented. This can be done by adopting healthy eating habits, doing some physical exercise regularly, avoiding stress, etc. Individuals should work on weight reduction in order to avoid obesity.

Obesity is indeed a health concern and needs to be prioritized. The management of obesity revolves around healthy eating habits and physical activity. Obesity, if not controlled in its initial stage can cause many severe health issues. So it is wiser to exercise daily and maintain a healthy lifestyle rather than being the victim of obesity.

Obesity can be defined as the clinical condition where accumulation of excessive fat takes place in the adipose tissue leading to worsening of health condition. Usually, the fat is deposited around the trunk and also the waist of the body or even around the periphery.

Obesity is actually a disease that has been spreading far and wide. It is preventable and certain measures are to be taken to curb it to a greater extend. Both in the developing and developed countries, obesity has been growing far and wide affecting the young and the old equally.

The alarming increase in obesity has resulted in stimulated death rate and health issues among the people. There are several methods adopted to lose weight and they include different diet types, physical activity and certain changes in the current lifestyle. Many of the companies are into minting money with the concept of inviting people to fight obesity.

In patients associated with increased risk factor related to obesity, there are certain drug therapies and other procedures adopted to lose weight. There are certain cost effective ways introduced by several companies to enable clinic-based weight loss programs.

Obesity can lead to premature death and even cause Type 2 Diabetes Mellitus. Cardiovascular diseases have also become the part and parcel of obese people. It includes stroke, hypertension, gall bladder disease, coronary heart disease and even cancers like breast cancer, prostate cancer, endometrial cancer and colon cancer. Other less severe arising due to obesity includes osteoarthritis, gastro-esophageal reflux disease and even infertility.

Hence, serious measures are to be taken to fight against this dreadful phenomenon that is spreading its wings far and wide. Giving proper education on benefits of staying fit and mindful eating is as important as curbing this issue. Utmost importance must be given to healthy eating habits right from the small age so that they follow the same until the end of their life.

Obesity is majorly a lifestyle disease attributed to the extra accumulation of fat in the body leading to negative health effects on a person. Ironically, although prevalent at a large scale in many countries, including India, it is one of the most neglect health problems. It is more often ignored even if told by the doctor that the person is obese. Only when people start acquiring other health issues such as heart disease, blood pressure or diabetes, they start taking the problem of obesity seriously.

Obesity Statistics in India:

As per a report, India happens to figure as the third country in the world with the most obese people. This should be a troubling fact for India. However, we are yet to see concrete measures being adopted by the people to remain fit.

Causes of Obesity:

Sedentary lifestyle, alcohol, junk food, medications and some diseases such as hypothyroidism are considered as the factors which lead to obesity. Even children seem to be glued to televisions, laptops and video games which have taken away the urge for physical activities from them. Adding to this, the consumption of junk food has further aggravated the growing problem of obesity in children.

In the case of adults, most of the professions of today make use of computers which again makes people sit for long hours in one place. Also, the hectic lifestyle of today makes it difficult for people to spare time for physical activities and people usually remain stressed most of the times. All this has contributed significantly to the rise of obesity in India.

Obesity and BMI:

Body Mass Index (BMI) is the measure which allows a person to calculate how to fit he or she is. In other words, the BMI tells you if you are obese or not. BMI is calculated by dividing the weight of a person in kg with the square of his / her height in metres. The number thus obtained is called the BMI. A BMI of less than 25 is considered optimal. However, if a person has a BMI over 30 he/she is termed as obese.

What is a matter of concern is that with growing urbanisation there has been a rapid increase of obese people in India? It is of utmost importance to consider this health issue a serious threat to the future of our country as a healthy body is important for a healthy soul. We should all be mindful of what we eat and what effect it has on our body. It is our utmost duty to educate not just ourselves but others as well about this serious health hazard.

Obesity can be defined as a condition (medical) that is the accumulation of body fat to an extent that the excess fat begins to have a lot of negative effects on the health of the individual. Obesity is determined by examining the body mass index (BMI) of the person. The BMI is gotten by dividing the weight of the person in kilogram by the height of the person squared.

When the BMI of a person is more than 30, the person is classified as being obese, when the BMI falls between 25 and 30, the person is said to be overweight. In a few countries in East Asia, lower values for the BMI are used. Obesity has been proven to influence the likelihood and risk of many conditions and disease, most especially diabetes of type 2, cardiovascular diseases, sleeplessness that is obstructive, depression, osteoarthritis and some cancer types.

In most cases, obesity is caused through a combination of genetic susceptibility, a lack of or inadequate physical activity, excessive intake of food. Some cases of obesity are primarily caused by mental disorder, medications, endocrine disorders or genes. There is no medical data to support the fact that people suffering from obesity eat very little but gain a lot of weight because of slower metabolism. It has been discovered that an obese person usually expends much more energy than other people as a result of the required energy that is needed to maintain a body mass that is increased.

It is very possible to prevent obesity with a combination of personal choices and social changes. The major treatments are exercising and a change in diet. We can improve the quality of our diet by reducing our consumption of foods that are energy-dense like those that are high in sugars or fat and by trying to increase our dietary fibre intake.

We can also accompany the appropriate diet with the use of medications to help in reducing appetite and decreasing the absorption of fat. If medication, exercise and diet are not yielding any positive results, surgery or gastric balloon can also be carried out to decrease the volume of the stomach and also reduce the intestines’ length which leads to the feel of the person get full early or a reduction in the ability to get and absorb different nutrients from a food.

Obesity is the leading cause of ill-health and death all over the world that is preventable. The rate of obesity in children and adults has drastically increased. In 2015, a whopping 12 percent of adults which is about 600 million and about 100 million children all around the world were found to be obese.

It has also been discovered that women are more obese than men. A lot of government and private institutions and bodies have stated that obesity is top of the list of the most difficult and serious problems of public health that we have in the world today. In the world we live today, there is a lot of stigmatisation of obese people.

We all know how troubling the problem of obesity truly is. It is mainly a form of a medical condition wherein the body tends to accumulate excessive fat which in turn has negative repercussions on the health of an individual.

Given the current lifestyle and dietary style, it has become more common than ever. More and more people are being diagnosed with obesity. Such is its prevalence that it has been termed as an epidemic in the USA. Those who suffer from obesity are at a much higher risk of diabetes, heart diseases and even cancer.

In order to gain a deeper understanding of obesity, it is important to learn what the key causes of obesity are. In a layman term, if your calorie consumption exceeds what you burn because of daily activities and exercises, it is likely to lead to obesity. It is caused over a prolonged period of time when your calorie intake keeps exceeding the calories burned.

Here are some of the key causes which are known to be the driving factors for obesity.

If your diet tends to be rich in fat and contains massive calorie intake, you are all set to suffer from obesity.

Sedentary Lifestyle:

With most people sticking to their desk jobs and living a sedentary lifestyle, the body tends to get obese easily.

Of course, the genetic framework has a lot to do with obesity. If your parents are obese, the chance of you being obese is quite high.

The weight which women gain during their pregnancy can be very hard to shed and this is often one of the top causes of obesity.

Sleep Cycle:

If you are not getting an adequate amount of sleep, it can have an impact on the hormones which might trigger hunger signals. Overall, these linked events tend to make you obese.

Hormonal Disorder:

There are several hormonal changes which are known to be direct causes of obesity. The imbalance of the thyroid stimulating hormone, for instance, is one of the key factors when it comes to obesity.

Now that we know the key causes, let us look at the possible ways by which you can handle it.

Treatment for Obesity:

As strange as it may sound, the treatment for obesity is really simple. All you need to do is follow the right diet and back it with an adequate amount of exercise. If you can succeed in doing so, it will give you the perfect head-start into your journey of getting in shape and bidding goodbye to obesity.

There are a lot of different kinds and styles of diet plans for obesity which are available. You can choose the one which you deem fit. We recommend not opting for crash dieting as it is known to have several repercussions and can make your body terribly weak.

The key here is to stick to a balanced diet which can help you retain the essential nutrients, minerals, and, vitamins and shed the unwanted fat and carbs.

Just like the diet, there are several workout plans for obesity which are available. It is upon you to find out which of the workout plan seems to be apt for you. Choose cardio exercises and dance routines like Zumba to shed the unwanted body weight. Yoga is yet another method to get rid of obesity.

So, follow a blend of these and you will be able to deal with the trouble of obesity in no time. We believe that following these tips will help you get rid of obesity and stay in shape.

Obesity and overweight is a top health concern in the world due to the impact it has on the lives of individuals. Obesity is defined as a condition in which an individual has excessive body fat and is measured using the body mass index (BMI) such that, when an individual’s BMI is above 30, he or she is termed obese. The BMI is calculated using body weight and height and it is different for all individuals.

Obesity has been determined as a risk factor for many diseases. It results from dietary habits, genetics, and lifestyle habits including physical inactivity. Obesity can be prevented so that individuals do not end up having serious complications and health problems. Chronic illnesses like diabetes, heart diseases and relate to obesity in terms of causes and complications.

Factors Influencing Obesity:

Obesity is not only as a result of lifestyle habits as most people put it. There are other important factors that influence obesity. Genetics is one of those factors. A person could be born with genes that predispose them to obesity and they will also have difficulty in losing weight because it is an inborn factor.

The environment also influences obesity because the diet is similar in certain environs. In certain environments, like school, the food available is fast foods and the chances of getting healthy foods is very low, leading to obesity. Also, physical inactivity is an environmental factor for obesity because some places have no fields or tracks where people can jog or maybe the place is very unsafe and people rarely go out to exercise.

Mental health affects the eating habits of individuals. There is a habit of stress eating when a person is depressed and it could result in overweight or obesity if the person remains unhealthy for long period of time.

The overall health of individuals also matter. If a person is unwell and is prescribed with steroids, they may end up being obese. Steroidal medications enable weight gain as a side effect.

Complications of Obesity:

Obesity is a health concern because its complications are severe. Significant social and health problems are experienced by obese people. Socially, they will be bullied and their self-esteem will be low as they will perceive themselves as unworthy.

Chronic illnesses like diabetes results from obesity. Diabetes type 2 has been directly linked to obesity. This condition involves the increased blood sugars in the body and body cells are not responding to insulin as they should. The insulin in the body could also be inadequate due to decreased production. High blood sugar concentrations result in symptoms like frequent hunger, thirst and urination. The symptoms of complicated stages of diabetes type 2 include loss of vision, renal failure and heart failure and eventually death. The importance of having a normal BMI is the ability of the body to control blood sugars.

Another complication is the heightened blood pressures. Obesity has been defined as excessive body fat. The body fat accumulates in blood vessels making them narrow. Narrow blood vessels cause the blood pressures to rise. Increased blood pressure causes the heart to start failing in its physiological functions. Heart failure is the end result in this condition of increased blood pressures.

There is a significant increase in cholesterol in blood of people who are obese. High blood cholesterol levels causes the deposition of fats in various parts of the body and organs. Deposition of fats in the heart and blood vessels result in heart diseases. There are other conditions that result from hypercholesterolemia.

Other chronic illnesses like cancer can also arise from obesity because inflammation of body cells and tissues occurs in order to store fats in obese people. This could result in abnormal growths and alteration of cell morphology. The abnormal growths could be cancerous.

Management of Obesity:

For the people at risk of developing obesity, prevention methods can be implemented. Prevention included a healthy diet and physical activity. The diet and physical activity patterns should be regular and realizable to avoid strains that could result in complications.

Some risk factors for obesity are non-modifiable for example genetics. When a person in genetically predisposed, the lifestyle modifications may be have help.

For the individuals who are already obese, they can work on weight reduction through healthy diets and physical exercises.

In conclusion, obesity is indeed a major health concern because the health complications are very serious. Factors influencing obesity are both modifiable and non-modifiable. The management of obesity revolves around diet and physical activity and so it is important to remain fit.

In olden days, obesity used to affect only adults. However, in the present time, obesity has become a worldwide problem that hits the kids as well. Let’s find out the most prevalent causes of obesity.

Factors Causing Obesity:

Obesity can be due to genetic factors. If a person’s family has a history of obesity, chances are high that he/ she would also be affected by obesity, sooner or later in life.

The second reason is having a poor lifestyle. Now, there are a variety of factors that fall under the category of poor lifestyle. An excessive diet, i.e., eating more than you need is a definite way to attain the stage of obesity. Needless to say, the extra calories are changed into fat and cause obesity.

Junk foods, fried foods, refined foods with high fats and sugar are also responsible for causing obesity in both adults and kids. Lack of physical activity prevents the burning of extra calories, again, leading us all to the path of obesity.

But sometimes, there may also be some indirect causes of obesity. The secondary reasons could be related to our mental and psychological health. Depression, anxiety, stress, and emotional troubles are well-known factors of obesity.

Physical ailments such as hypothyroidism, ovarian cysts, and diabetes often complicate the physical condition and play a massive role in abnormal weight gain.

Moreover, certain medications, such as steroids, antidepressants, and contraceptive pills, have been seen interfering with the metabolic activities of the body. As a result, the long-term use of such drugs can cause obesity. Adding to that, regular consumption of alcohol and smoking are also connected to the condition of obesity.

Harmful Effects of Obesity:

On the surface, obesity may look like a single problem. But, in reality, it is the mother of several major health issues. Obesity simply means excessive fat depositing into our body including the arteries. The drastic consequence of such high cholesterol levels shows up in the form of heart attacks and other life-threatening cardiac troubles.

The fat deposition also hampers the elasticity of the arteries. That means obesity can cause havoc in our body by altering the blood pressure to an abnormal range. And this is just the tip of the iceberg. Obesity is known to create an endless list of problems.

In extreme cases, this disorder gives birth to acute diseases like diabetes and cancer. The weight gain due to obesity puts a lot of pressure on the bones of the body, especially of the legs. This, in turn, makes our bones weak and disturbs their smooth movement. A person suffering from obesity also has higher chances of developing infertility issues and sleep troubles.

Many obese people are seen to be struggling with breathing problems too. In the chronic form, the condition can grow into asthma. The psychological effects of obesity are another serious topic. You can say that obesity and depression form a loop. The more a person is obese, the worse is his/ her depression stage.

How to Control and Treat Obesity:

The simplest and most effective way, to begin with, is changing our diet. There are two factors to consider in the diet plan. First is what and what not to eat. Second is how much to eat.

If you really want to get rid of obesity, include more and more green vegetables in your diet. Spinach, beans, kale, broccoli, cauliflower, asparagus, etc., have enough vitamins and minerals and quite low calories. Other healthier options are mushrooms, pumpkin, beetroots, and sweet potatoes, etc.

Opt for fresh fruits, especially citrus fruits, and berries. Oranges, grapes, pomegranate, pineapple, cherries, strawberries, lime, and cranberries are good for the body. They have low sugar content and are also helpful in strengthening our immune system. Eating the whole fruits is a more preferable way in comparison to gulping the fruit juices. Fruits, when eaten whole, have more fibers and less sugar.

Consuming a big bowl of salad is also great for dealing with the obesity problem. A salad that includes fibrous foods such as carrots, radish, lettuce, tomatoes, works better at satiating the hunger pangs without the risk of weight gain.

A high protein diet of eggs, fish, lean meats, etc., is an excellent choice to get rid of obesity. Take enough of omega fatty acids. Remember to drink plenty of water. Keeping yourself hydrated is a smart way to avoid overeating. Water also helps in removing the toxins and excess fat from the body.

As much as possible, avoid fats, sugars, refined flours, and oily foods to keep the weight in control. Control your portion size. Replace the three heavy meals with small and frequent meals during the day. Snacking on sugarless smoothies, dry fruits, etc., is much recommended.

Regular exercise plays an indispensable role in tackling the obesity problem. Whenever possible, walk to the market, take stairs instead of a lift. Physical activity can be in any other form. It could be a favorite hobby like swimming, cycling, lawn tennis, or light jogging.

Meditation and yoga are quite powerful practices to drive away the stress, depression and thus, obesity. But in more serious cases, meeting a physician is the most appropriate strategy. Sometimes, the right medicines and surgical procedures are necessary to control the health condition.

Obesity is spreading like an epidemic, haunting both the adults and the kids. Although genetic factors and other physical ailments play a role, the problem is mostly caused by a reckless lifestyle.

By changing our way of living, we can surely take control of our health. In other words, it would be possible to eliminate the condition of obesity from our lives completely by leading a healthy lifestyle.

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Causes and Effects of Obesity Essay

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Introduction

Laziness as the main cause of obesity, social effects of obesity, effects of obesity: health complications.

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Maintaining good body weight is highly recommended by medical doctors as a way of promoting a healthy status of the body. This is to say that there is allowed body weight, which a person is supposed to maintain. Extreme deviations from this weight expose a person to several health complications.

While being underweight is not encouraged, cases of people who are overweight and increasing effects of this condition have raised concerns over the need of addressing the issue of obesity in the society today, where statistics are rising day and night. What is obesity? This refers to a medical condition in which a person’s body has high accumulation of body fat to the level of being fatal or a cause of serious health complications. Additionally, obesity is highly associated with one’s body mass index, abbreviated as BMI.

This denotes the value obtained when a person’s weight in kilograms is divided by the square of their height in meters (Burniat 3). According to medical experts, obesity occurs when the BMI exceeds 30kg/m 2 . While this is the case, people who have a BMI of between 25 and 29 and considered to be overweight. Obesity has a wide-range of negative effects, which may be a threat to the life of a person.

The fist effect of obesity is that it encourages laziness in the society. It is doubtless that obese people find it hard and strenuous to move from one point to the other because of accumulated fats. As a result, most of these people lead a sedentary lifestyle, which is usually characterized by minimal or no movement. In such scenarios, victims prefer being helped doing basic activities, including moving from one point to another.

Moreover, laziness makes one to be inactive and unproductive. For example, a student who is obese may find it hard to attend to his or her homework and class assignments, thus affecting performance. With regard to physical exercises, obese people perceive exercises as punishment, which is not meant for them (Korbonits 265). As a result, they do not accept simple activities like jogging because of their inability to move.

In line with this, obese people cannot participate in games like soccer, athletics, and rugby among others. Based on this sedentary lifestyle, obese people spend a lot of their time watching television, movies, and playing video games, which worsen the situation.

The main effect of obesity is health complications. Research indicates that most of the killer diseases like diabetes, heart diseases, and high blood pressure are largely associated with obesity. In the United States, obesity-related complications cost the nation approximately 150 billion USD and result into 0.3 million premature deaths annually.

When there is increase in body fat, it means that the body requires more nutrients and oxygen to support body tissues (Burniat 223). Since these elements can only be transported by the blood to various parts of the body, the workload of the heart is increased.

This increase in the workload of the heart exerts pressure on blood vessels, leading to high blood pressure. An increase in the heart rate may also be dangerous due to the inability of the body to supply required blood to various parts. Moreover, obesity causes diabetes, especially among adults as the body may become resistant to insulin. This resistance may lead to a high level of blood sugar, which is fatal.

Besides health complications, obesity causes an array of psychological effects, including inferiority complex among victims. Obese people suffer from depression, emanating from negative self-esteem and societal rejection. In some cases, people who become obese lose their friends and may get disapproval from teachers and other personalities (Korbonits 265). This is mainly based on the assumption that people become obese due to lack of self-discipline. In extreme cases, obese people may not be considered for promotion at workplaces, because of the negative perception held against them.

Due to inferiority complex, obese people avoid being in public and prefer being alone. This is because they imagine how the world sees them and may also find it hard being involved in public activities because of their sizes.

This further makes them to consider themselves unattractive based on their deviation from what is considered as the normal body size and shape. Regardless of how obese people are treated, they always believe that they are being undermined because of their body size.

In summary, obesity is a major cause of premature deaths in the United States and around the world. This health condition occurs when there is excess accumulation of body fat, caused by unhealthy lifestyles. Obesity is largely associated with several killer diseases like high blood pressure, diabetes, and diseases of the heart.

These diseases drain world economies since most of them are fatal and expensive to manage. Additionally, obesity promotes sedentary life where victims minimize movement by adopting an inactive lifestyle. Moreover, obese victims suffer psychologically because of societal rejection. In general, obesity has a wide-range of negative effects, which may be a threat to the life of a person.

Burniat, Walter. Child and Adolescent Obesity: Causes and Consequences, Prevention and Management . United Kingdom: Cambridge University Press, 2002. Print.

Korbonits, Márta. Obesity and Metabolism . Switzerland: Karger Publishers, 2008. Print.

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Overview of Obesity

Facts about obesity.

Overweight and obesity together make up one of the leading preventable causes of death in the U.S. Obesity is a chronic disease that can seriously affect your health.

Overweight means that you have extra body weight. Obesity means having a high amount of extra body fat. Being overweight or obese raises your risk for health problems. These include:

Coronary heart disease

Type 2 diabetes

High cholesterol

Osteoarthritis

High blood pressure

Sleep apnea

Some types of cancer.

Public health experts agree that overweight and obesity have reached epidemic proportions in this country and around the world. More than one-third of U.S. adults are obese. People ages 60 and older are more likely to be obese than younger adults, according to the most recent data from the National Health and Nutrition Examination Survey. And the problem also affects children. Approximately 20% of U.S. children and teens ages 2 to 19 are obese.

Who's obese?

Overweight and obesity are different points on a scale that ranges from being underweight to being morbidly obese. Where you fit on this scale is determined by your body mass index (BMI).

BMI is a measure of your weight as it relates to your height. BMI often gives you a good idea of the amount of body fat you have. Your healthcare providers use BMI to find out your risk for obesity-related diseases. Sometimes some very muscular people may have a BMI in the overweight range. But these people are not considered overweight because muscle tissue weighs more than fat tissue.

In general, a BMI from 20 to 24.9 in adults is considered ideal. A BMI between 25 and 29.9 is considered overweight. A person is considered obese if the BMI is 30 or higher.

In general, after the age of 50, the weight of a person assigned male at birth weight tends to stay the same and often decreases slightly between ages 60 and 74. In contrast, the weight of a person assigned female at birth tends to increase until age 60, and then begins to decrease.

Obesity can also be measured by waist-to-hip ratio. This is a measurement tool that looks at the amount of fat on your waist, compared with the amount of fat on your hips and buttocks. The waist circumference tells the amount of stomach fat. Increased stomach fat is linked to type 2 diabetes, high cholesterol, high blood pressure, and heart disease. A waist circumference of more than 40 inches in people assigned male at birth and more than 35 inches in people assigned female at birth may increase the risk for heart disease and other diseases tied to being overweight.

Talk with your healthcare provider if you have questions about healthy body weight.

What causes obesity?

In many ways, obesity is a puzzling disease. Experts don't know exactly how your body regulates your weight and body fat. What they do know is that a person who eats more calories than they use for energy each day will gain weight.

But the risk factors that determine obesity can be complex. They are often a combination of your genes, socioeconomic factors, metabolism, and lifestyle choices. Some endocrine disorders, diseases, and medicines may also affect a person's weight.

Factors that may affect obesity include the following.

Studies show that the likelihood of becoming obese is passed down through a family's genes. Researchers have found several genes that seem to be linked with obesity. Genes, for instance, may affect where you store extra fat in your body. But most researchers think that it takes more than just 1 gene to cause an obesity epidemic. They are continuing to do more research to better understand how genes and lifestyle interact to cause obesity. Because families eat meals together and share other activities, environment and lifestyle also play a role.

Metabolism factors

How your body uses energy is different from how another person's uses it. Metabolism and hormones differ from person to person. And these factors play a role in how much weight you gain. One example is ghrelin, the hunger hormone that regulates appetite. Researchers have found that ghrelin may help set off hunger. Another hormone called leptin can decrease appetite. Another example is polycystic ovary syndrome (PCOS), a condition caused by high levels of certain hormones. A person with PCOS is more likely to be obese.

Socioeconomic factors

How much money you make may affect whether you are obese. This is especially true for people assigned female at birth. Those who are poor and of lower social status are more likely to be obese than those of higher socioeconomic status. This is especially true among minority groups.

Lifestyle choices

Overeating and a lack of exercise both contribute to obesity. But you can change these lifestyle choices. If many of your calories come from refined foods or foods high in sugar or fat, you will likely gain weight. If you don't get much if any exercise, you'll find it hard to lose weight or maintain a healthy weight.

Medicines like corticosteroids, beta-blockers, some antidepressants, and antiseizure medicines can cause you to gain some extra weight.

Emotional eating–eating when you're bored or upset–can lead to weight gain. Too little sleep may also contribute to weight gain. People who sleep fewer than 5 hours a night are more likely to become obese than people who get 7 to 8 hours of sleep a night.

Health effects of obesity

Obesity has a far-ranging negative effect on health. Each year in the U.S., obesity-related conditions cost more than $150 billion and cause premature deaths. The health effects linked with obesity include:

Excess weight needs more blood to circulate to the fat tissue and causes the blood vessels to become narrow (coronary artery disease). This makes the heart work harder because it must pump more blood against more resistance from the blood vessels and can lead to a heart attack (myocardial infarction). More circulating blood and more resistance also means more pressure on the artery walls. Higher pressure on the artery walls increases the blood pressure. Excess weight also raises blood cholesterol and triglyceride levels and lowers HDL (good) cholesterol levels, adding to the risk of heart disease.

Obesity is the major cause of type 2 diabetes. Obesity can make your body resistant to insulin, the hormone that regulates blood sugar. When obesity causes insulin resistance, your blood sugar level rises. Even moderate obesity dramatically increases the risk for diabetes.

Heart disease

Atherosclerosis, or hardening of the arteries, happens more often in obese people. Coronary artery disease is also more common in obese people because fatty deposits build up in arteries that supply the heart. Narrowed arteries and reduced blood flow to the heart can cause chest pain called angina or a heart attack. Blood clots can also form in narrowed arteries and travel to the brain, causing a stroke.

Joint problems, including osteoarthritis

Obesity can affect the knees and hips because extra weight stresses the joints. Joint replacement surgery may not be a good choice for an obese person. That's because the artificial joint has a higher risk of loosening and causing more damage.

Sleep apnea and respiratory problems are also related to obesity

Sleep apnea causes people to stop breathing for brief periods during sleep. Sleep apnea interrupts sleep. It causes sleepiness during the day. It also causes heavy snoring. Sleep apnea is also linked to high blood pressure, increased risk for heart disease, stroke, diabetes, and can even cause an early death. Breathing problems tied to obesity happen when added weight of the chest wall squeezes the lungs. This restricts breathing.

Being overweight or obese increases your risk for a variety of cancers, according to the American Cancer Society. Among obese people assigned female at birth, the risk increases for cancer of the endometrium or the lining of the uterus. Obese people assigned female at birth also increase their risk for breast cancers in those who have gone through menopause. People assigned male at birth who are overweight have a higher risk for prostate cancer. People who are obese are at increased risk for colorectal cancer.

Metabolic syndrome

The National Cholesterol Education Program says that metabolic syndrome is a risk factor for cardiovascular disease. Metabolic syndrome has several major risk factors. These are stomach obesity, high blood triglyceride levels, low HDL cholesterol levels, high blood pressure, and insulin resistance (severe type 2 diabetes). Having at least 3 of these risk factors confirms the diagnosis of metabolic syndrome. 

Psychosocial effects

People who are overweight or obese can have problems socially or psychologically. This is because the culture in the U.S. often values a body image that's overly thin. Overweight and obese people are often blamed for their condition. Other people may think of them as lazy or weak-willed. It's not uncommon for people who are overweight or obese to earn less than other people. Or to have fewer or no romantic relationships. Some people's disapproval and bias against those who are overweight may lead to discrimination and even bullying. Depression and anxiety are more common in people who are overweight and obese. 

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Essays About Obesity: Top 5 Examples and 7 Writing Prompts

Obesity is a pressing health issue many people must deal with in their lives. If you are writing essays about obesity, check out our guide for helpful examples and writing prompts. 

In the world we live in today, certain diseases such as obesity are becoming more significant problems. People suffering from obesity have excess fat, which threatens their health significantly. This can lead to strokes, high blood pressure, heart attacks, and even death. It also dramatically alters one’s physical appearance.

However, we must not be so quick to judge and criticize obese people for their weight and supposed “lifestyle choices.” Not every obese person makes “bad choices” and is automatically “lazy,” as various contributing causes exist. Therefore, we must balance concern for obese people’s health and outright shaming them. 

To write insightful essays about obesity, you can start by reading essay examples. 

5 Best Essay examples

1. obesity as a social issue by earnest washington, 2. is there such a thing as ‘healthy obesity’ by gillian mohney, 3. problems of child obesity by peggy maldonado, 4.  what is fat shaming are you a shamer by jamie long.

• 5. ​​The Dangerous Link Between Coronavirus and Obesity by Rami Bailony

Writing Prompts for Essays About Obesity

1. what causes obesity, 2. what are the effects of obesity, 3. how can you prevent obesity, 4. what is “fat shaming”, 5. why is obesity rate so higher, 6. obesity in the united states, 7. your experience with obesity.

“Weight must be considered as a genuine risk in today’s world. Other than social issues like body shaming, obesity has significantly more to it and is a risk to human life. It must be dealt with and taken care of simply like some other interminable illness and we as people must recollect that machines and innovation has progressed to help us not however not make us unenergetic.”

Washington writes about the dangers of obesity, saying that it can significantly damage your digestive and cardiovascular systems and even cause cancer. In addition, humans’ “expanded reliance on machines” has led us to become less active and more sedentary; as a result, we keep getting fatter. While he acknowledges that shaming obese people does no good, Washington stresses the dangers of being too heavy and encourages people to get fit. 

“‘I think we need to move away from using BMI as categorizing one as obese/overweight or unhealthy,” Zarabi told Healthline. “The real debate here is how do we define health? Is the vegetarian who has a BMI of 30, avoiding all saturated fats from meats and consuming a diet heavy in simple carbohydrates [and thus] reducing his risk of cardiac disease but increasing likelihood of elevated triglycerides and insulin, considered healthy?

Mohney, writing for Healthline, explains how “healthy obesity” is nuanced and should perhaps be retired. Some people may be metabolically healthy and obese simultaneously; however, they are still at risk of diseases associated with obesity. Others believe that health should be determined by more factors than BMI, as some people eat healthily and exercise but remain heavy. People have conflicting opinions on this term, and Mohney describes suggestions to instead focus on getting treatment for “healthy obese” people

“The absence of physical movement is turning into an increasingly normal factor as youngsters are investing more energy inside, and less time outside. Since technology is turning into an immense piece of present-day youngsters’ lives, exercises, for example, watching TV, gaming, messaging and playing on the PC, all of which require next to no vitality and replaces the physical exercises.”

In her essay, Maldonado discusses the causes and effects of childhood obesity. For example, hereditary factors and lack of physical activity make more children overweight; also, high-calorie food and the pressure on kids to “finish their food” make them consume more. 

Obesity leads to high blood pressure and cholesterol, heart disease, and cancer; children should not suffer as they are still so young. 

“Regardless of the catalyst at the root of fat shaming, it persists quite simply because we as a society aren’t doing enough to call it out and stand in solidarity against it. Our culture has largely bought into the farce that thinness equals health and success. Instead, the emphasis needs to shift from the obsession of appearance to promoting healthy lifestyle behaviors for all, regardless of body size. A lean body shouldn’t be a requisite to be treated with dignity and respect. Fat shaming is nonsensical and is the manifestation of ignorance and possibly, hate.”

Long warns readers of the dangers of fat shaming, declaring that it is reprehensible and should not be done. People may have “good intentions” when criticizing overweight or obese people, but it does not, in fact, help with making them healthier. Long believes that society should highlight a healthy lifestyle rather than a “healthy” body, as everyone’s bodies are different and should not be the sole indicator of health. 

5. ​​ The Dangerous Link Between Coronavirus and Obesity by Rami Bailony

“In a study out of NYU, severe obesity (BMI >40) was a greater risk factor for hospitalization among Covid-19 patients than heart failure, smoking status, diabetes, or chronic kidney disease. In China, in a small case series of critically ill Covid-19 patients, 88.24% of patients who died had obesity versus an obesity rate of 18.95% in survivors. In France, patients with a BMI greater than 35 were seven times more likely to require mechanical ventilation than patients with a BMI below 25.”

Bailony’s essay sheds light on research conducted in several countries regarding obesity and COVID-19. The disease is said to be “a leading risk factor in mortality and morbidity” from the virus; studies conducted in the U.S., China, and France show that most obese people who contracted the coronavirus died. Bailony believes obesity is not taken seriously enough and should be treated as an actual disease rather than a mere “lifestyle choice.”

It is well-known that obesity is an excess buildup of body fat, but what exactly causes this? It is not simply due to “eating a lot,” as many people simply understand it; there are other factors besides diet that affect someone’s body size. Look into the different causes of obesity, explaining each and how they are connected.

Obesity can result in the development of many diseases. In addition, it can significantly affect one’s physique and digestive, respiratory, and circulatory systems. For your essay, discuss the different symptoms of obesity and the health complications it can lead to in the future.

It can be safely assumed that no one wants to be obese, as it is detrimental to one’s health. Write an essay guide of some sort, giving tips on managing your weight, staying healthy, and preventing obesity. Include some dietary guidelines, exercise suggestions, and the importance of keeping the balance between these two.

“Fat shaming” is a phenomenon that has become more popular with the rise in obesity rates. Define this term, explain how it is seen in society, and explain why it is terrible. Also, include ways that you can speak about the dangers of obesity without making fun of obese people or making them feel bad for their current state. 

The 21st century has seen a dramatic rise in obesity rates worldwide compared to previous decades. Why is this the case? Explore one or more probable causes for the increase in obese people. You should mention multiple causes in your essay, but you may choose to focus on one only- explain it in detail.

The United States, in particular, is known to be a country with many obese people. This is due to a combination of factors, all connected in some way. Research obesity in the U.S. and write about why it is a bigger problem than in other countries- take a look at portion size, fitness habits, and food production. 

If applicable, you may write about your experience with obesity. Whether you have struggled or are struggling with it in the past or know someone who has, discuss how this makes you feel. Reflect on how this knowledge has impacted you as a person and any lessons this may have taught you. 

For help with your essays, check out our round-up of the best essay checkers .If you’re looking for more ideas, check out our essays about bullying topic guide !

Obesity Essay

Last updated on: Feb 9, 2023

Obesity Essay: A Complete Guide and Topics

By: Nova A.

11 min read

Reviewed By: Jacklyn H.

Published on: Aug 31, 2021

Are you assigned to write an essay about obesity? The first step is to define obesity.

The obesity epidemic is a major issue facing our country right now. It's complicated- it could be genetic or due to your environment, but either way, there are ways that you can fix it!

Learn all about what causes weight gain and get tips on how you can get healthy again.

On this Page

What is Obesity

What is obesity? Obesity and BMI (body mass index) are both tools of measurement that are used by doctors to assess body fat according to the height, age, and gender of a person. If the BMI is between 25 to 29.9, that means the person has excess weight and body fat.

If the BMI exceeds 30, that means the person is obese. Obesity is a condition that increases the risk of developing cardiovascular diseases, high blood pressure, and other medical conditions like metabolic syndrome, arthritis, and even some types of cancer.

Obesity Definition

Obesity is defined by the World Health Organization as an accumulation of abnormal and excess body fat that comes with several risk factors. It is measured by the body mass index BMI, body weight (in kilograms) divided by the square of a person’s height (in meters).

Obesity in America

Obesity is on the verge of becoming an epidemic as 1 in every 3 Americans can be categorized as overweight and obese. Currently, America is an obese country, and it continues to get worse.

Paper Due? Why Suffer? That's our Job!

Causes of obesity

Do you see any obese or overweight people around you?

You likely do.

This is because fast-food chains are becoming more and more common, people are less active, and fruits and vegetables are more expensive than processed foods, thus making them less available to the majority of society. These are the primary causes of obesity.

Obesity is a disease that affects all age groups, including children and elderly people.

Now that you are familiar with the topic of obesity, writing an essay won’t be that difficult for you.

How to Write an Obesity Essay

The format of an obesity essay is similar to writing any other essay. If you need help regarding how to write an obesity essay, it is the same as writing any other essay.

Obesity Essay Introduction

The trick is to start your essay with an interesting and catchy sentence. This will help attract the reader's attention and motivate them to read further. You don’t want to lose the reader’s interest in the beginning and leave a bad impression, especially if the reader is your teacher.

A hook sentence is usually used to open the introductory paragraph of an essay in order to make it interesting. When writing an essay on obesity, the hook sentence can be in the form of an interesting fact or statistic.

Head on to this detailed article on hook examples to get a better idea.

Once you have hooked the reader, the next step is to provide them with relevant background information about the topic. Don’t give away too much at this stage or bombard them with excess information that the reader ends up getting bored with. Only share information that is necessary for the reader to understand your topic.

Next, write a strong thesis statement at the end of your essay, be sure that your thesis identifies the purpose of your essay in a clear and concise manner. Also, keep in mind that the thesis statement should be easy to justify as the body of your essay will revolve around it.

Body Paragraphs

The details related to your topic are to be included in the body paragraphs of your essay. You can use statistics, facts, and figures related to obesity to reinforce your thesis throughout your essay.

If you are writing a cause-and-effect obesity essay, you can mention different causes of obesity and how it can affect a person’s overall health. The number of body paragraphs can increase depending on the parameters of the assignment as set forth by your instructor.

Start each body paragraph with a topic sentence that is the crux of its content. It is necessary to write an engaging topic sentence as it helps grab the reader’s interest. Check out this detailed blog on writing a topic sentence to further understand it.

End your essay with a conclusion by restating your research and tying it to your thesis statement. You can also propose possible solutions to control obesity in your conclusion. Make sure that your conclusion is short yet powerful.

Obesity Essay Examples

Essay about Obesity (PDF)

Childhood Obesity Essay (PDF)

Obesity in America Essay (PDF)

Essay about Obesity Cause and Effects (PDF)

Satire Essay on Obesity (PDF) 

Obesity Argumentative Essay (PDF)

Obesity Essay Topics

Choosing a topic might seem an overwhelming task as you may have many ideas for your assignment. Brainstorm different ideas and narrow them down to one, quality topic.

If you need some examples to help you with your essay topic related to obesity, dive into this article and choose from the list of obesity essay topics.

Childhood Obesity

As mentioned earlier, obesity can affect any age group, including children. Obesity can cause several future health problems as children age.

Here are a few topics you can choose from and discuss for your childhood obesity essay:

• What are the causes of increasing obesity in children?
• Obese parents may be at risk for having children with obesity.
• What is the ratio of obesity between adults and children?
• What are the possible treatments for obese children?
• Are there any social programs that can help children with combating obesity?
• Has technology boosted the rate of obesity in children?
• Are children spending more time on gadgets instead of playing outside?
• Schools should encourage regular exercises and sports for children.
• How can sports and other physical activities protect children from becoming obese?
• Can childhood abuse be a cause of obesity among children?
• What is the relationship between neglect in childhood and obesity in adulthood?
• Does obesity have any effect on the psychological condition and well-being of a child?
• Are electronic medical records effective in diagnosing obesity among children?
• Obesity can affect the academic performance of your child.
• Do you believe that children who are raised by a single parent can be vulnerable to obesity?
• You can promote interesting exercises to encourage children.
• What is the main cause of obesity, and why is it increasing with every passing day?
• Schools and colleges should work harder to develop methodologies to decrease childhood obesity.
• The government should not allow schools and colleges to include sweet or fatty snacks as a part of their lunch.
• If a mother is obese, can it affect the health of the child?
• Children who gain weight frequently can develop chronic diseases.

Obesity Argumentative Essay Topics

Do you want to write an argumentative essay on the topic of obesity?

The following list can help you with that!

Here are some examples you can choose from for your argumentative essay about obesity:

• Can vegetables and fruits decrease the chances of obesity?
• Should you go for surgery to overcome obesity?
• Are there any harmful side effects?
• Can obesity be related to the mental condition of an individual?
• Are parents responsible for controlling obesity in childhood?
• What are the most effective measures to prevent the increase in the obesity rate?
• Why is the obesity rate increasing in the United States?
• Can the lifestyle of a person be a cause of obesity?
• Does the economic situation of a country affect the obesity rate?
• How is obesity considered an international health issue?
• Can technology and gadgets affect obesity rates?
• What can be the possible reasons for obesity in a school?
• How can we address the issue of obesity?
• Is obesity a chronic disease?
• Is obesity a major cause of heart attacks?
• Are the junk food chains causing an increase in obesity?
• Do nutritional programs help in reducing the obesity rate?
• How can the right type of diet help with obesity?
• Why should we encourage sports activities in schools and colleges?
• Can obesity affect a person’s behavior?

Health Related Topics for Research Paper

If you are writing a research paper, you can explain the cause and effect of obesity.

Here are a few topics that link to the cause and effects of obesity.Review the literature of previous articles related to obesity. Describe the ideas presented in the previous papers.

• Can family history cause obesity in future generations?
• Can we predict obesity through genetic testing?
• What is the cause of the increasing obesity rate?
• Do you think the increase in fast-food restaurants is a cause of the rising obesity rate?
• Is the ratio of obese women greater than obese men?
• Why are women more prone to be obese as compared to men?
• Stress can be a cause of obesity. Mention the reasons how mental health can be related to physical health.
• Is urban life a cause of the increasing obesity rate?
• People from cities are prone to be obese as compared to people from the countryside.
• How obesity affects the life expectancy of people? What are possible solutions to decrease the obesity rate?
• Do family eating habits affect or trigger obesity?
• How do eating habits affect the health of an individual?
• How can obesity affect the future of a child?
• Obese children are more prone to get bullied in high school and college.
• Why should schools encourage more sports and exercise for children?

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Topics for Essay on Obesity as a Problem

Do you think a rise in obesity rate can affect the economy of a country?

Here are some topics for your assistance regarding your economics related obesity essay.

• Does socioeconomic status affect the possibility of obesity in an individual?
• Analyze the film and write a review on “Fed Up” – an obesity epidemic.
• Share your reviews on the movie “The Weight of The Nation.”
• Should we increase the prices of fast food and decrease the prices of fruits and vegetables to decrease obesity?
• Do you think healthy food prices can be a cause of obesity?
• Describe what measures other countries have taken in order to control obesity?
• The government should play an important role in controlling obesity. What precautions should they take?
• Do you think obesity can be one of the reasons children get bullied?
• Do obese people experience any sort of discrimination or inappropriate behavior due to their weight?
• Are there any legal protections for people who suffer from discrimination due to their weight?
• Which communities have a higher percentage of obesity in the United States?
• Discuss the side effects of the fast-food industry and their advertisements on children.
• Describe how the increasing obesity rate has affected the economic condition of the United States.
• What is the current percentage of obesity all over the world? Is the obesity rate increasing with every passing day?
• Why is the obesity rate higher in the United States as compared to other countries?
• Do Asians have a greater percentage of obese people as compared to Europe?
• Does the cultural difference affect the eating habits of an individual?
• Obesity and body shaming.
• Why is a skinny body considered to be ideal? Is it an effective way to reduce the obesity rate?

Obesity Solution Essay Topics

With all the developments in medicine and technology, we still don’t have exact measures to treat obesity.

Here are some insights you can discuss in your essay:

• How do obese people suffer from metabolic complications?
• Describe the fat distribution in obese people.
• Is type 2 diabetes related to obesity?
• Are obese people more prone to suffer from diabetes in the future?
• How are cardiac diseases related to obesity?
• Can obesity affect a woman’s childbearing time phase?
• Describe the digestive diseases related to obesity.
• Obesity may be genetic.
• Obesity can cause a higher risk of suffering a heart attack.
• What are the causes of obesity? What health problems can be caused if an individual suffers from obesity?
• What are the side effects of surgery to overcome obesity?
• Which drugs are effective when it comes to the treatment of obesity?
• Is there a difference between being obese and overweight?
• Can obesity affect the sociological perspective of an individual?
• Explain how an obesity treatment works.
• How can the government help people to lose weight and improve public health?

Writing an essay is a challenging yet rewarding task. All you need is to be organized and clear when it comes to academic writing.

• Choose a topic you would like to write on.
• Organize your thoughts.
• Pen down your ideas.
• Compose a perfect essay that will help you ace your subject.
• Proofread and revise your paper.

Were the topics useful for you? We hope so!

However, if you are still struggling to write your paper, you can pick any of the topics from this list, and our essay writer will help you craft a perfect essay.

Are you struggling to write an effective essay?

If writing an essay is the actual problem and not just the topic, you can always hire an essay writing service for your help. Essay experts at 5StarEssays can help compose an impressive essay within your deadline.

All you have to do is contact us. We will get started on your paper while you can sit back and relax.

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Marketing, Thesis

As a Digital Content Strategist, Nova Allison has eight years of experience in writing both technical and scientific content. With a focus on developing online content plans that engage audiences, Nova strives to write pieces that are not only informative but captivating as well.

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Prevention, prevention, prevention.

Losing weight is hard to do.

In the U.S., only one in six adults who have dropped excess pounds actually keep off at least 10 percent of their original body weight. The reason: a mismatch between biology and environment. Our bodies are evolutionarily programmed to put on fat to ride out famine and preserve the excess by slowing metabolism and, more important, provoking hunger. People who have slimmed down and then regain their weight don’t lack willpower—their bodies are fighting them every inch of the way.

This inborn predisposition to hold on to added weight reverberates down the life course. Few children are born obese, but once they become heavy, they are usually destined to be heavy adolescents and heavy adults. According to a 2016 study in the New England Journal of Medicine , approximately 90 percent of children with severe obesity will become obese adults with a BMI of 35 or higher. Heavy young adults are generally heavy in middle and old age. Obesity also jumps across generations; having a mother who is obese is one of the strongest predictors of obesity in children.

All of which means that preventing child obesity is key to stopping the epidemic. By the time weight piles up in adulthood, it is usually too late. Luckily, preventing obesity in children is easier than in adults, partly because the excess calories they absorb are minimal and can be adjusted by small changes in diet—substituting water, for example, for sugary fruit juices or soda.

Still, the bulk of the obesity problem—literally—is in adults. According to Frank Hu, chair of the Harvard Chan Department of Nutrition, “Most people gain weight during young and middle adulthood. The weight-gain trajectory is less than 1 pound per year, but it creeps up steadily from age 18 to age 55. During this time, people gain fat mass, not muscle mass. When they reach age 55 or so, they begin to lose their existing muscle mass and gain even more fat mass. That’s when all the metabolic problems appear: insulin resistance, high cholesterol, high blood pressure.”

Adds Walter Willett, Frederick John Stare Professor of Epidemiology and Nutrition at Harvard Chan, “The first 5 pounds of weight gain at age 25—that’s the time to be taking action. Because someone is on a trajectory to end up being 30 pounds overweight by the time they’re age 50.”

The most realistic near-term public health goal, therefore, is not to reverse but rather to slow down the trend—and even this will require strong commitment from government at many levels. In May 2017, the Trump administration rolled back recently-enacted standards for school meals, delaying a rule to lower sodium and allowing waivers for regulations requiring cafeterias to serve foods rich in whole grains. If recent expansions in food entitlements and school meals are undermined, “It would be a ‘disaster,’ to use the president’s word,” says Marlene Schwartz, director of the Rudd Center for Obesity & Food Policy at the University of Connecticut. “The federal food programs are incredibly important, not just because of the food and money they provide families, but because supporting better nutrition in child care, schools, and the WIC [Women, Infants, and Children] program has created new social norms. We absolutely cannot undo the progress that we’ve made in helping this generation transition to a healthier diet.”

Get the science right.

It is impossible to prescribe solutions to obesity without reminding ourselves that nutrition scientists botched things decades ago and probably sent the epidemic into overdrive. Beginning in the 1970s, the U.S. government and major professional groups recommended for the first time that people eat a low-fat/high-carbohydrate diet. The advice was codified in 1977 with the first edition of The Dietary Goals for the United States , which aimed to cut diet-related conditions such as heart disease and diabetes. What ensued amounted to arguably the biggest public health experiment in U.S. history, and it backfired.

At the time, saturated fat and dietary cholesterol were believed to be the main factors responsible for cardiovascular disease—an oversimplified theory that ignored the fact that not all fats are created equal. Soon, the public health blitz against saturated fat became a war on all fat. In the American diet, fat calories plummeted and carb calories shot up.

“We can’t blame industry for this. It was a bandwagon effect in the scientific community, despite the lack of evidence—even with evidence to the contrary,” says Willett. “Farmers have known for thousands of years that if you put animals in a pen, don’t let them run around, and load them up with grains, they get fat. That’s basically what has been happening to people: We created the great American feedlot. And we added in sugar, coloring, and seductive promotion for low-fat junk food.”

Scientists now know that whole fruits and vegetables (other than potatoes), whole grains, high-quality proteins (such as from fish, chicken, beans, and nuts), and healthy plant oils (such as olive, peanut, or canola oil) are the foundations of a healthy diet.

But there is also a lot scientists don’t yet know. One unanswered question is why some people with obesity are spared the medical complications of excess weight. Another concerns the major mechanisms by which obesity ushers in disease. Although surplus body weight can itself directly cause problems—such as arthritis due to added load on joints, or breast cancer caused by hormones secreted by fat cells—in general, obesity triggers myriad biological processes. Many of the resulting conditions—such as atherosclerosis, diabetes, and even Alzheimer’s disease—are mediated by inflammation, in which the body’s immune response becomes damagingly self-perpetuating. In this sense, today’s food system is as inflammagenic as it is obesigenic.

Scientists also need to ferret out the nuanced effects of particular foods. For example, do fermented products—such as yogurt, tempeh, or sauerkraut—have beneficial properties? Some studies have found that yogurt protects against weight gain and diabetes, and suggest that healthy live bacteria (known as probiotics) may play a role. Other reports point to fruits being more protective than vegetables in weight control and diabetes prevention, although the types of fruits and vegetables make a difference.

A 2017 article in the American Journal of Clinical Nutrition showed that substituting whole grains for refined grains led to a loss of nearly 100 calories a day—by speeding up metabolism, cutting the number of calories that the body hangs on to, and, more surprisingly, by changing the digestibility of other foods on the plate. That extra energy lost daily—by substituting, say, brown rice for white rice or barley for pita bread—was equivalent to a brisk 30-minute walk. One hundred calories a day, sustained over years, and multiplied by the population is one mathematical equivalent of the obesity epidemic.

A companion study found that adults who ate a whole-grain-rich diet developed healthier gut bacteria and improved immune responses. That particular foods alter the gut microbiome—the dense and vital community of bacteria and other microorganisms that work symbiotically with the body’s own digestive system—is another critical insight. The microbiome helps determine weight by controlling how our bodies extract calories and store fat in the liver, and the microbiomes of obese individuals are startlingly efficient at harvesting calories from food. [To learn more about Harvard Chan research on the gut microbiome, read “ Bugs in the System .”] The hormonal effects of sleep deprivation and stress—two epidemics concurrent and intertwined with the obesity trend—are other promising avenues of research.

And then there are the mystery factors. One recent hypothesis is that an agent known as adenovirus 36 partly accounts for our collective heft. A 2010 article in The Royal Society described a study in which researchers examined samples of more than 20,000 animals from eight species living with or around humans in industrialized nations, a menagerie that included macaques, chimpanzees, vervets, marmosets, lab mice and rats, feral rats, and domestic dogs and cats. Like their Homo sapiens counterparts, all of the study populations had gained weight over the past several decades—wild, domestic, and lab animals alike. The chance that this is a coincidence is, according to the scientists’ estimate, 1 in 10 million. The stumped authors surmise that viruses, gene expression changes, or “as-of-yet unidentified and/or poorly understood factors” are to blame.

Master the art of persuasion.

A 2015 paper in the American Journal of Public Health revealed the philosophical chasm that hampers America’s progress on obesity prevention. It found that 72 to 98 percent of obesity-related media reports emphasize personal responsibility for weight, compared with 40 percent of scientific papers.

A recent study by Drexel University researchers also quantified the political polarization around public health measures. From 1998 through 2013, Democrats voted in line with recommendations from the American Public Health Association 88.3 percent of the time, on average, while Republicans voted for the proposals just 21.3 percent of the time.

Clearly, we can’t count on bipartisan goodwill to stem the obesity crisis. But we can ask what kinds of messages appeal to politically divergent audiences. A stealth strategy may be to avoid even uttering the word “obesity.” On January 1 of this year, Philadelphia’s 1.5-cents-per-ounce excise tax on sugar-sweetened and diet beverages took effect. When Philadelphia Mayor Jim Kenney lobbied voters to approve the tax, his bid centered not on improving health—the unsuccessful pitch of his predecessor—but on raising $91 million annually for prekindergarten programs.

“That’s something lots of people care about and can get behind—it’s a feel-good policy, and it makes sense,” says psychologist Christina Roberto, assistant professor of medical ethics and health policy at the University of Pennsylvania, and a former assistant professor of social and behavioral sciences and nutrition at Harvard Chan. The provision for taxing diet beverages was also shrewd, she adds, because it spread the tax’s pain; since wealthier people are more likely than less-affluent individuals to buy diet drinks, the tax could not be slapped with the label “regressive.”

But Roberto sees a larger lesson in the Philadelphia story. Public health messaging that appeals to values that transcend the individual is less fraught, less stigmatizing, and perhaps more effective. As she puts it, “It’s very different to hear the message, ‘Eat less red meat, help the planet’ versus ‘Eat less red meat, help yourself avoid saturated fat and cardiovascular disease.’”

Supermarket makeovers

Supermarket aisles are other places where public health can shuffle a deck stacked against healthy consumer choices.

With slim profit margins and 50,000-plus products on their shelves, grocery stores depend heavily on food manufacturers’ promotional incentives to make their bottom lines. “Manufacturers pay slotting fees to get their products on the shelf, and they pay promotion allowances: We’ll give you this much off a carton of Coke if you put it on sale for a certain price or if you put it on an end-of-aisle display,” says José Alvarez, former president and chief executive officer of Stop & Shop/Giant-Landover, now senior lecturer of business administration at Harvard Business School. Such promotional payments, Alvarez adds, often exceed retailers’ net profits.

Healthy new products—like flash-frozen dinners prepared with heaps of vegetables and whole grains, and relatively little salt—can’t compete for prized shelf space against boxed mac and cheese or cloying breakfast cereals. One solution, says Alvarez, is for established consumer packaged goods companies to buy out what he calls the “hippie in the basement” firms that have whipped up more nutritious items. The behemoths could apply their production, marketing, and distribution prowess to the new offerings—and indeed, this has started to happen over the last five years.

Another approach is to make nutritious foods more convenient to eat. “We have all of these cooking shows and upscale food magazines, but most people don’t have the time or inclination—or the skills, quite frankly—to cook,” says Alvarez. “Instead, we should focus on creating high-quality, healthy, affordable prepared foods.”

An additional model is suggested by Jeff Dunn, a 20-year veteran of the soft drink industry and former president of Coca-Cola North America, who went on to become an advocate for fresh, healthy food. Dunn served as president and chief executive officer of Bolthouse Farms from 2008 to 2015, where he dramatically increased sales of baby carrots by using marketing techniques common in the junk food business. “We operated on the principles of the three 3 A’s: accessibility, availability, and affordability,” says Dunn. “That, by the way, is Coke’s more-than-70-year-old formula for success.”

Show them the money.

Obesity kills budgets. According to the Campaign to End Obesity, a collaboration of leaders from industry, academia, public health, and policymakers, annual U.S. health costs related to obesity approach $200 billion. In 2010, the nonpartisan Congressional Budget Office reported that nearly 20 percent of the rise in health care spending from 1987 to 2007 was linked to obesity. And the U.S. Centers for Disease Control and Prevention (CDC) found that full-time workers in the U.S. who are overweight or obese and have other chronic health conditions miss an estimated 450 million more days of work each year than do healthy employees—upward of $153 billion in lost productivity annually.

But making the money case for obesity prevention isn’t straightforward. For interventions targeting children and youth, only a small fraction of savings is captured in the first decade, since most serious health complications don’t emerge for many years. Long-term obesity prevention, in other words, doesn’t fit into political timetables for elected officials.

Yet lawmakers are keen to know how “best for the money” obesity-prevention programs can help them in the short run. Over the past two years, Harvard Chan’s Steve Gortmaker and his colleagues have been working with state health departments in Alaska, Mississippi, New Hampshire, Oklahoma, Washington, and West Virginia and with the city of Philadelphia and other locales, building cost-effectiveness models using local data for a wide variety of interventions—from improved early child care to healthy school environments to communitywide campaigns. “We collaborate with health departments and community stakeholders, provide them with the evidence base, help assess how much different options cost, model the results over a decade, and they pick what they want to work on. One constant that we’ve seen—and these are very different political environments—is a strong interest in cost-effectiveness,” he says.

In a 2015 study in Health Affairs , Gortmaker and colleagues outlined three interventions that would more than pay for themselves: an excise tax on sugar-sweetened beverages implemented at the state level; elimination of the tax subsidy for advertising unhealthy food to children; and strong nutrition standards for food and drinks sold in schools outside of school meals. Implemented nationally, these interventions would prevent 576,000, 129,100, and 345,000 cases of childhood obesity, respectively, by 2025. The projected net savings to society in obesity-related health care costs for each dollar invested: $31, $33, and $4.60, respectively.

Gortmaker is one of the leaders of a collaborative modeling effort known as CHOICES—for Childhood Obesity Intervention Cost-Effectiveness Study—an acronym that seems a pointed rebuttal to the reflexive conservative argument that government regulation tramples individual choice. Having grown up not far from Des Plaines, Illinois, site of the first McDonald’s franchise in the country, he emphasizes to policymakers that at this late date, America cannot treat its way out of obesity, given current medical know-how. Only a thoroughgoing investment in prevention will turn the tide. “Clinical interventions produce too small an effect, with too small a population, and at high cost,” Gortmaker says. “The good news is that there are many cost-effective options to choose from.”

While Gortmaker underscores the importance of improving both food choices and options for physical activity, he has shown that upgrading the food environment offers much more benefit for the buck. This is in line with the gathering scientific consensus that what we eat plays a greater role in obesity than does sedentary lifestyle (although exercise protects against many of the metabolic consequences of excess weight). “The easiest way to explain it,” Gortmaker says, “is to talk about a sugary beverage—140 calories. You could quickly change a kid’s risk of excess energy balance by 140 calories a day just by switching from a sugary drink a day to water or sparkling water. But for a 10-year-old boy to burn an extra 140 calories, he’d have to replace an hour-and-a-half of sitting with an hour-and-a-half of walking.”

Small tweaks in adults’ diets can likewise make a big difference in short order. “With adults, health care costs rise rapidly with excess weight gain,” Gortmaker says. “If you can slow the onset of obesity, you slow the onset of diabetes, and potentially not only save health care costs but also boost people’s productivity in the workforce.”

One of Gortmaker’s most intriguing calculations spins off of the food industry’s estimated $633 million spent on television marketing aimed at kids. Currently, federal tax treatment of advertising as an ordinary business expense means that the government, in effect, subsidizes hawking of junk food to children. Gortmaker modeled a national intervention that would eliminate this subsidy of TV ads for nutritionally empty foods and beverages aimed at 2- to 19-year-olds. Drawing on well-delineated relationships between exposure to these advertisements and subsequent weight gain, he found that the intervention would save $260 million in downstream health care costs. Although the effect would probably be small at the individual level, it would be significant at the population level.

Level the playing field through taxes and regulation.

When public health took on cigarette smoking, starting in the 1960s, it did so with robust policies banning television ads and other marketing, raising taxes to increase prices, making public places smoke-free, and offering people treatment such as the nicotine patch. In 1965, the smoking rate for U.S. adults was 42.2 percent; today, it is 16.8 percent.

Similarly, America reduced the rate of deaths caused by motor vehicle accidents—a 90 percent decrease over the 20th century, according to the CDC—with mandatory seat belt laws, safer car designs, stop signs, speed limits, rumble strips, and the stigmatization of drunk driving.

Change the product. Change the environment. Change the culture. That is also the policy recipe for stopping obesity.

Laws that make healthy behaviors easier are often followed by positive changes in those behaviors. And people who are trying to adopt healthy behaviors tend to support policies that make their personal aspirations achievable, which in turn nudges lawmakers to back the proposals.

One debate today revolves around whether recipients of federal Supplemental Nutrition Assistance Program (SNAP) benefits (formerly known as food stamps) should be restricted from buying sodas or junk food. The largest component of the USDA budget, SNAP feeds one in seven Americans. A USDA report, issued last November, found that the number-one purchase by SNAP households was sweetened beverages, a category that included soft drinks, fruit juices, energy drinks, and sweetened teas, accounting for nearly 10 percent of SNAP money spent on food. Is the USDA therefore underwriting the soda industry and planting the seeds for chronic disease that the government will pay to treat years down the line?

Eric Rimm, a professor in the Departments of Epidemiology and Nutrition at the Harvard Chan School, frames the issue differently. In a 2017 study in the American Journal of Preventive Medicine , he and his colleagues asked SNAP participants whether they would prefer the standard benefits package or a “SNAP-plus” that prohibited the purchase of sugary beverages but offered 50 percent more money for buying fruits and vegetables. Sixty-eight percent of the participants chose the healthy SNAP-plus option.

“A lot of work around SNAP policy is done by academics and politicians, without reaching out to the beneficiaries,” says Rimm. “We haven’t asked participants, ‘What’s your say in this? How can we make this program better for you?’” To be sure, SNAP is riddled with nutritional contradictions. Under current rules, for example, participants can use benefits to buy a 12-pack of Pepsi or a Snickers bar or a giant bag of Lay’s potato chips but not real food that happens to be heated, such as a package of rotisserie chicken. “This is the most vulnerable population in the country,” says Rimm. “We’re not listening well enough to our constituency.”

Other innovative fiscal levers to alter behavior could also drive down obesity. In 2014, a trio of strong voices on food industry practices—Dariush Mozaffarian, DrPH ’06, dean of Tufts University’s Friedman School of Nutrition Science and Policy and former associate professor of epidemiology at the Harvard Chan School; Kenneth Rogoff, professor of economics at Harvard; and David Ludwig, professor in the Department of Nutrition at Harvard Chan and a physician at Boston Children’s Hospital—broached the idea of a “meaningful” tax on nearly all packaged retail foods and many chain restaurants, with the proceeds used to pay for minimally processed foods and healthier meals for school kids. In essence, the tax externalizes the social costs of harmful individual behavior.

“We made a straightforward proposal to tax all processed foods and then use the income to subsidize whole foods in a short-term, revenue-neutral way,” explains Ludwig. “The power of this idea is that, since there is so much processed food consumption, even a modest tax—in the 10 to 15 percent range—is not going to greatly inflate the cost of these foods. Their price would increase moderately, but the proceeds would not disappear into government coffers. Instead, the revenue would make healthy foods affordable for virtually the entire population, and the benefits would be immediately evident. Yes, people will pay moderately more for their Coke or for their cinnamon bear claw but a lot less for nourishing, whole foods.”

Another suggestion comes from Sandro Galea, dean of the Boston University School of Public Health, and Abdulrahman M. El-Sayed, a public health physician and epidemiologist. In a 2015 issue of the American Journal of Public Health , they called for “calorie offsets,” similar to the carbon offsets used to mitigate environmental harm caused by the gas and oil industries. A “calorie offset” scheme could hand the food and beverage industries a chance at redemption by inviting them to invest in such undertakings as city farms, cooking classes for parents, healthy school cafeterias, and urban green spaces.

These ambitious proposals face almost impossibly high hurdles. Political battle lines typically pit public health against corporations, with Big Food casting doubt on solid nutrition science, deeming government regulation a threat to free choice, and making self-policing pledges that it has never kept. On the website for the Americans for Food and Beverage Choice, a group spearheaded by the American Beverage Association, is the admonition: “[W]hether it’s at a restaurant or in a grocery store, it’s never the government’s job to decide what you choose to eat and drink.”

Yet surprisingly, many public health professionals are convinced that the only way to stop obesity is to make common cause with the food industry. “This isn’t like tobacco, where it’s a fight to the death. We need the food industry to make healthier food and to make a profit,” says Mozaffarian. “The food industry is much more diverse and heterogeneous than tobacco or even cars. As long as we can help them—through carrots and sticks, tax incentives and disincentives—to move towards healthier products, then they are part of the solution. But we have to be vigilant, because they use a lot of the same tactics that tobacco did.”

Sow what we want to reap.

Americans overeat what our farmers overproduce.

“The U.S. food system is egregiously terrible for human and planetary health,” says Walter Willett. It’s so terrible, Willett made a pie chart of American grain production consumed domestically. It shows that most of the country’s agricultural land goes to the two giant commodity crops: corn and soy. Most of those crops, in turn, go to animal fodder and ethanol, and are also heavily used in processed snack foods. Today, only about 10 percent of grain grown in the U.S. for domestic use is eaten directly by human beings. According to a 2013 report from the Union of Concerned Scientists, only 2 percent of U.S. farmland is used to grow fruits and vegetables, while 59 percent is devoted to commodity crops.

Historically, those skewed proportions made sense. Federal food policies, drafted with the goal of alleviating hunger, preferentially subsidize corn and soy production. And whereas corn or soybeans could be shipped for days on a train, fruits and vegetables had to be grown closer to cities by truck farmers so the produce wouldn’t spoil. But those long-ago constraints don’t explain today’s upside-down agricultural priorities.

In a now-classic 2016 Politico article titled “The farm bill drove me insane,” Marion Nestle illustrated the irrational gap between what the government recommends we eat and what it subsidizes: “If you were to create a MyPlate meal that matched where the government historically aimed its subsidies, you’d get a lecture from your doctor. More than three-quarters of your plate would be taken up by a massive corn fritter (80 percent of benefits go to corn, grains and soy oil). You’d have a Dixie cup of milk (dairy gets 3 percent), a hamburger the size of a half dollar (livestock: 2 percent), two peas (fruits and vegetables: 0.45 percent) and an after-dinner cigarette (tobacco: 2 percent). Oh, and a really big linen napkin (cotton: 13 percent) to dab your lips.”

In this sense, the USDA marginalizes human health. Many of the foods that nutritionists agree are best for us—notably, fruits, vegetables, and tree nuts—fall under the bureaucratic rubric “specialty crops,” a category that also includes “dried fruits, horticulture, and nursery crops (including floriculture).” Farm bills, which get passed every five years or so, fortify the status quo. The 2014 Farm Bill, for example, provided $73 million for the Specialty Crop Block Grant Program in 2017, out of a total of about $25 billion for the USDA’s discretionary budget. (The next Farm Bill, now under debate, will be coming out in 2018.)

By contrast, a truly anti-obesigenic agricultural system would stimulate USDA support for crop diversity—through technical assistance, research, agricultural training programs, and financial aid for farmers who are newly planting or transitioning their land into produce. It would also enable farmers, most of whom survive on razor-thin profit margins, to make a decent living.

In the early 1970s, Finland’s death rate from coronary heart disease was the highest in the world, and in the eastern region of North Karelia—a pristine, sparsely populated frontier landscape of forest and lakes—the rate was 40 percent worse than the national average. Every family saw physically active men, loggers and farmers who were strong and lean, dying in their prime.

Thus was born the North Karelia Project, which became a model worldwide for saving lives by transforming lifestyles. The project was launched in 1972 and officially ended 25 years later. While its initial goal was to reduce smoking and saturated fat in the diet, it later resolved to increase fruit and vegetable consumption.

The North Karelia Project fulfilled all of these ambitions. When it started, for example, 86 percent of men and 82 percent of women smeared butter on their bread; by the early 2000s, only 10 percent of men and 4 percent of women so indulged. Use of vegetable oil for cooking jumped from virtually zero in 1970 to 50 percent in 2009. Fruit and vegetables, once rare visitors to the dinner plate, became regulars. Over the project’s official quarter-century existence, coronary heart disease deaths in working-age North Karelian men fell 82 percent, and life expectancy rose seven years.

The secret of North Karelia’s success was an all-out philosophy. Team members spent innumerable hours meeting with residents and assuring them that they had the power to improve their own health. The volunteers enlisted the assistance of an influential women’s group, farmers’ unions, homemakers’ organizations, hunting clubs, and church congregations. They redesigned food labels and upgraded health services. Towns competed in cholesterol-cutting contests. The national government passed sweeping legislation (including a total ban on tobacco advertising). Dairy subsidies were thrown out. Farmers were given strong incentives to produce low-fat milk, or to get paid for meat and dairy products based not on high-fat but on high-protein content. And the newly established East Finland Berry and Vegetable Project helped locals switch from dairy farming—which had made up more than two-thirds of agriculture in the region—to cultivation of cold-hardy currants, gooseberries, and strawberries, as well as rapeseed for heart-healthy canola oil.

“A mass epidemic calls for mass action,” says the project’s director, Pekka Puska, “and the changing of lifestyles can only succeed through community action. In this case, the people pulled the government—the government didn’t pull the people.”

Could the United States in 2017 learn from North Karelia’s 1970s grand experiment?

“Americans didn’t become an obese nation overnight. It took a long time—several decades, the same timeline as in individuals,” notes Frank Hu. “What were we doing over the past 20 years or 30 years, before we crossed this threshold? We haven’t asked these questions. We haven’t done this kind of soul-searching, as individuals or society as a whole.”

Today, Americans may finally be willing to take a hard look at how food figures in their lives. In a July 2015 Gallup phone poll of Americans 18 and older, 61 percent said they actively try to avoid regular soda (the figure was 41 percent in 2002); 50 percent try to avoid sugar; and 93 percent try to eat vegetables (but only 57.7 percent in 2013 reported they ate five or more servings of fruits and vegetables at least four days of the previous week).

Individual resolve, of course, counts for little in problems as big as the obesity epidemic. Most successes in public health bank on collective action to support personal responsibility while fighting discrimination against an epidemic’s victims. [To learn more about the perils of stigma against people with obesity, read “ The Scarlet F .”]

Yet many of public health’s legendary successes also took what seems like an agonizingly long time to work. Do we have that luxury?

“Right now, healthy eating in America is like swimming upstream. If you are a strong swimmer and in good shape, you can swim for a little while, but eventually you’re going to get tired and start floating back down,” says Margo Wootan, SD ’93, director of nutrition policy for the Center for Science in the Public Interest. “If you’re distracted for a second—your kid tugs on your pant leg, you had a bad day, you’re tired, you’re worried about paying your bills—the default options push you toward eating too much of the wrong kinds of food.”

But Wootan has not lowered her sights. “What we need is mobilization,” she says. “Mobilize the public to address nutrition and obesity as societal problems—recognizing that each of us makes individual choices throughout the day, but that right now the environment is stacked against us. If we don’t change that, stopping obesity will be impossible.”

The passing of power to younger generations may aid the cause. Millennials are more inclined to view food not merely as nutrition but also as narrative—a trend that leaves Duke University’s Kelly Brownell optimistic. “Younger people have been raised to care about the story of their food. Their interest is in where it came from, who grew it, whether it contributes to sustainable agriculture, its carbon footprint, and other factors. The previous generation paid attention to narrower issues, such as hunger or obesity. The Millennials are attuned to the concept of food systems.”

We are at a public health inflection point. Forty years from now, when we gaze at the high-resolution digital color photos from our own era, what will we think? Will we realize that we failed to address the obesity epidemic, or will we know that we acted wisely?

The question brings us back to the 1970s, and to Pekka Puska, the physician who directed the North Karelia Project during its quarter-century existence. Puska, now 71, was all of 27 and burning with big ideas when he signed up to lead the audacious effort. He knows the promise and the perils of idealism. “Changing the world may have been utopic,” he says, “but changing public health was possible.”

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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.

• Body Mass Index (BMI)
• WHO Child Growth Standards
• Growth reference data for 5-19 years

WHO Strategy

• Global Strategy on Diet, Physical Activity and Health
• Global Health Observatory (GHO)

More information

• WHO's work on obesity
• WHO's work on nutrition

Obesity - Free Essay Examples And Topic Ideas

Obesity is a medical condition in which excess body fat has accumulated to an extent that it may have a negative effect on health. Essays on obesity could explore its causes, the health risks associated, and the societal costs. Discussions might also revolve around various interventions to address obesity at an individual and community level. We have collected a large number of free essay examples about Obesity you can find at PapersOwl Website. You can use our samples for inspiration to write your own essay, research paper, or just to explore a new topic for yourself.

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How To Write an Essay About Obesity

Understanding obesity.

Before writing an essay about obesity, it's crucial to understand what obesity is and its implications. Obesity is a medical condition characterized by an excess accumulation of body fat, often defined by a body mass index (BMI) of 30 or higher. It is not just a cosmetic concern but a complex health issue associated with various diseases, such as heart disease, diabetes, and high blood pressure. Start your essay by outlining the causes of obesity, which may include genetic factors, lack of physical activity, unhealthy eating patterns, and environmental and psychological factors. Discuss the global prevalence of obesity and its rise in recent decades, indicating a significant public health concern.

Developing a Thesis Statement

A strong essay on obesity should be centered around a clear, concise thesis statement. This statement should present a specific viewpoint or argument about obesity. For instance, you might discuss the societal factors contributing to the rise of obesity, analyze the effectiveness of current interventions and policies, or argue the need for a multifaceted approach to tackle this health issue. Your thesis will guide the direction of your essay and ensure a structured and coherent analysis.

Gathering Supporting Evidence

To support your thesis, gather evidence from a variety of sources, including medical studies, public health reports, and statistical data. This might include data on obesity rates in different populations, research on the health risks associated with obesity, or studies evaluating the effectiveness of diet and exercise programs. Use this evidence to support your thesis and build a persuasive argument. Be sure to consider different perspectives and address potential counterarguments.

Analyzing the Impact of Obesity

Dedicate a section of your essay to analyzing the impact of obesity. Discuss the physical health consequences, such as increased risk of chronic diseases, as well as the psychological and social implications, including stigma and reduced quality of life. Consider the economic burden of obesity on healthcare systems and society. This analysis should provide a comprehensive understanding of the far-reaching effects of obesity.

Concluding the Essay

Conclude your essay by summarizing the main points of your discussion and restating your thesis in light of the evidence provided. Your conclusion should tie together your analysis and emphasize the significance of addressing obesity as a critical public health issue. You might also want to suggest areas for future research or propose potential strategies to combat the obesity epidemic.

Reviewing and Refining Your Essay

After completing your essay, review and edit it for clarity and coherence. Ensure that your arguments are well-structured and supported by evidence. Check for grammatical accuracy and ensure that your essay flows logically from one point to the next. Consider seeking feedback from peers, healthcare professionals, or educators to further refine your essay. A well-written essay on obesity will not only demonstrate your understanding of the issue but also your ability to engage with complex health and societal challenges.

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Argumentative Essay on Obesity

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Published: Mar 5, 2024

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• < Previous chapter

26 Conclusion: Obesity and its prevention in the 21st century

• Published: September 2010
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The case for a preventative approach to the obesity epidemic is compelling. Obesity poses what is arguably one of the most significant threats to population health that is currently faced. The data presented in this book highlight just how common obesity has become in children and in adults across the globe, and how it impacts disproportionately on the poor. This chapter presents a summary of the discussions in the preceding chapters.

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• Singapore Med J
• v.64(3); 2023 Mar
• PMC10071857

The impact of obesity: a narrative review

Benjamin chih chiang lam.

1 Family and Community Medicine, Khoo Teck Puat Hospital, Singapore

2 Integrated Care for Obesity and Diabetes, Khoo Teck Puat Hospital, Singapore

Amanda Yuan Ling Lim

3 Singapore Association for the Study of Obesity, Singapore

4 Division of Endocrinology, Department of Medicine, National University Hospital, Singapore

Soo Ling Chan

5 Division of Endocrinology, Department of Medicine, Ng Teng Fong General Hospital, Singapore

Mabel Po Shan Yum

6 Psychology Service, Khoo Teck Puat Hospital, Singapore

Natalie Si Ya Koh

7 Department of Cardiology, National Heart Centre, Singapore

Eric Andrew Finkelstein

8 Health Services and Systems Research, Duke-NUS Medical School, Singapore

Obesity is a disease with a major negative impact on human health. However, people with obesity may not perceive their weight to be a significant problem and less than half of patients with obesity are advised by their physicians to lose weight. The purpose of this review is to highlight the importance of managing overweight and obesity by discussing the adverse consequences and impact of obesity. In summary, obesity is strongly related to >50 medical conditions, with many of them having evidence from Mendelian randomisation studies to support causality. The clinical, social and economic burdens of obesity are considerable, with these burdens potentially impacting future generations as well. This review highlights the adverse health and economic consequences of obesity and the importance of an urgent and concerted effort towards the prevention and management of obesity to reduce the burden of obesity.

INTRODUCTION

The prevalence of obesity has increased significantly over the last two decades worldwide, including in Singapore, a multiethnic Southeast Asian country.[ 1 , 2 ] Recent national health surveys of adult Singaporeans suggest a continuation of this rising trend after a brief period of stabilisation.[ 3 ] Obesity, which is characterised by excessive adiposity, is not benign.

Obesity predisposes affected individuals to a large array of diseases that are often interconnected, leading to an increased risk of simple (two comorbid diseases) and complex (four or more comorbid diseases) multimorbidity in these individuals, when compared to people with healthy weight.[ 4 ] For example, in a large Finnish cohort of 114,657 people aged 16–78 years, with a mean follow-up of 12.1 years, people with obesity were five times more likely to develop simple multimorbidity and 12 times more likely to develop complex multimorbidity, with stronger associations found in people with more severe obesity.[ 4 ] This dose–response relationship between obesity and multimorbidity is also observed in other populations, including Asian populations.[ 5 , 6 ] In Singapore, the proportion of disability-adjusted life years, a composite measure of all health loss within a population, contributed by overweight and obesity, increased from 3.9% in 1990 to 6.4% in 2017, making it the fifth leading risk factor affecting health in Singapore.[ 7 ] Hence, obesity is a disease with a major negative impact on human health and has become a major global and regional health problem.

However, according to international surveys and interviews, people with obesity may not perceive their weight to be a significant problem,[ 8 ] with evidence also suggesting that less than half of patients with obesity are advised by their physicians to lose weight.[ 9 , 10 ] Hence, the purpose of this narrative review, as part of a series on obesity, is to highlight the importance of managing overweight and obesity by presenting and summarising the latest evidence on the adverse consequences and impact of obesity [ Figure 1 ]. The causal role of excess adiposity on obesity-related conditions (as established by the many epidemiological evidence already described in literature) will be explored. In addition, data from Singapore, if any, will be included in the review for each section, with the review on the economic burden of overweight and obesity focusing on Singapore.

Diagram shows a summary of the diseases and conditions associated with obesity and the potential impacts. *Supported by mendelian randomisation studies. T1DM: type 1 diabetes mellitus, T2DM: type 2 diabetes mellitus

EVIDENCE FOR CAUSAL ROLE OF EXCESS ADIPOSITY ON OBESITY-RELATED DISEASES

The hypertrophy of adipose tissue is associated with proinflammatory adipokine production and macrophage infiltration. In addition, the failure of adipose tissue to continually expand leads to lipotoxicity and ectopic fat deposition in lean tissues such as the heart, liver, pancreas and kidneys.[ 11 , 12 ] These phenomena contribute to a proinflammatory and insulin-resistant milieu and, together with increased mechanical stress due to increased adipose tissue mass,[ 11 , 13 ] are the main pathophysiological mechanisms responsible for the development of multiple medical conditions. Hence, there are reasonable pathways to link outcome to exposure (i.e. plausibility), one of the principles useful for establishing a causal relationship.[ 14 ]

This causal role of obesity is further supported by evidence from Mendelian randomisation (MR) studies. MR is an analytical technique involving genetic variants that are associated with exposures (risk factors such as obesity) as instrumental variables to investigate the effects of these exposures on an outcome of interest (e.g. a disease).[ 15 ] Since these genetic variants are fixed, randomly allocated at conception and temporally precede the outcome, MR is less likely to be subject to bias, confounding and reverse causation, which are frequent in conventional observational studies.[ 15 ] ’BMI’, ’obesity’, ’Mendelian randomisation’, ’Mendelian randomization’ and the outcome of interest (e.g. ’diabetes’) were used as search terms, and all studies relevant to this review were considered. These obesity-related diseases, with evidence for the causal role of obesity (plausible biological mechanisms and MR studies), and the various impacts of obesity will be discussed next.

Diabetes mellitus, dyslipidaemia and hypertension

As highlighted, obesity leads to insulin resistance. Additionally, elevated free fatty acid from the adipose tissues and ectopic fat deposition cause pancreatic β-cell dysfunction.[ 16 , 17 ] Hence, the various pathological mechanisms synergistically exacerbate the onset of type 2 diabetes mellitus (T2DM). In particular, visceral fat deposition plays an important role in the development of T2DM.[ 18 ] Hepatic fat worsens hepatic insulin resistance, while pancreatic fat affects insulin secretion and glucose tolerance.[ 18 ] In a meta-analysis of MR studies, genetically predicted higher body mass index (BMI) was consistently associated with T2DM, with a combined odds ratio (OR) of 2.03 (95% confidence interval [CI] 1.88–2.19) per 1 standard deviation increase in BMI.[ 19 ] In Singapore, multiple observational studies confirm the increased risk of T2DM with increasing BMI in all major ethnic groups,[ 20 , 21 , 22 ] although there might be ethnic-specific sensitivity to the effects of increasing adiposity.[ 23 ]

There is also increasing evidence for the role of obesity in the increased incidence of type 1 diabetes mellitus (T1DM), with studies from North America and the UK suggesting an increasing prevalence of overweight and obesity in people with T1DM.[ 24 ] It has been hypothesised that obesity-induced insulin resistance may be responsible for the accelerated loss of pancreatic β cells through excessive stimulation[ 25 ] and a chronic proinflammatory state.[ 26 ] This causal role is supported by MR studies, although the evidence is not as consistent (compared to obesity and T2DM), with high heterogeneity between the studies.[ 19 ]

Obesity is associated with dyslipidaemia, which is characterised by increased triglycerides (TGs) and free fatty acids, decreased high-density lipoprotein-cholesterol (HDL-C) with HDL dysfunction and increased low-density lipoprotein cholesterol (LDL-C), in particular, small dense LDL-C, which is particularly atherogenic.[ 27 ] The underlying mechanisms involve hepatic fat accumulation, insulin resistance and chronic inflammation.[ 27 , 28 ] In a recent MR study based on participants from the UK Biobank, genetically predicted higher BMI was significantly associated with dyslipidaemia (low HDL-C levels).[ 29 ] In Singapore, in a multiethnic sample of 4,723 adult participants, elevated TG was more common in people with obesity, with the prevalence of elevated TG increasing with higher BMI and waist-to-hip ratio (WHR),[ 20 ] consistent with the evidence.

Hypertension is more than twice as prevalent in people with obesity compared to people with normal weight.[ 30 ] The mechanisms for obesity-induced hypertension are varied (involving adipokines, cytokines, free fatty acids, insulin, the rennin–angiotensin–aldosterone system) and interconnected, with the final common pathways being endothelial dysfunction, extracellular fluid overload and sympathetic nervous system activation.[ 30 , 31 ] Hence, obesity is an established risk factor for hypertension, and its causal role is supported by MR studies,[ 19 , 32 ] particularly that of higher adiposity with a more unfavourable metabolic profile (higher visceral and ectopic fat).[ 32 ] In Singapore, the increased prevalence of hypertension with higher BMI and WHR is consistent, especially in males.[ 20 ]

Nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is a condition in which fat accumulates in the liver in the absence of excessive alcohol consumption. Genetic variants that increase hepatic fat content have been shown to be associated with increased liver enzymes, hepatocellular damage and fibrosis, suggesting that hepatic fat accumulation mediates the development of liver fibrosis, independent of inflammation.[ 33 ] Hence, NAFLD may lead to nonalcoholic steatohepatitis (NASH), and ultimately, cirrhosis or hepatocellular carcinoma.

The prevalence of NAFLD has risen in tandem with the global epidemic of obesity, with NAFLD now being the most common cause of chronic liver disease worldwide.[ 34 ] A meta-analysis of MR studies confirms the causal effect of obesity on NAFLD,[ 19 ] with central adiposity (waist circumference) having the strongest relationship (OR 2.93, 95% CI 1.85–4.63) among the various obesity measures.[ 35 ] In Singapore, studies consistently show that participants with evidence of NAFLD have significantly higher BMI and waist circumference.[ 36 , 37 ]

Cardiovascular diseases

The association between obesity and increased incidence of cardiovascular diseases such as heart failure, coronary heart disease and stroke has long been established.[ 38 ] For example, based on pooled data from 97 prospective cohort studies involving 1.8 million participants, the hazard ratio (HR) for each 5 kg/m 2 higher BMI was 1.27 (95% CI 1.23–1.31) for coronary heart disease and 1.18 (95% CI 1.14–1.22) for stroke after adjustment for potential confounders.[ 39 ] Additional adjustment for diabetes mellitus, hypertension and dyslipidaemia reduced the HRs to 1.15 (95% CI 1.12–1.18) and 1.04 (95% CI 1.01–1.08) for coronary heart disease and stroke, respectively, suggesting that 46% (95% CI 42%–50%) of the excess risk of BMI for coronary heart disease and 76% (95% CI 65%–91%) for stroke were mediated by these conditions,[ 39 ] which are common in people with obesity.[ 4 , 30 ]

Obesity itself leads to an increased risk of these cardiovascular events, likely via mechanisms such as the secretion of adipokines, proinflammatory cytokines and hypofibrinolytic factors, that together could lead to increased oxidative stress and endothelial dysfunction resulting in atherosclerosis.[ 40 ] Additionally, excessive adiposity results in haemodynamic alterations via various neurohormonal and metabolic abnormalities, causing left ventricular (LV) hypertrophy and subsequent dysfunction, leading to LV failure. LV failure, facilitated by pulmonary arterial hypertension from hypoxia due to obstructive sleep apnoea (OSA) and/or obesity hypoventilation syndrome (OHS), may subsequently lead to right ventricular failure.[ 41 ] This causal role of obesity is supported by multiple MR studies,[ 19 , 29 , 32 ] with the strongest association between BMI and heart failure, followed by BMI and coronary artery disease, then BMI and stroke.[ 19 , 32 ]

Another obesity-related cardiovascular disease is atrial fibrillation (AF), with evidence suggesting that obesity is an independent risk factor for AF, even after accounting for OSA.[ 41 ] Also, studies have demonstrated a strong graded association between higher BMI and the risk of persistent AF and higher BMI, with increased risk of postablation AF.[ 41 ] The mechanisms linking obesity and AF are complex and incompletely understood, with increased left atrial and ventricular abnormalities, altered haemodynamics, increased epicardial and pericardial fat, inflammation, and metabolic and neurohormonal abnormalities being the potential causal mechanisms.[ 41 ] This causal relationship is similarly supported by MR studies which consistently show that genetically predicted BMI is associated with AF.[ 19 , 32 , 42 ]

In Singapore, a longitudinal study involving 2,605 Chinese participants found that the adjusted HR for cardiovascular and stroke mortality was highest in the group with obesity (BMI ≥30 kg/m 2 ) among those aged ≥65 years,[ 43 ] which is consistent with the association between obesity and increased incidence of cardiovascular diseases.

Obstructive sleep apnoea and hypoventilation syndrome

The increased intra-abdominal and intrathoracic pressure as a result of excessive adiposity impedes inflation of the lung, which can significantly affect the lung function, thereby leading to hypoventilation and ventilation–perfusion imbalance.[ 44 ] A constellation of obesity, daytime hypoventilation characterised by hypercapnia and hypoxaemia, and sleep-disordered breathing, without an alternative cause for hypoventilation, is known as OHS, with an estimated prevalence of 8%–20% in patients with obesity who were referred to sleep centres for evaluation of sleep-disordered breathing.[ 45 ]

The most common sleep-disordered breathing in such patients and people with obesity is OSA, as fat accumulation around the upper airways predisposes to the collapse of these airways.[ 44 ] About 50% of people with OSA have obesity, and approximately 40%–90% of people who are overweight suffer from OSA.[ 44 , 45 ] Consistent with epidemiological observations and genetic correlation (between OSA and BMI), an MR study shows that genetically predicted BMI is strongly associated with OSA, supporting the causal effect of BMI on OSA.[ 46 ] In Singapore, a study based on 587 Chinese participants reported that people with OSA had significantly higher BMI, and also BMI remained an important predictor of OSA after adjusting for hypertension and smoking,[ 47 ] in line with the overall evidence.

Polycystic ovary syndrome

Obesity is strongly associated with polycystic ovary syndrome (PCOS),[ 48 ] which is characterised by reproductive dysfunction (oligo-amenorrhoea, infertility), hyperandrogenism (hirsutism, acne, androgenic alopecia and biochemical hyperandrogenism) and a polycystic ovarian morphology (high antral follicle counts or increased ovarian volume).[ 49 ] Up to 88% of women with PCOS are overweight or obese,[ 48 ] with a meta-analysis showing that women with obesity had a twofold to threefold higher risk for PCOS when compared to women without obesity.[ 50 ] The pathogenesis of PCOS involves primarily insulin resistance, with the ensuing secondary hyperinsulinaemia resulting in enhanced steroidogenesis in the ovaries, particularly androgen production.[ 48 ] Hence, the insulin-resistant milieu associated with obesity can lead to the development of PCOS. This causal effect of obesity on PCOS is supported by MR studies,[ 32 , 51 ] with one MR study suggesting that this effect is predominantly metabolic in nature.[ 32 ] In Singapore, a study based on a multiethnic population of 389 participants reported that women with PCOS had significantly higher BMI compared to women without PCOS,[ 52 ] consistent with the evidence.

Cognitive impact and dementia

Experimental studies have shown that cellular mechanisms such as oxidative stress and inflammation can affect the brain structure and function.[ 53 ] Obesity is an established risk factor for dementia,[ 54 ] and has been associated with cognitive impairment[ 55 , 56 ] and decreased grey matter volume linked with executive functioning.[ 53 , 57 ] However, while MR studies have found causal relationships between BMI and grey matter volumes,[ 58 ] evidence for BMI and dementia has so far not been significant.[ 32 , 58 , 59 ] In Singapore, a longitudinal analysis of 1,519 cognitively normal older persons (>55 years) of Chinese ethnicity showed that central obesity was associated with a higher risk of developing mild cognitive impairment,[ 60 ] consistent with the overall evidence that higher adiposity has a negative impact on the brain.

Chronic kidney disease

Excess adiposity results in pathological processes such as lipotoxicity, inflammation, oxidative stress and activation of the renin–angiotensin–aldosterone system, leading to glomerular and tubular injuries (obesity-induced nephropathy).[ 61 ] Multiple MR studies have confirmed this causal relationship between obesity and kidney disease,[ 32 , 62 , 63 ] including one study conducted in an East Asian population using BMI-associated variants validated in East Asia.[ 63 ] In Singapore, longitudinal gain in adiposity was associated with progressive renal decline in a prospective multiethnic cohort with T2DM, suggesting that increasing adiposity would lead to adverse renal outcomes over time.[ 64 ]

Obesity is known to be associated with 13 types of cancers: oesophageal adenocarcinoma, renal cell carcinoma, postmenopausal breast cancer, endometrial cancer, colorectal cancer, meningioma, multiple myeloma, and cancer of the gastric cardia, liver, gallbladder, pancreas, ovary and thyroid.[ 65 ] In Singapore, these obesity-associated cancers make up four out of the top five cancers affecting women (breast, colorectal, endometrial and ovarian) and two of the top five cancers affecting men (colorectal and liver).[ 66 ] Potential mechanisms of increased cancer risk in obesity include hyperinsulinaemia, chronic inflammation and oestrogen excess.[ 67 ] This causal role of obesity in cancer is supported by MR studies,[ 19 , 32 ] particularly for cancers of the digestive system, with all of them (oesophageal, colorectal, gastric, liver, gallbladder, pancreas) positively associated with genetically predicted BMI based on a meta-analysis of MR studies.[ 19 ]

Depression and anxiety

The prevalence of depression is much higher among people with obesity than that in the general population.[ 68 , 69 ] Similarly, anxiety occurs more frequently in people who are overweight or obese compared to people with normal weight, and the relationship is stronger among those who are more severely obese.[ 70 , 71 , 72 ] Research findings consistently show that people with obesity frequently suffer from psychological issues ranging from stress associated with weight-related issues, perceived weight discrimination and stigmatisation to body image dissatisfaction.[ 68 , 69 ] Additionally, there is evidence that the dysfunctional adipose tissues present in obesity result in metabolic abnormalities, such as altered glucocorticoid, adipokine, insulin, leptin and inflammatory signalling, which either directly or indirectly impact the control of emotions and mood.[ 73 , 74 ] Hence, the causal relationship between obesity and depression/anxiety is likely to have both psychological and biological components. This is supported by MR studies which demonstrate the relationship between genetically predicted BMI (and fat mass) and depression,[ 75 , 76 , 77 ] even when using a genetic instrument that omits the metabolic consequences of higher BMI.[ 75 ]

In Singapore, a study based on 83 patients with obesity at a weight management clinic reported that the prevalence of anxiety symptoms and depressive symptoms was 28% and 11%, respectively,[ 78 ] suggesting that symptoms of depression and anxiety are highly prevalent in people with obesity in Singapore and are higher than the national prevalence of depression and anxiety,[ 79 ] consistent with international data.

Severe coronavirus disease-19

The dysfunctional physiological milieu of obesity has been associated with altered lymphoid tissue integrity, shifts in leukocyte populations and proinflammatory profiles, such that immune responses and pathogen defence are impaired.[ 80 ] This is demonstrated in previous influenza outbreaks[ 81 ] and the current coronavirus disease 2019 (COVID-19) pandemic, where obesity (high adiposity) is a major risk factor for severe COVID-19 (death and hospitalisation), as supported by multiple epidemiological studies worldwide[ 82 ] and MR studies[ 83 , 84 , 85 , 86 ] using data from the COVID-19 Host Genetics Initiative (an international collaboration that aims to uncover the genetic determinants of outcomes related to COVID-19 susceptibility and severity). In Singapore, where the COVID-19 mortality rate is low (<0.001),[ 87 ] a subgroup analysis of younger (<60 years) COVID-19 patients found that a BMI ≥25 kg/m 2 was significantly associated with the need for low-flow supplemental oxygen and mechanical ventilation,[ 88 ] consistent with observations internationally.

Other diseases

Other diseases with established epidemiological and strong MR evidence include asthma,[ 32 ] gastro-oesophageal reflux disease,[ 19 , 32 ] diverticular disease,[ 19 , 32 ] gallstone disease,[ 19 , 32 ] Crohn's disease,[ 19 , 89 ] osteoarthritis,[ 32 , 90 ] intervertebral degeneration (including back pain and sciatica),[ 91 , 92 ] peripheral arterial disease,[ 19 , 32 ] venous thromboembolism,[ 19 , 32 ] deep vein thrombosis,[ 19 , 32 ] aortic valve stenosis,[ 19 ] atopic dermatitis,[ 93 ] psoriasis,[ 32 ] gout[ 32 ] and rheumatoid arthritis.[ 32 ]

IMPACT ON MOTHER AND CHILD

Maternal obesity has been associated with adverse outcomes, including increased mortality, for both mother and child.[ 94 ] Mothers with obesity are more likely to develop pregnancy complications such as gestational hypertension, preeclampsia, gestational diabetes mellitus and thromboembolic disease, with a higher risk of preterm delivery, caesarian section, stillbirth, intrauterine growth retardation and foetus that is large for gestational age.[ 94 , 95 , 96 ] In an MR study, genetically elevated maternal BMI was associated with higher offspring birthweight, supporting a causal relationship.[ 97 ] These adverse outcomes can lead to complications and disability, with increased birth weight being associated with childhood adiposity and metabolic disorders during life.[ 94 ] Hence, the impact of obesity may extend beyond the current generation (mother) to the next generation (child). In Singapore, findings from the Growing Up in Singapore Towards Healthy Outcomes (GUSTO) study, a prospective mother–offspring birth cohort, showed that pre-pregnancy BMI and maternal obesity were associated with child size and adiposity[ 98 ] and childhood obesity,[ 99 ] respectively, confirming the generational impact of obesity.

PSYCHOSOCIAL IMPACT

Obesity negatively impacts health-related quality of life, with greater degrees of obesity associated with greater impairments.[ 100 , 101 , 102 ] While most individuals often report significant difficulties with physical and occupational functioning, many also experience problems with social functioning, such as social withdrawal[ 103 ] and social isolation.[ 104 ] This could be due to perceived negative attitudes and discrimination towards people with obesity, increased self-consciousness and self-blame for being overweight.[ 69 , 104 ] People with obesity, especially females, are often dissatisfied with their body image, which is exacerbated by society's expectation of thinness, with the degree of dissatisfaction positively correlated with the amount of excess weight.[ 102 , 105 , 106 ] Taken together, obesity can negatively impact an individual's self-esteem,[ 69 ] thereby affecting self-efficacy,[ 107 ] possibly resulting in a vicious circle and downward spiral.

ECONOMIC IMPACT

There are substantially higher healthcare utilisation and medical costs among people who are overweight or obese due to treatment of medical conditions caused by excess adiposity and for direct obesity treatments, which may include weight loss surgeries and medications.[ 108 ] In addition to direct medical costs, there is also an increase in indirect costs as a result of increased absenteeism (workdays missed due to illness or injury) and presenteeism (reduced productivity while working).[ 109 ]

The economic burden of overweight and obesity has been well described and quantified in North America,[ 108 , 110 ] Europe,[ 111 , 112 , 113 , 114 ] Brazil,[ 115 ] Australia,[ 116 , 117 ] China[ 118 ] and Saudi Arabia,[ 119 ] with an estimated cost of 0.8%–2.4% of gross domestic product (GDP) in 2019 based on eight countries.[ 120 ] As for Singapore, a recent study has attempted to quantify the economic burden of overweight and obesity.[ 121 ] Using econometric methods and cross-sectional data from the Singapore Epidemiology of Eye Diseases (SEED) cohort, which includes measured height and weight, self-reported healthcare utilisation and absenteeism/presenteeism (based on a modified version of the Work Productivity Activity Impairment questionnaire), the incremental per capita and aggregate direct and indirect costs of excess weight among a multiethnic population of older adults (aged 40–80) were estimated.

Among Chinese, individuals who were overweight missed one additional workday per year compared to those who were of normal weight. Individuals in the obese category had SGD720 per year greater medical expenditures, but missed workdays were not statistically different from those in the normal weight category. Among Indians, differences were not significant between normal and overweight categories, but Indians in the obese category incurred an additional SGD310 per year in absenteeism costs than those of normal weight. For Malays, no significant differences by BMI category were identified.[ 121 ]

In aggregate, the predicted total medical expenditures attributable to overweight and obesity in Singapore were estimated to be SGD178 million, representing 1.6% of Singapore's total healthcare expenditures (SGD11,300 million in 2019). This figure is on the low end of published estimates, which range between 2.9% and 9.7% of the total healthcare spending.[ 121 ] Including absenteeism increases this estimate to SGD261 million, although this estimate is likely to be conservative because it does not include costs for presenteeism (reduced productivity while working), retraining, injuries or other costs resulting from excess weight in the workplace.[ 121 ] By ethnicity, Malays are responsible for 19% of the total costs of excess weight, even though they make up only 12% of the Singapore population.[ 121 ] This disproportionate burden is consistent with the disproportionately higher rates of overweight and obesity among Malays.[ 3 ]

LIMITATIONS OF REVIEW

First, this review discussed mainly the impact of adult obesity, with a focus on diseases that have shown a strong relationship with obesity, especially those supported by MR studies. Hence, the impact of paediatric obesity is not discussed and not all diseases have been covered. Second, not all the diseases supported by evidence from MR studies were discussed in detail. Nonetheless, they are listed in the section ’Other diseases’ and included in Figure 1 . Third, interventional studies which show significant weight loss-improving health outcomes were not discussed. These studies, by showing the positive impact of weight loss, would have further supported the negative impact of obesity. Lastly, while there are some MR studies based on Asian cohorts, the majority of MR studies were based on genetic data derived from individuals of European ancestry or large cohorts that were predominantly European. Hence, the inference of causality may be limited in non-European populations.

As discussed, obesity is strongly related to more than 50 medical conditions [summarised in Figure 1 ], with evidence from MR studies to support causality for many of these conditions. Based on the 2017 Global Burden of Diseases study, the top four causes (cardiovascular diseases, cancers, musculoskeletal disorders and mental disorders) of disability-adjusted life years in Singapore account for more than 50% of the total burden,[ 7 ] with many of the common conditions in these four causes related to obesity. Hence, the clinical, social and economic burdens of obesity are considerable, potentially impacting future generations as well. This review, therefore, highlights the importance of an urgent and concerted effort towards the prevention and management of obesity to reduce the burden of obesity.

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obesity summary

obesity , Excessive body fat . It is usually caused by sedentary habits and a diet high in fat, alcohol , or total calories. Calories consumed but not used are stored as fat. Rare causes include glandular defects and excess steroid s ( see Cushing syndrome ). Obesity raises the risk of heart disease and diabetes mellitus . Treatment, by reducing calorie intake and increasing exercise, is best undertaken with a doctor’s advice.

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• Review Article
• Published: 23 September 2021

The genetics of obesity: from discovery to biology

• Ruth J. F. Loos   ORCID: orcid.org/0000-0002-8532-5087 1 , 2 , 3 , 4 &
• Giles S. H. Yeo   ORCID: orcid.org/0000-0001-8823-3615 5  

Nature Reviews Genetics volume  23 ,  pages 120–133 ( 2022 ) Cite this article

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• Disease genetics
• Endocrine system and metabolic diseases
• Genetic association study
• Genetic variation

The prevalence of obesity has tripled over the past four decades, imposing an enormous burden on people’s health. Polygenic (or common) obesity and rare, severe, early-onset monogenic obesity are often polarized as distinct diseases. However, gene discovery studies for both forms of obesity show that they have shared genetic and biological underpinnings, pointing to a key role for the brain in the control of body weight. Genome-wide association studies (GWAS) with increasing sample sizes and advances in sequencing technology are the main drivers behind a recent flurry of new discoveries. However, it is the post-GWAS, cross-disciplinary collaborations, which combine new omics technologies and analytical approaches, that have started to facilitate translation of genetic loci into meaningful biology and new avenues for treatment.

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Introduction.

Obesity is associated with premature mortality and is a serious public health threat that accounts for a large proportion of the worldwide non-communicable disease burden, including type 2 diabetes, cardiovascular disease, hypertension and certain cancers 1 , 2 . Mechanical issues resulting from substantially increased weight, such as osteoarthritis and sleep apnoea, also affect people’s quality of life 3 . The impact of obesity on communicable disease, in particular viral infection 4 , has recently been highlighted by the discovery that individuals with obesity are at increased risk of hospitalization and severe illness from COVID-19 (refs 5 , 6 , 7 ).

On the basis of the latest data from the NCD Risk Factor Collaboration, in 2016 almost 2 billion adults (39% of the world’s adult population) were estimated to be overweight (defined by a body mass index (BMI) of ≥25 kg m − 2 ), 671 million (12% of the world’s adult population) of whom had obesity (BMI ≥30 kg m − 2 ) — a tripling in the prevalence of obesity since 1975 (ref. 8 ) (Fig.  1 ). Although the rate of increase in obesity seems to be declining in most high-income countries, it continues to rise in many low-income and middle-income countries and prevalence remains high globally 8 . If current trends continue, it is expected that 1 billion adults (nearly 20% of the world population) will have obesity by 2025. Particularly alarming is the global rise in obesity among children and adolescents; more than 7% had obesity in 2016 compared with less than 1% in 1975 (ref. 8 ).

The prevalence of obesity has risen steadily over the past four decades in children, adolescents (not shown) and adults worldwide. a | Prevalence of obesity (body mass index (BMI) ≥30 kg m −2 ) in women and men ≥20 years of age, from 1975 to 2016. b | Prevalence of obesity (weight ≥2 s.d. above the median of the WHO growth reference) in 5-year-old girls and boys from 1975 to 2016. Geographical regions are represented by different colours. Graphs are reproduced from the NCD Risk Factor Collaboration (NCD RisC) website and are generated from data published in ref. 8 .

Although changes in the environment have undoubtedly driven the rapid increase in prevalence, obesity results from an interaction between environmental and innate biological factors. Crucially, there is a strong genetic component underlying the large interindividual variation in body weight that determines people’s response to this ‘obesogenic’ environment . Twin, family and adoption studies have estimated the heritability of obesity to be between 40% and 70% 9 , 10 . As a consequence, genetic approaches can be leveraged to characterize the underlying physiological and molecular mechanisms that control body weight.

Classically, we have considered obesity in two broad categories (Fig.  2 ): so-called monogenic obesity , which is inherited in a Mendelian pattern, is typically rare, early-onset and severe and involves either small or large chromosomal deletions or single-gene defects; and polygenic obesity (also known as common obesity), which is the result of hundreds of polymorphisms that each have a small effect. Polygenic obesity follows a pattern of heritability that is similar to other complex traits and diseases. Although often considered to be two distinct forms, gene discovery studies of monogenic and polygenic obesity have converged on what seems to be broadly similar underlying biology. Specifically, the central nervous system (CNS) and neuronal pathways that control the hedonic aspects of food intake have emerged as the major drivers of body weight for both monogenic and polygenic obesity. Furthermore, early evidence shows that the expression of mutations causing monogenic obesity may — at least in part — be influenced by the individual’s polygenic susceptibility to obesity 11 .

Key features of monogenic and polygenic forms of obesity .

In this Review, we summarize more than 20 years of genetic studies that have characterized the molecules and mechanisms that control body weight, specifically focusing on overall obesity and adiposity, rather than fat distribution or central adiposity. Although most of the current insights into the underlying biology have been derived from monogenic forms of obesity, recent years have witnessed several successful variant-to-function translations for polygenic forms of obesity. We also explore how the ubiquity of whole-exome sequencing (WES) and genome sequencing has begun to blur the line that used to demarcate the monogenic causes of obesity from common polygenic obesity. Syndromic forms of obesity, such as Bardet–Biedl, Prader–Willi, among many others 12 , are not reviewed here. Although obesity is often a dominant feature of these syndromes, the underlying genetic defects are often chromosomal abnormalities and typically encompass multiple genes, making it difficult to decipher the precise mechanisms directly related to body-weight regulation. Finally, as we enter the post-genomic era, we consider the prospects of genotype-informed treatments and the possibility of leveraging genetics to predict and hence prevent obesity.

Gene discovery approaches

The approaches used to identify genes linked to obesity depend on the form of obesity and genotyping technology available at the time. Early gene discovery studies for monogenic forms of obesity had a case-focused design: patients with severe obesity, together with their affected and unaffected family members, were examined for potential gene-disrupting causal mutations via Sanger sequencing. By contrast, genetic variation associated with common forms of obesity have been identified in large-scale population studies, either using a case–control design or continuous traits such as BMI. Gene discovery for both forms of obesity was initially hypothesis driven; that is, restricted to a set of candidate genes that evidence suggests have a role in body-weight regulation. Over the past two decades, however, advances in high-throughput genome-wide genotyping and sequencing technologies, combined with a detailed knowledge of the human genetic architecture, have enabled the interrogation of genetic variants across the whole genome for their role in body-weight regulation using a hypothesis-generating approach.

Gene discovery for monogenic obesity

Many of the candidate genes and pathways linked to body-weight regulation were initially identified in mice, such as the obese ( ob ) 13 and diabetes ( db ) 14 mouse lines, in which severe hyperphagia and obesity spontaneously emerged. Using reverse genetics , the ob gene was shown to encode leptin, a hormone produced from fat, and it was demonstrated that leptin deficiency resulting from a mutation in the ob gene caused the severe obesity seen in the ob/ob mouse 15 (Fig.  3 ). Shortly after the cloning of ob , the db gene was cloned and identified as encoding the leptin receptor (LEPR) 16 . Reverse genetics was also used to reveal that the complex obesity phenotype of Agouti ‘lethal yellow’ mice is caused by a rearrangement in the promoter sequence of the agouti gene that results in ectopic and constitutive expression of the agouti peptide 17 , 18 , which antagonizes the melanocortin 1 and 4 receptors (MC1R and MC4R) 19 , 20 . This finding linked the melanocortin pathway to body-weight regulation, thereby unveiling a whole raft of new candidate genes for obesity.

Genes identified for monogenic obesity in a given year are shown on the left. Discoveries made for polygenic obesity are shown on the right, including a cumulative count of newly discovered loci per year and by ancestry. Although candidate gene and genome-wide linkage studies became available in the late 1990s, findings were limited, and these study designs are not as frequently used as genome-wide association studies.

Once the genes for leptin and its receptor were identified, they became candidate genes for human obesity, and in 1997 the first humans with congenital leptin deficiency were identified 21 . This discovery was rapidly followed by the report of humans with mutations in the gene encoding the leptin receptor ( LEPR ) 22 , as well as in genes encoding multiple components of the melanocortin pathway, including PCSK1 (ref. 23 ), MC4R 24 , 25 , 26 and POMC 27 , 28 , 29 , all of which were found to result in severe early-onset obesity (Table  1 ).

Advances in high-throughput DNA sequencing led to candidate gene screening being replaced by WES, an unbiased approach that allows all coding sequences to be screened for mutations. However, it rapidly became clear that, whereas candidate gene studies yielded few mutations, WES identified too many potential obesity-associated variants such that the noise often masked the true causative mutations. However, with improved algorithms to predict the pathogenicity of mutations, as well as a rapidly expanding toolkit of functional assays, it has become easier to filter the likely pathogenic mutations. Several success stories have been reported in which WES has identified novel pathways and genes linked to obesity, such as the class 3 semaphorins (SEMA3A–G), which have been shown to direct the development of certain hypothalamic neurons, including those expressing pro-opiomelanocortin (POMC) 30 (see ‘Other neuronal circuits and molecules linked to severe obesity’).

Most monogenic obesity mutations have been identified in cohorts of patients with severe and early-onset (<10 years old) obesity. Additionally, as monogenic obesity often demonstrates a recessive inheritance pattern 31 , consanguinity in populations has further increased the chance of identifying mutations, owing to greater chances of homozygosity of deleterious mutations 32 . For example, studies have reported that mutations in the genes encoding leptin, LEPR and MC4R explain 30% of cases of severe obesity in children from a consanguineous Pakistani population 33 , and single-gene defects more broadly account for nearly 50% 34 .

Gene discovery for polygenic obesity

The discovery of genes that influence polygenic obesity, which is common in the general population, started off slowly with candidate gene studies and genome-wide linkage studies . The candidate gene approach was first applied in the mid-1990s and aimed to validate genes identified through human and animal models of extreme obesity for a role in common obesity (Fig.  3 ). Common variants in such candidate genes were tested for association with obesity risk, BMI or other body composition traits. Over the subsequent 15 years, hundreds of genes were studied as candidates, but variants in only six ( ADRB3 (ref. 35 ), BDNF 36 , CNR1 (ref. 37 ), MC4R 38 , PCSK1 (ref. 39 ) and PPARG 40 ) showed reproducible association with obesity outcomes. The genome-wide linkage approach made its entrance into the field towards the end of the 1990s (Fig.  3 ). Genome-wide linkage studies rely on the relatedness of individuals and test whether certain chromosomal regions co-segregate with a disease or trait across generations. Even though more than 80 genome-wide linkage studies identified >300 chromosomal loci with suggestive evidence of linkage with obesity traits, few loci were replicated and none was successfully fine-mapped to pinpoint the causal gene or genes 41 . Ultimately, candidate gene and genome-wide linkage studies, constrained by small sample sizes, sparse coverage of genetic variation across the genome and lack of replication, only had a marginal impact on the progression of gene discovery for common obesity outcomes.

However, the pace of gene discovery for common diseases accelerated with the advent of genome-wide association studies (GWAS) (Fig.  3 ). The first GWAS for obesity traits were published in 2007 and identified a cluster of common variants in the first intron of the FTO locus that was convincingly associated with BMI 42 , 43 . Many more GWAS followed and, to date, nearly 60 GWAS have identified more than 1,100 independent loci associated with a range of obesity traits 44 (Supplementary Tables 1 , 2 ).

As sample sizes increase with each consecutive GWAS, the statistical power to identify more loci also increases, in particular for loci that are less common and/or have smaller effects. For example, the first GWAS were relatively small ( n = ~5,000) and identified only the FTO locus 42 , 43 . The BMI-increasing allele of FTO is common, particularly in populations of European ancestry (minor allele frequency (MAF) 40–45%), and has a relatively large effect on BMI (0.35 kg m −2 per allele; equivalent to 1 kg for a person who is 1.7 m tall). Ten years and numerous GWAS later, the most recent GWAS for BMI included nearly 800,000 individuals, identified more than 750 loci, with MAFs as small as 1.6% and per-allele effects as low as 0.04 kg m −2 per allele (equivalent to 120 g for a person who is 1.7 m tall) 45 . Combined, these genome-wide significant loci explained 6% of variation in BMI 45 . Large-scale international collaborations have been formed, such as the Genetic Investigation for Anthropometric Traits (GIANT) consortium , that combine summary statistics of individual GWAS to generate data sets comprising hundreds of thousands of individuals. Furthermore, many GWAS efforts have maximized sample size by focusing on BMI as the primary obesity outcome, an inexpensive and easy-to-obtain measurement that is readily available in most studies. As such, the vast majority of loci have been identified first in GWAS of BMI, but their effects typically transfer to other overall adiposity outcomes.

Even though BMI is widely used, it is considered a crude proxy of overall adiposity because it does not distinguish between lean and fat mass 46 . Therefore, GWAS have been performed for more refined obesity traits, such as body fat percentage 47 , 48 , fat-free mass 49 , imaging-derived adipose tissue 50 , circulating leptin levels 51 and LEPR levels 52 . In addition, two GWAS have focused on persistent healthy thinness, assuming that genes that determine resistance to weight gain may also inform obesity prevention and weight loss maintenance 53 , 54 . Although GWAS of more refined and alternative obesity outcomes are generally much smaller than those for BMI, the phenotypes are often a more accurate representation of body-weight regulation and, as such, the loci identified tend to more often point to relevant biological pathways that underlie obesity.

Almost all GWAS loci for obesity outcomes were first identified in adults. Most of these loci also associate with obesity and/or BMI in children and adolescents, highlighting the fact that the genetic underpinning of obesity is relatively constant across the course of life 55 , 56 , 57 . Similarly to gene discovery for other common diseases, the obesity genetics field has suffered from a strong bias in population representation, with the vast majority of GWAS being performed in populations that are exclusively or predominantly of European ancestry. Nevertheless, some loci have first been discovered in populations of Asian 58 , African 59 , 60 , Hispanic or other ancestry 61 , despite their much smaller sample sizes. Broadly, loci identified in one ancestry demonstrate good transferability (that is, directionally consistent associations) across other ancestries, even though effect sizes and allele frequencies may differ. The modest-to-high genetic correlations across ancestries observed for BMI ( r  = 0.78) are consistent with good transferability 62 , but also suggest that ancestry-specific loci remain to be discovered. Besides increasing the sample sizes of GWAS in populations of non-European ancestry, demographic, evolutionary and/or genomic features of specific populations (such as founder, consanguineous or isolated populations) have been leveraged for gene discovery, identifying genetic variants with large effects that are common in the discovery population, such as CREBRF , first identified in Samoan populations, and ADCY3 , first identified in the Greenlandic population, but rare or nonexistent in most others 63 , 64 , 65 , 66 . CREBRF has been shown to play a role in cellular energy storage and use, and may be implicated in cellular and organismal adaptation to nutritional stress 65 . ADCY3 colocalizes with MC4R at the primary cilia of a subset of hypothalamic neurons that have been implicated in body-weight regulation 67 .

GWAS have typically focused on biallelic, common genetic variation (MAF >5%), but have also been used to screen for the role of copy number variants (CNVs) in obesity. So far, only a few CNVs have been identified that have a convincing association with BMI, such as the 1p31.1 45-kb deletion near NEGR1 (ref. 68 ), which encodes a cell-adhesion molecule expressed in the brain 69 ; the 16p12.3 21-kb deletion upstream of GPRC5B 70 , which may modulate insulin secretion 71 ; the 10q11.22 CNV in PPYR1 (also known as NPY4R ) 72 , which encodes a potent anti-obesity agent known to inhibit food intake 73 ; and the 1p21.1 multi-allele CNV encompassing AMY1A 74 , which produces salivary α-amylase, a key enzyme in starch digestion 75 .

To determine the role of other types of variation in obesity, alternative genome-wide screens have been performed. For example, the impact of low-frequency and rare protein-coding variants has been tested using exome sequencing and exome array data 76 , 77 , 78 , 79 . It was speculated that low-frequency (MAF 1–5%) and rare (MAF <1%) variants would have larger effects than common variants, and thus be easier to detect. Nevertheless, even large-scale studies identified only a few robust associations for rare coding variants. For example, exome-wide screening based on array data from more than 400,000 individuals identified p.Tyr35Ter (rs13447324) in MC4R ; p.Arg190Gln (rs139215588) and p.Glu288Gly (rs143430880) in GIPR , which stimulates insulin secretion and mediates fat deposition 80 ; p.Arg95Ter (rs114285050) in GRP151 , which modulates habenular function that controls addiction vulnerability 81 ; and p.Arg769Ter (rs533623778) in PKHD1L1 , which has been involved in cancer development 77 , 78 . A recent study that leveraged WES data for more than 600,000 individuals identified 16 genes for which the burden of rare nonsynonymous variants was associated with BMI, including five brain-expressed G protein-coupled receptors ( CALCR , MC4R , GIPR , GPR151 and GPR75 ) 79 .

As obesity is a complex, multifactorial condition, some GWAS have integrated demographic factors (such as sex and age 82 ) and environmental factors (such as physical activity 83 , diet 84 or smoking 85 ) into their analyses. Despite sample sizes of more than 200,000 individuals, these genome-wide gene-by-environment (G×E) interaction analyses remain challenging and so far only 12 loci have been identified, the effects of which on obesity are attenuated or exacerbated by non-genetic factors. Nevertheless, the G×E interaction between the FTO locus and a healthy lifestyle has been robustly replicated. Specifically, increased physical activity or a healthy diet can attenuate the effect of the FTO locus on obesity risk by 30–40% 86 , 87 .

The increasing availability of large-scale cohorts and biobanks, such as the UK Biobank , the Million Veterans Project , All of Us , Biobank Japan and 23andMe , combined with ongoing work by the GIANT consortium, will boost sample sizes further to easily exceed 4 million participants in meta-analyses, expediting the discovery of many more obesity-associated loci. However, translation of GWAS-identified loci into new biological insights remains a major challenge.

From genes to biology

Despite the difficulties in validating causative mutations and variants, genetic studies into both rare and common obesity over the past two decades have revealed two surprisingly cogent, overarching biological messages: first, the leptin–melanocortin pathway is a key appetitive control circuit 31 , 88 (Fig.  4 ); and second, genes that are either enriched or exclusively expressed within the brain and CNS have a central role in obesity 89 .

Pro-opiomelanocortin (POMC)-expressing neurons and agouti-related protein (AGRP)-expressing neurons within the arcuate nucleus of the hypothalamus (ARC) act to sense circulating leptin (LEP) levels, which reflect fat mass. These neurons signal to melanocortin 4 receptor (MC4R)-expressing neurons in the paraventricular nucleus of the hypothalamus (PVN), which controls appetite, thus linking long-term energy stores to feeding behaviour. Binding of class 3 semaphorins (SEMA3) to their receptors NRP and PLXNA influences the projection of POMC neurons to the PVN. Binding of brain-derived neurotrophic factor (BDNF) to its receptor neurotrophic receptor tyrosine kinase 2 (NTRK2) is thought to be an effector of leptin-mediated synaptic plasticity of neurons, including those in the ARC and PVN. The transcription factor SIM1 is crucial for the proper development of the PVN. +, agonist; −, antagonist; LEPR, leptin receptor; MRAP2, melanocortin receptor accessory protein 2; MSH, melanocyte-stimulating hormone; SH2B1, SH2B adaptor protein 1.

The leptin–melanocortin pathway and MC4R

Leptin is a key hormone secreted by adipocytes, which circulates at levels in proportion to fat mass 90 . Leptin also responds to acute changes in energy state, as its levels decrease with food deprivation and are restored during re-feeding. Administration of leptin to fasted mice abrogates many of the neuroendocrine consequences of starvation, suggesting that the normal biological role of leptin is to initiate the starvation response 91 . Leptin signals through the LEPR, which exists in several different isoforms. However, obesity-related effects of leptin are predominantly mediated by a long isoform that contains an intracellular domain (LEPRb), which is expressed in various regions of the CNS 90 .

Within the arcuate nucleus (ARC) of the hypothalamus, LEPRb is found on two populations of neurons at the heart of the melanocortin pathway, one of which expresses POMC and the other agouti-related protein (AGRP) 92 (Fig.  4 ). POMC is post-translationally processed by prohormone convertases to produce several biologically active moieties, including β-lipotrophin and β-endorphin, and, crucially, the melanocortin peptides adrenocorticotrophin (ACTH) and α-, β- and γ-melanocyte-stimulating hormone (MSH) 93 . The ARC POMC neurons project to MC4R neurons within the paraventricular nucleus (PVN) where melanocortin peptides signal to decrease food intake 92 . By contrast, AGRP acts as an endogenous antagonist of MC4R to increase food intake 92 , 94 . MC3R is another centrally expressed receptor that binds to both melanocortin peptides and AGRP; however, as mice with targeted deletions in the gene are not obese but instead have altered fat to lean mass ratio, MC3R is less likely to be related to food intake and more likely to be involved in nutrient partitioning 95 , 96 .

We can state with confidence that the fine balance of melanocortinergic agonism and AGRP antagonism of MC4R, in response to peripheral nutritional cues such as leptin, plays a central part in influencing appetitive drive 92 . The genetic evidence clearly supports this contention, with mutations in most genes of the melanocortin pathway resulting in hyperphagia and severe obesity in both humans and mice 31 , 88 . In fact, the vast majority of single-gene disruptions causing severe early-onset obesity in humans fall within this pathway, including LEPR , POMC , AGRP , MCR4R , PCSK1 (ref. 23 ), SH2B1 (ref. 97 ), PHIP 98 , MRAP2 (ref. 99 ) and SIM1 (ref. 100 ) (Fig.  4 ; Table  1 ). Mutations in MC4R in particular, are the most common single-gene defect leading to hyperphagia and obesity. Pathogenic mutations in MC4R are found in up to 5% of cases of severe childhood obesity 101 and up to 0.3% of the general population 101 , 102 . Of note, the degree of receptor dysfunction, as measured by in vitro assays, can predict the amount of food eaten at a test meal by an individual harbouring that particular mutation 101 . Thus MC4R does not act in a binary on/off manner, but as a rheostat; put simply, the melanocortin pathway is a ‘tunable’ system. In addition to regulating food intake, it also regulates food preference, with individuals who carry mutations in MC4R showing a preference for food with higher fat content 103 .

The importance of the melanocortin pathway in regulating feeding behaviour is highlighted by the identification of naturally occurring mutations in pathway genes in a wide range of different species where the appropriate selection pressure has been present (Table  1 ). For example, studies have found that 20–25% of Labrador retrievers, which are known to be more food-motivated than other dog breeds, carry a 14-bp deletion in POMC that disrupts the β-MSH and β-endorphin coding sequences and is associated with greater food motivation and increased body weight 104 . Also, certain breeds of pig have been shown to carry MC4R missense mutations that are associated with fatness, growth and food intake traits 105 . MC4R mutations even contribute to the adaptation and survival of blind Mexican cavefish to the nutrient-poor conditions of their ecosystem 106 .

Other neuronal circuits and molecules linked to severe obesity

It is now clear that in addition to engaging classical neuropeptide–receptor systems within the brain, leptin also rapidly modifies synaptic connections between neurons 107 , and that this structural plasticity is crucial to its downstream functions. One of the ways in which this plasticity is thought to be achieved is via brain-derived neurotrophic factor (BDNF) signalling to its receptor TrkB. BDNF is widely expressed in the CNS where it plays an important part in neuronal development 108 , 109 . In the hippocampus, BDNF contributes to synaptic plasticity and long-term potentiation associated with memory and learning 110 . However, evidence has emerged that implicates BDNF and TrkB in the regulation of mammalian eating behaviour and energy balance 111 . BDNF is downregulated by nutritional deprivation and upregulated by leptin within the ventromedial nucleus (VMN) of the hypothalamus 112 , although this regulation is probably indirect, as very few VMN BDNF neurons express the LEPR 113 (Fig.  4 ) and some evidence indicates that it acts at least in part downstream of melanocortin signalling 112 . Crucially, genetic disruption of BDNF 114 , 115 and TrkB 112 , 116 in both humans and mice results in hyperphagia and severe obesity.

Another group of neuronal proteins important in the development of neuronal circuitry and linked to energy balance are the class 3 semaphorins (SEMA3A–G). A study in humans found that 40 rare loss-of-function variants in SEMA3A–G and their receptors (PLXNA1–4, NRP1 and NRP2) were significantly enriched in 982 individuals with severe obesity compared with 4,449 controls 30 . Disruption of several of these genes in zebrafish caused increased somatic growth and/or adiposity, and experiments with mouse hypothalamic explants suggest that SEMA3 signalling via NRP2 receptors drives the development of POMC projections from the ARC to the PVN 30 . However, given that these results are from a single study, more data are required to confirm the exact role of class 3 semaphorins in energy homeostasis.

Insights from genetic loci linked to common obesity

Unlike candidate gene studies, GWAS make no a priori assumptions about the underlying biology that links genetic variants to a disease of interest. While this agnostic approach allows for new biological insights, the vast majority of GWAS-identified variants map to the non-coding parts of genes or to regions between genes. As such, they do not directly disrupt the protein-coding regions, but instead overlap with regulatory elements that influence expression of genes in close proximity or even over long distances.

However, even if the causative genes are unknown, pathway, tissue and functional enrichment analyses based on the genes located in the GWAS loci can provide insights into potential mechanisms. Since the very first GWAS for BMI 68 , 117 , such analyses have pointed to the CNS being a key player in body-weight regulation, consistent with insights from human and animal models of extreme obesity. Recent analyses that include the latest BMI-associated loci, combined with updated multi-omics databases and advanced computational tools, have further refined these observations. In addition to the hypothalamus and pituitary gland (which are both known appetite regulation sites), other brain areas have been highlighted, including the hippocampus and the limbic system (which are involved in learning, cognition and emotion) and the insula and the substantia nigra (which are related to addiction and reward) 58 , 89 , 118 , 119 . The enrichment of immune-related cells (such as lymphocytes and B cells) and adipose tissue was found to be weaker 58 .

Although enrichment analyses provide preliminary insights into the broad biology represented by genes in the GWAS loci, determining which genes, variants and/or underlying mechanisms are causal has proved an arduous task. For example, the FTO locus, which was identified more than a decade ago and harbours six genes, is the most extensively studied GWAS-identified obesity locus (Fig.  5 ). Despite its highly significant and widely replicated association with obesity 120 , the causal variants and/or genes in the FTO locus have not yet been pinpointed with convincing evidence, and the mechanisms by which the locus affects body weight have not been fully elucidated. Early functional follow-up analyses suggested that FTO itself might be responsible, as Fto deficiency in mice results in a lean phenotype, whereas Fto overexpression is associated with increased body weight 121 , 122 . Studies in mice have suggested that FTO plays a role in cellular nutrient sensing 123 , 124 . Other studies found evidence that FTO influences brain regions that affect appetite, reward processing and incentive motivation by regulating ghrelin levels in humans 125 or by controlling dopaminergic signalling in mice 126 , 127 . In addition, variants in the FTO locus were shown to alter a regulatory element that controls the transcription of Rpgrip1l in mice, a ciliary gene located immediately upstream of Fto 128 , 129 , 130 . Mice with reduced Rpgrip1l activity exhibit hyperphagic obesity, possibly mediated through diminished leptin signalling 128 , 129 , 130 . In recent years, studies in human and animal models have shown that variants in the FTO locus directly interact with the promoter of Irx3 , a gene located 0.5 Mb downstream of FTO . Irx3 -deficient mice were found to exhibit weight loss and increased metabolic rate with browning of white adipose tissue, without changes in physical activity or appetite 131 , 132 . Further in-depth functional characterization showed that rs1421085 in the FTO locus disrupts a conserved binding motif for the transcriptional repressor ARID5B, which leads to a doubling of IRX3 and IRX5 expression during early adipocyte differentiation 132 . The authors argue that increased expression of these genes results in a developmental shift from energy-dissipating beige adipocytes to energy-storing white adipocytes, a fivefold reduction in mitochondrial thermogenesis and increased lipid storage 132 . However, given that multiple studies have shown that the FTO locus is robustly associated with food intake, with no evidence to date linking it to changes in energy expenditure, the relevance of this observation to the actual observed human phenotype still needs to be explored 133 . A recent study reports that the FTO locus affects gene expression in multiple tissues, including adipose tissue and brain, and, more broadly, that the genetic architecture of disease-associated loci may involve extensive pleiotropy and allelic heterogeneity across tissues 134 .

FTO contains nine exons (depicted by blue rectangles) and the body mass index (BMI)-associated SNP identified in genome-wide association studies (depicted by a red ×) maps to intron 1. IRX3 and RPGRIP1L have both been proposed to be the causal genes for obesity within the locus and to act on body weight through distinct mechanisms. HFD, high-fat diet.

Besides the FTO locus, functional follow-up analyses have been performed for only a few obesity-associated GWAS loci. For example, early studies identified a cluster of variants just downstream of TMEM18 (refs 68 , 117 ). TMEM18 encodes a poorly characterized transmembrane protein that is highly conserved across species and widely expressed across tissues, including in several regions of the brain 135 , 136 . Tmem18 deficiency in mice results in a higher body weight owing to increased food intake, whereas Tmem18 overexpression reduces food intake and limits weight gain 136 . A knockdown experiment in Drosophila melanogaster suggests that TMEM18 affects carbohydrate and lipid levels by disrupting insulin and glucagon signalling 137 .

Two other GWAS loci for which functional analyses have been performed are located just upstream of CADM1 (ref. 82 ) and in CADM2 (ref. 70 ), genes that encode cell-adhesion proteins of the immunoglobulin superfamily and mediate synaptic assembly in the CNS 138 . The BMI-increasing alleles at each locus are associated with increased expression of CADM1 and CADM2 in the hypothalamus 139 , 140 . Deficiency of either Cadm1 or Cadm2 in mice results in a lower body weight and increased insulin sensitivity, glucose tolerance and energy expenditure without any change in food intake 139 , 140 . Conversely, increased neuronal expression of either Cadm1 or Cadm2 is associated with elevated body weight 139 , 140 . Furthermore, CADM1 is expressed in POMC neurons and Cadm1 deficiency leads to an increase in the number of excitatory synapses, suggestive of an increased synaptic plasticity 140 . Cadm2 -deficient mice exhibit increased locomotor activity and higher core body temperature 139 .

Another GWAS locus, just upstream of NEGR1 , harbours two deletions associated with increased obesity risk 68 , 117 , 141 . These deletions do not overlap with the coding sequence of NEGR1 , but encompass a conserved transcription factor-binding site for NKX6.1 , a potent transcriptional repressor 68 , 141 . Loss of binding of NKX6.1 leads to higher NEGR1 expression 141 , which is consistent with the observation that BMI-increasing alleles (that is, deletions) at this locus are associated with higher NEGR1 expression in the brain. Similar to CADM1 and CADM2, NEGR1 is a cell-adhesion molecule of the immunoglobulin superfamily that is expressed in several regions of the brain and has been shown to have a role in brain connectivity 69 , 142 , a process believed to be important in obesity 143 . NEGR1 deficiency in mice was shown to result in lower body weight, mainly due to reduced lean mass, mediated by lower food intake 144 . However, two other functional studies, one in mice and one in rats, found that knockdown of Negr1 expression resulted in the opposite phenotype — increased body weight and food intake 145 , 146 . While NEGR1 deficiency in mice was found to impair core behaviours, so far, findings and proposed mechanisms are not fully aligned 69 , 147 , 148 , 149 .

Taken together, functional follow-up analyses for these loci are slowly expanding our understanding of the pathophysiology that drives weight gain. However, many more obesity-associated loci are waiting to be translated into new biological insights. A major hurdle in translating GWAS loci into plausible candidate genes and appropriate paradigms for functional research is the annotation of the associated variants in a locus. Defining the regulatory function of the non-coding variants, identifying their putative effector transcripts and determining their tissues of action remains an ongoing challenge. The advent of high-throughput genome-scale technologies for mapping regulatory elements, combined with comprehensive multi-omics databases, advanced computational tools and the latest genetic engineering and molecular phenotyping approaches, is poised to speed up the translation of GWAS loci into meaningful biology 150 .

Converging results from monogenic and polygenic forms of obesity

Gene discovery is often dichotomized by allele frequency and disease prevalence; that is, mutations are sought for monogenic forms of obesity and common variants for polygenic obesity (Fig.  2 ). However, it is increasingly recognized that monogenic and polygenic forms of obesity are not discrete entities. Instead, they lie on a spectrum and share — at least in part — the same biology. As GWAS have continued to discover more obesity-associated loci, an increasing number of these loci harbour genes that were first identified for extreme and early-onset obesity in humans or animal models, including MC4R 151 , 152 , BDNF 117 , SH2B1 (refs 68 , 117 ), POMC 70 , LEP 51 , 153 , LEPR 52 , 154 , NPY 155 , SIM1 (ref. 155 ), NTRK2 (ref. 58 ), PCSK1 (ref. 154 ) and KSR2 (ref. 77 ). In fact, most of these genes encode components of the leptin–melanocortin and BDNF–TrkB signalling pathways (Table  1 ). Thus, whereas genetic disruption of components of these pathways results in severe obesity, genetic variants in or near these same genes that have more subtle effects on their expression will influence where an individual might sit in the normal distribution of BMI.

Although most genes have been first identified for extreme forms of obesity, a locus harbouring ADCY3 was first identified in GWAS for common obesity 77 , and ADCY3 was subsequently confirmed as having a role in extreme obesity 63 , 64 . ADCY3 encodes an adenylate cyclase that catalyses the synthesis of cAMP, an important second messenger in signalling pathways. There is some evidence that ADCY3 (adenylate cyclase) colocalizes with MC4R at the primary cilia of PVN neurons 67 and that cilia are required specifically on MC4R-expressing neurons for the control of energy homeostasis 156 . In mice, disruption of Adcy3 or Mc4r in the cilia of these neurons impairs melanocortin signalling, resulting in hyperphagia and obesity 67 .

As more GWAS loci are reported, we expect that findings across different lines of obesity research will continue to converge, providing accumulating evidence for new biology.

From genes to clinical care

Genetic insights from gene discovery efforts are increasingly being used in the context of precision medicine in ways that directly affect health. Knowing a patient’s genotype may enable a more precise diagnosis of the type of obesity, which in turn allows the prescription of personalized treatment or prevention strategies. Furthermore, knowing an individual’s genetic susceptibility to obesity early in life may help to more accurately predict those most at risk of gaining weight in the future.

Use of genotype information in treatment of obesity

When a disease is caused by a single mutation and the environmental contribution is limited, as is the case for some forms of extreme and early-onset obesity, a genetic test can be instrumental in correctly diagnosing patients. Although no standard genetic testing panel is currently available for extreme and early-onset obesity, some clinics, research centres and pharmaceutical companies sequence well-known candidate genes to identify the functional mutation that may be the cause of a patient’s excess body weight. Such a genetic diagnosis can lessen the feelings of guilt and blame for the patient, and alleviate social stigma and discrimination. Importantly, a genetic diagnosis can inform disease prognosis and, in some cases, it will determine treatment. To date, there are two treatments for obesity that are tailored to patient genotype.

The prototype of genotype-informed treatment for obesity is the administration of recombinant human leptin in patients who are leptin-deficient owing to mutations in the LEP gene 157 , 158 . Although congenital leptin deficiency is exceptionally rare (only 63 cases have been reported to date 28 ), leptin replacement therapy has been remarkably beneficial for these patients by substantially reducing food intake, body weight and fat mass, and normalizing endocrine function 157 , 158 . It has literally transformed their lives.

The second genotype-informed treatment for obesity is setmelanotide, a selective MC4R agonist that was recently approved by the FDA for rare monogenic obesity conditions including LEPR, PCSK1 and POMC deficiency 159 . Setmelanotide acts as a substitute for the absent MSH in patients with POMC deficiency owing to mutations in POMC or PCSK1 , and in patients with LEPR deficiency owing to mutations in LEPR , which is essential for POMC function 160 , 161 , 162 . Daily subcutaneous injection of setmelanotide results in substantial weight loss and in reduction of hunger 160 , 161 , 162 . After a 1-year treatment with setmelanotide in phase III trials, patients with POMC deficiency lost on average 25.6% of their initial weight, with 80% of patients achieving at least a 10% weight loss 162 . The adverse effects of setmelanotide treatment are minor, and include hyperpigmentation, nausea and/or vomiting, penile erection and injection site reactions. Weight loss in patients with LEPR deficiency was less pronounced; on average, they lost 12.5% of their initial weight, with only 45% of patients achieving at least a 10% weight loss 162 . The difference in weight loss between the two patient groups may be because POMC deficiency directly affects the production of MC4R ligands (α-MSH and β-MSH), whereas LEPR deficiency affects signalling upstream of POMC 162 . As such, setmelanotide may be able to completely restore MC4R signalling in POMC deficiency, but only partially in LEPR deficiency. Even though the average weight loss in POMC-deficient patients was twice that in LEPR-deficient patients, the reduction in hunger was substantially larger in LEPR-deficient patients (−43.7%) than in POMC-deficient patients (−27.1%) 162 . The reasons for the discrepancy between weight loss and reduction in hunger remain to be studied in greater depth. It has been estimated that in the USA, >12,800 individuals carry mutations in the melanocortin pathway for whom setmelanotide may be more effective for weight loss than any other treatment 163 . Although 12,800 carriers represent only a fraction (0.004%) of the adult population in the USA, and not all of these mutation carriers are overweight or obese, for the patients for whom setmelanotide is effective, it may end a lifelong battle to lose weight 163 . In patients without genetic defects, neither setmelanotide nor leptin administration have, to date, demonstrated a substantial effect on weight loss 164 , 165 .

These two genotype-informed treatments show how insight into the underlying biological mechanisms can guide the development of molecules and medications that restore impaired pathways, at least in monogenic forms of obesity caused by deficiency of one protein. Nevertheless, there remain substantial obstacles in the transition from conventional to precision medicine for monogenic obesity, which would require the adoption of systematic WES for individuals suspected to be carriers of deleterious mutations, and eventually even standardized screening at birth. We are clearly a long way from such a scenario at present.

Use of genotype information in prediction of obesity

As more variants are being discovered for common obesity, there is a growing expectation that genetic information will soon be used to identify individuals at risk of obesity. Knowing a person’s genetic susceptibility would allow for a more accurate prediction of who is at risk of gaining weight and give an opportunity to intervene earlier to prevent obesity more effectively. Genetic susceptibility to complex disease, including obesity, is assessed using a polygenic score (PGS). PGSs to assess obesity susceptibility are based on GWAS for BMI (PGS BMI ), the latest of which includes data on more than 2 million variants and explains 8.4% of the variation in BMI 166 . The average BMI of individuals with a high PGS BMI (top decile) is 2.9 kg m −2 (equivalent to 8 kg in body weight) higher and their odds of severe obesity (BMI ≥40 kg m −2 ) is 4.2-fold higher than those with a lower PGS BMI (lowest nine deciles) 166 .

Despite these strong associations with BMI and obesity, the predictive performance of the PGS BMI is weak, which is unsurprising given its limited explained variance. For example, using the same PGS BMI and data from the UK Biobank, we estimate that the area under the receiver operating characteristic curve (AUC ROC ) is only 0.64 to predict obesity. This means that the probability that an individual with obesity has a higher PGS BMI than an individual without obesity is 0.64. However, for a PGS to have clinical utility, the AUC ROC needs to be much higher (>0.80). In addition, we calculated the extent to which a PGS BMI ≥90th percentile correctly classifies individuals with obesity (Fig.  6 ). We found that such a predictive test (PGS BMI ≥90th percentile) has a positive predictive value of 0.43, meaning that of those who were predicted to develop obesity, only 43% actually developed obesity. Its sensitivity is 0.19, which means that of the individuals who developed obesity, only 19% had been correctly classified by the PGS BMI . Given that the current treatment options for obesity are low risk, or even generally beneficial, the high false-positive rate is less concerning than the low sensitivity, as some at-risk individuals may miss the opportunity for early prevention.

The outcome is illustrated for a polygenic score (PGS) that assumes that individuals with a score in the highest decile (≥90th percentile (pct)) will develop obesity, has a positive predictive value of 0.4 and a sensitivity of 0.19. Of ten individuals with a high score classified by the PGS as ‘with obesity’, four will be classified correctly but the other six will be misclassified and will not develop obesity — a positive predictive value of 0.4. Likewise, 17 of the 90 individuals with a score <90th pct who are predicted to not develop obesity, will develop obesity. Thus, only four of the 21 individuals who developed obesity were correctly classified by the PGS — a sensitivity of 0.19. Misclassified individuals are indicated by the red boxes, individuals correctly classified as ‘with obesity’ are indicated by a blue box. Adapted with permission from ref. 170 , Elsevier.

Thus, the current PGS BMI has a high rate of misclassification and does not reliably predict who is at risk of developing obesity and who is not. The predictive ability of PGSs are expected to improve as GWAS increase in sample size and algorithms to calculate the scores become more refined. Nevertheless, given the importance of socio-demographic, lifestyle and clinical risk factors in the aetiology of obesity, it is unlikely that a PGS BMI will ever be able to accurately predict obesity on its own. Instead, effective prediction models will have to include genetic and non-genetic factors, including a broad spectrum of demographic, environmental, clinical and possibly molecular markers, as well.

Conclusions and future perspectives

What initially began as two apparently distinct approaches, one studying rare Mendelian causes of extreme obesity, and the other exploring complex polygenic influences of population body-weight distribution, have eventually converged on the central role of the brain in regulating body weight. In particular, both approaches have highlighted the roles of the leptin–melanocortin pathway and TrkB–BDNF signalling. Perhaps it seems obvious now, but it was by no means certain that, just because genetic disruption of a pathway resulted in a severe phenotype, polymorphisms within that same pathway would produce a more subtle and nuanced result.

The GWAS approach is hypothesis-free, with the promise to reveal new genes that point to new biology and pathways. However, for the vast majority of the >1,000 GWAS-identified loci, we do not know which genes are causal, what cells, tissues and organs they act in to affect body weight, and we do not understand the underlying mechanisms. The translation from variant to function is a well-known challenge 167 , but with increasing availability of new omics data, high-throughput technologies and advanced analytical approaches, there is an unprecedented opportunity to speed up the translation of hundreds of GWAS loci.

Sample size remains a major driver for gene discovery. In an ongoing collaboration that combines data from more than 3 million individuals of diverse ancestry from the GIANT consortium, the UK Biobank and 23andMe, the number of BMI-associated GWAS loci is set to double. Also, a recent WES effort of more than 640,000 individuals has demonstrated that rare mutations are discoverable when sample sizes are sufficiently large 79 . However, alternative study designs, a focus on more refined phenotypes or a focus on population subgroups (that is, more homogeneous groups of individuals with similar outcomes) could further add to gene discovery.

Translation of only a few dozen of the GWAS-identified loci could tremendously improve our insights into the biology of obesity and possibly reveal new therapeutic targets. It would also take us a little closer to the ‘holy grail’ — the ability to move away from a failed ‘one-size-fits-all’ strategy, and towards true precision medicine for obesity, metabolic disease and other diet-related illnesses.

GBD 2015 Obesity Collaborators. Health effects of overweight and obesity in 195 countries over 25 years. N. Engl. J. Med. 377 , 13–27 (2017).

Article   Google Scholar  

Must, A. et al. The disease burden associated with overweight and obesity. JAMA 282 , 1523–1529 (1999).

Article   CAS   PubMed   Google Scholar  

Fontaine, K. R. & Barofsky, I. Obesity and health-related quality of life. Obes. Rev. 2 , 173–182 (2001).

Bhattacharya, I., Ghayor, C., Perez Dominguez, A. & Weber, F. E. From influenza virus to novel corona virus (SARS-CoV-2)—the contribution of obesity. Front. Endocrinol. 11 , 556962 (2020).

Petrilli, C. M. et al. Factors associated with hospital admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study. BMJ 369 , m1966 (2020).

Article   PubMed   PubMed Central   Google Scholar  

Cummings, M. J. et al. Epidemiology, clinical course, and outcomes of critically ill adults with COVID-19 in New York City: a prospective cohort study. Lancet 395 , 1763–1770 (2020).

Article   CAS   PubMed   PubMed Central   Google Scholar  

Zhao, X. et al. Obesity increases the severity and mortality of influenza and COVID-19: a systematic review and meta-analysis. Front. Endocrinol. 11 , 595109 (2020).

Abarca-Gómez, L. et al. Worldwide trends in body-mass index, underweight, overweight, and obesity from 1975 to 2016: a pooled analysis of 2416 population-based measurement studies in 128.9 million children, adolescents, and adults. Lancet 390 , 2627–2642 (2017).

Maes, H. H., Neale, M. C. & Eaves, L. J. Genetic and environmental factors in relative body weight and human obesity. Behav. Genet. 27 , 325–351 (1997).

Elks, C. E. et al. Variability in the heritability of body mass index: a systematic review and meta-regression. Front. Endocrinol. 3 , 29 (2012). This paper reports a large-scale meta-analysis of heritability data of twin and family studies .

Chami, N., Preuss, M., Walker, R. W., Moscati, A. & Loos, R. J. F. The role of polygenic susceptibility to obesity among carriers of pathogenic mutations in MC4R in the UK Biobank population. PLoS Med. 17 , e1003196 (2020). This study shows that the effect of MC4R mutations on BMI and obesity risk is attenuated by the polygenic background .

Kaur, Y., de Souza, R. J., Gibson, W. T. & Meyre, D. A systematic review of genetic syndromes with obesity. Obes. Rev. 18 , 603–634 (2017).

Ingalls, A. M., Dickie, M. M. & Snell, G. D. Obese, a new mutation in the house mouse. J. Hered. 41 , 317–318 (1950).

Hummel, K. P., Dickie, M. M. & Coleman, D. L. Diabetes, a new mutation in the mouse. Science 153 , 1127–1128 (1966).

Zhang, Y. et al. Positional cloning of the mouse obese gene and its human homologue. Nature 372 , 425–432 (1994). This paper reports the cloning of leptin, which provided the first molecular evidence that feeding and regulation of body weight had a hormonal basis .

Article   CAS   Google Scholar  

Chen, H. et al. Evidence that the diabetes gene encodes the leptin receptor: identification of a mutation in the leptin receptor gene in db / db mice. Cell 84 , 491–495 (1996). This paper reports the cloning of the LEPR and the localization of its signalling version, which highlights the role of the brain in the control of appetitive behaviour .

Bultman, S. J., Michaud, E. J. & Woychik, R. P. Molecular characterization of the mouse agouti locus. Cell 71 , 1195–1204 (1992).

Miller, M. W. et al. Cloning of the mouse agouti gene predicts a secreted protein ubiquitously expressed in mice carrying the lethal yellow mutation. Genes Dev. 7 , 454–467 (1993).

Lu, D. et al. Agouti protein is an antagonist of the melanocyte-stimulating-hormone receptor. Nature 371 , 799–802 (1994).

Fan, W., Boston, B. A., Kesterson, R. A., Hruby, V. J. & Cone, R. D. Role of melanocortinergic neurons in feeding and the agouti obesity syndrome. Nature 385 , 165–168 (1997).

Montague, C. T. et al. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 387 , 903–908 (1997). This work demonstrates that leptin signalling is also relevant in the human context, and provides early evidence, together with mutations in PCSK1 , of a monogenic cause of severe human obesity .

Clement, K. et al. A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature 392 , 398–401 (1998). This work confirms the observations from mice about leptin signalling to the brain .

Jackson, R. S. et al. Obesity and impaired prohormone processing associated with mutations in the human prohormone convertase 1 gene. Nat. Genet. 16 , 303–306 (1997). This study, together with mutations in the leptin gene, provides early evidence of a monogenic cause of severe human obesity, and also highlights the role of the nascent melanocortin pathway in body-weight regulation .

Huszar, D. et al. Targeted disruption of the melanocortin-4 receptor results in obesity in mice. Cell 88 , 131–141 (1997).

Yeo, G. S. et al. A frameshift mutation in MC4R associated with dominantly inherited human obesity. Nat. Genet. 20 , 111–112 (1998).

Vaisse, C., Clement, K., Guy-Grand, B. & Froguel, P. A frameshift mutation in MC4R is associated with a dominant form of obesity. Nat. Genet. 20 , 113–114 (1998). This paper, together with Yeo et al. (1998), shows that heterozygous mutations in MC4R result in severe human obesity, establishing the role of the central melanocortin pathway in regulating human appetitive behaviour .

Krude, H. et al. Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans. Nat. Genet. 19 , 155–157 (1998). This paper provides direct evidence that melanocortin peptides play a key role in the regulation of energy homeostasis .

Yaswen, L., Diehl, N., Brennan, M. B. & Hochgeschwender, U. Obesity in the mouse model of pro-opiomelanocortin deficiency responds to peripheral melanocortin. Nat. Med. 5 , 1066–1070 (1999).

Challis, B. G. et al. Mice lacking pro-opiomelanocortin are sensitive to high-fat feeding but respond normally to the acute anorectic effects of peptide-YY(3-36). Proc. Natl Acad. Sci. USA 101 , 4695–4700 (2004).

van der Klaauw, A. A. et al. Human semaphorin 3 variants link melanocortin circuit development and energy balance. Cell 176 , 729–742.e18 (2019).

Farooqi, S. & O’Rahilly, S. Genetics of obesity in humans. Endocr. Rev. 27 , 710–718 (2006).

Saeed, S., Arslan, M. & Froguel, P. Genetics of obesity in consanguineous populations: toward precision medicine and the discovery of novel obesity genes. Obesity 26 , 474–484 (2018).

Article   PubMed   Google Scholar  

Saeed, S. et al. Genetic variants in LEP, LEPR, and MC4R explain 30% of severe obesity in children from a consanguineous population. Obesity 23 , 1687–1695 (2015).

Saeed, S. et al. Genetic causes of severe childhood obesity: a remarkably high prevalence in an inbred population of Pakistan. Diabetes 69 , 1424–1438 (2020).

Kurokawa, N. et al. The ADRB3 Trp64Arg variant and BMI: a meta-analysis of 44 833 individuals. Int. J. Obes. 32 , 1240–1249 (2008).

Shugart, Y. Y. et al. Two British women studies replicated the association between the Val66Met polymorphism in the brain-derived neurotrophic factor (BDNF) and BMI. Eur. J. Hum. Genet. 17 , 1050–1055 (2009).

Benzinou, M. et al. Endocannabinoid receptor 1 gene variations increase risk for obesity and modulate body mass index in European populations. Hum. Mol. Genet. 17 , 1916–1921 (2008).

Wang, D. et al. Association of the MC4R V103I polymorphism with obesity: a Chinese case–control study and meta-analysis in 55,195 individuals. Obesity 18 , 573–579 (2010).

Nead, K. T. et al. Contribution of common non-synonymous variants in PCSK1 to body mass index variation and risk of obesity: a systematic review and meta-analysis with evidence from up to 331 175 individuals. Hum. Mol. Genet. 24 , 3582–3594 (2015).

Tonjes, A., Scholz, M., Loeffler, M. & Stumvoll, M. Association of Pro12Ala polymorphism in peroxisome proliferator-activated receptor gamma with pre-diabetic phenotypes: meta-analysis of 57 studies on nondiabetic individuals. Diabetes Care 29 , 2489–2497 (2006).

Rankinen, T. et al. The human obesity gene map: the 2005 update. Obesity 14 , 529–644 (2006).

Frayling, T. M. et al. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science 316 , 889–894 (2007). This paper describes the first GWAS (for type 2 diabetes) to identify a locus ( FTO ) robustly associated with BMI .

Scuteri, A. et al. Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits. PLoS Genet. 3 , e115 (2007).

Buniello, A. et al. The NHGRI-EBI GWAS Catalog of published genome-wide association studies, targeted arrays and summary statistics 2019. Nucleic Acids Res. 47 , D1005–D1012 (2019).

Yengo, L. et al. Meta-analysis of genome-wide association studies for height and body mass index in approximately 700 000 individuals of European ancestry. Hum. Mol. Genet. 27 , 3641–3649 (2018).

Javed, A. et al. Diagnostic performance of body mass index to identify obesity as defined by body adiposity in children and adolescents: a systematic review and meta-analysis. Pediatr. Obes. 10 , 234–244 (2015).

Kilpelainen, T. O. et al. Genetic variation near IRS1 associates with reduced adiposity and an impaired metabolic profile. Nat. Genet. 43 , 753–760 (2011).

Lu, Y. et al. New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk. Nat. Commun. 7 , 10495 (2016).

Zillikens, M. C. et al. Large meta-analysis of genome-wide association studies identifies five loci for lean body mass. Nat. Commun. 8 , 80 (2017).

Chu, A. Y. et al. Multiethnic genome-wide meta-analysis of ectopic fat depots identifies loci associated with adipocyte development and differentiation. Nat. Genet. 49 , 125–130 (2017).

Kilpelainen, T. O. et al. Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels. Nat. Commun. 7 , 10494 (2016).

Sun, Q. et al. Genome-wide association study identifies polymorphisms in LEPR as determinants of plasma soluble leptin receptor levels. Hum. Mol. Genet. 19 , 1846–1855 (2010).

Riveros-McKay, F. et al. Genetic architecture of human thinness compared to severe obesity. PLoS Genet. 15 , e1007603 (2019).

Orthofer, M. et al. Identification of ALK in thinness. Cell 181 , 1246–1262.e22 (2020).

Bradfield, J. P. et al. A trans-ancestral meta-analysis of genome-wide association studies reveals loci associated with childhood obesity. Hum. Mol. Genet. 28 , 3327–3338 (2019).

Felix, J. F. et al. Genome-wide association analysis identifies three new susceptibility loci for childhood body mass index. Hum. Mol. Genet. 25 , 389–403 (2016).

Vogelezang, S. et al. Novel loci for childhood body mass index and shared heritability with adult cardiometabolic traits. PLoS Genet. 16 , e1008718 (2020).

Akiyama, M. et al. Genome-wide association study identifies 112 new loci for body mass index in the Japanese population. Nat. Genet. 49 , 1458–1467 (2017).

Ng, M. C. Y. et al. Discovery and fine-mapping of adiposity loci using high density imputation of genome-wide association studies in individuals of African ancestry: African Ancestry Anthropometry Genetics Consortium. PLoS Genet. 13 , e1006719 (2017).

Gurdasani, D. et al. Uganda genome resource enables insights into population history and genomic discovery in Africa. Cell 179 , 984–1002.e36 (2019).

Wojcik, G. L. et al. Genetic analyses of diverse populations improves discovery for complex traits. Nature 570 , 514–518 (2019).

Martin, A. R. et al. Clinical use of current polygenic risk scores may exacerbate health disparities. Nat. Genet. 51 , 584–591 (2019).

Grarup, N. et al. Loss-of-function variants in ADCY3 increase risk of obesity and type 2 diabetes. Nat. Genet. 50 , 172–174 (2018).

Saeed, S. et al. Loss-of-function mutations in ADCY3 cause monogenic severe obesity. Nat. Genet. 50 , 175–179 (2018).

Minster, R. L. et al. A thrifty variant in CREBRF strongly influences body mass index in Samoans. Nat. Genet. 48 , 1049–1054 (2016).

Andersen, M. K. et al. The derived allele of a novel intergenic variant at chromosome 11 associates with lower body mass index and a favorable metabolic phenotype in Greenlanders. PLoS Genet. 16 , e1008544 (2020).

Siljee, J. E. et al. Subcellular localization of MC4R with ADCY3 at neuronal primary cilia underlies a common pathway for genetic predisposition to obesity. Nat. Genet. 50 , 180–185 (2018).

Willer, C. J. et al. Six new loci associated with body mass index highlight a neuronal influence on body weight regulation. Nat. Genet. 41 , 25–34 (2009).

Singh, K. et al. Neural cell adhesion molecule Negr1 deficiency in mouse results in structural brain endophenotypes and behavioral deviations related to psychiatric disorders. Sci. Rep. 9 , 5457 (2019).

Speliotes, E. K. et al. Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index. Nat. Genet. 42 , 937–948 (2010).

Soni, A., Amisten, S., Rorsman, P. & Salehi, A. GPRC5B a putative glutamate-receptor candidate is negative modulator of insulin secretion. Biochem. Biophys. Res. Commun. 441 , 643–648 (2013).

Jarick, I. et al. Novel common copy number variation for early onset extreme obesity on chromosome 11q11 identified by a genome-wide analysis. Hum. Mol. Genet. 20 , 840–852 (2011).

Sainsbury, A. et al. Synergistic effects of Y2 and Y4 receptors on adiposity and bone mass revealed in double knockout mice. Mol. Cell Biol. 23 , 5225–5233 (2003).

Falchi, M. et al. Low copy number of the salivary amylase gene predisposes to obesity. Nat. Genet. 46 , 492–497 (2014).

Meisler, M. H. & Ting, C. N. The remarkable evolutionary history of the human amylase genes. Crit. Rev. Oral Biol. Med. 4 , 503–509 (1993).

Hendricks, A. E. et al. Rare variant analysis of human and rodent obesity genes in individuals with severe childhood obesity. Sci. Rep. 7 , 4394 (2017).

Turcot, V. et al. Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity. Nat. Genet. 50 , 26–41 (2018). This large-scale exome-wide discovery study reports the use of array data to identify rare coding variations associated with BMI .

Emdin, C. A. et al. Analysis of predicted loss-of-function variants in UK Biobank identifies variants protective for disease. Nat. Commun. 9 , 1613 (2018).

Akbari, P. et al. Sequencing of 640,000 exomes identifies GPR75 variants associated with protection from obesity. Science 373 , eabf8683 (2021). This large-scale exome-wide discovery study reports the use of WES data to identify mutations associated with BMI .

Baggio, L. L. & Drucker, D. J. Biology of incretins: GLP-1 and GIP. Gastroenterology 132 , 2131–2157 (2007).

Antolin-Fontes, B. et al. The habenular G-protein-coupled receptor 151 regulates synaptic plasticity and nicotine intake. Proc. Natl Acad. Sci. USA 117 , 5502–5509 (2020).

Winkler, T. W. et al. The influence of age and sex on genetic associations with adult body size and shape: a large-scale genome-wide interaction study. PLoS Genet. 11 , e1005378 (2015).

Graff, M. et al. Genome-wide physical activity interactions in adiposity — a meta-analysis of 200,452 adults. PLoS Genet. 13 , e1006528 (2017).

Smith, C. E. et al. Genome-wide interactions with dairy intake for body mass index in adults of European descent. Mol. Nutr. Food Res. 62 , 1700347 (2018).

Justice, A. E. et al. Genome-wide meta-analysis of 241,258 adults accounting for smoking behaviour identifies novel loci for obesity traits. Nat. Commun. 8 , 14977 (2017).

Qi, Q. et al. Fried food consumption, genetic risk, and body mass index: gene–diet interaction analysis in three US cohort studies. BMJ 348 , g1610 (2014).

Kilpelainen, T. O. et al. Physical activity attenuates the influence of FTO variants on obesity risk: a meta-analysis of 218,166 adults and 19,268 children. PLoS Med. 8 , e1001116 (2011).

Yeo, G. S. H. Genetics of obesity: can an old dog teach us new tricks? Diabetologia 60 , 778–783 (2017).

Locke, A. E. et al. Genetic studies of body mass index yield new insights for obesity biology. Nature 518 , 197–206 (2015). This large-scale GWAS for BMI shows that BMI-associated loci frequently localize in or near genes that act in the brain .

Friedman, J. M. & Halaas, J. L. Leptin and the regulation of body weight in mammals. Nature 395 , 763–770 (1998).

Ahima, R. S. et al. Role of leptin in the neuroendocrine response to fasting. Nature 382 , 250–252 (1996).

Cowley, M. A. et al. Integration of NPY, AGRP, and melanocortin signals in the hypothalamic paraventricular nucleus: evidence of a cellular basis for the adipostat. Neuron 24 , 155–163 (1999).

Bertagna, X. Proopiomelanocortin-derived peptides. Endocrinol. Metab. Clin. North Am. 23 , 467–485 (1994).

Ollmann, M. M. et al. Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein. Science 278 , 135–138 (1997).

Butler, A. A. et al. A unique metabolic syndrome causes obesity in the melanocortin-3 receptor-deficient mouse. Endocrinology 141 , 3518–3521 (2000).

Chen, A. S. et al. Inactivation of the mouse melanocortin-3 receptor results in increased fat mass and reduced lean body mass. Nat. Genet. 26 , 97–102 (2000).

Doche, M. E. et al. Human SH2B1 mutations are associated with maladaptive behaviors and obesity. J. Clin. Invest. 122 , 4732–4736 (2012).

Marenne, G. et al. Exome sequencing identifies genes and gene sets contributing to severe childhood obesity, linking PHIP variants to repressed POMC transcription. Cell Metab. 31 , 1107–1119.e12 (2020).

Asai, M. et al. Loss of function of the melanocortin 2 receptor accessory protein 2 is associated with mammalian obesity. Science 341 , 275–278 (2013).

Michaud, J. L. et al. Sim1 haploinsufficiency causes hyperphagia, obesity and reduction of the paraventricular nucleus of the hypothalamus. Hum. Mol. Genet. 10 , 1465–1473 (2001).

Farooqi, I. S. et al. Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. N. Engl. J. Med. 348 , 1085–1095 (2003).

Wade, K. H. et al. Loss-of-function mutations in the melanocortin 4 receptor in a UK birth cohort. Nat. Med. 27 , 1088–1096 (2021). This paper establishes the frequency of loss-of-function mutations in MC4R to be 0.3%, much more common than previously appreciated .

van der Klaauw, A. et al. Role of melanocortin signalling in the preference for dietary macronutrients in human beings. Lancet 385 , S12 (2015).

Raffan, E. et al. A deletion in the canine POMC gene is associated with weight and appetite in obesity-prone Labrador retriever dogs. Cell Metab. 23 , 893–900 (2016).

Kim, K. S., Larsen, N., Short, T., Plastow, G. & Rothschild, M. F. A missense variant of the porcine melanocortin-4 receptor (MC4R) gene is associated with fatness, growth, and feed intake traits. Mamm. Genome 11 , 131–135 (2000).

Aspiras, A. C., Rohner, N., Martineau, B., Borowsky, R. L. & Tabin, C. J. Melanocortin 4 receptor mutations contribute to the adaptation of cavefish to nutrient-poor conditions. Proc. Natl Acad. Sci. USA 112 , 9668–9673 (2015).

Pinto, S. et al. Rapid rewiring of arcuate nucleus feeding circuits by leptin. Science 304 , 110–115 (2004).

Davies, A. M. The role of neurotrophins in the developing nervous system. J. Neurobiol. 25 , 1334–1348 (1994).

McAllister, A. K., Katz, L. C. & Lo, D. C. Opposing roles for endogenous BDNF and NT-3 in regulating cortical dendritic growth. Neuron 18 , 767–778 (1997).

Korte, M. et al. Hippocampal long-term potentiation is impaired in mice lacking brain-derived neurotrophic factor. Proc. Natl Acad. Sci. USA 92 , 8856–8860 (1995).

Kernie, S. G., Liebl, D. J. & Parada, L. F. BDNF regulates eating behavior and locomotor activity in mice. EMBO J. 19 , 1290–1300 (2000).

Xu, B. et al. Brain-derived neurotrophic factor regulates energy balance downstream of melanocortin-4 receptor. Nat. Neurosci. 6 , 736–742 (2003).

Xu, B. & Xie, X. Neurotrophic factor control of satiety and body weight. Nat. Rev. Neurosci. 17 , 282–292 (2016).

Rios, M. et al. Conditional deletion of brain-derived neurotrophic factor in the postnatal brain leads to obesity and hyperactivity. Mol. Endocrinol. 15 , 1748–1757 (2001).

Gray, J. et al. Hyperphagia, severe obesity, impaired cognitive function, and hyperactivity associated with functional loss of one copy of the brain-derived neurotrophic factor (BDNF) gene. Diabetes 55 , 3366–3371 (2006).

Yeo, G. S. et al. A de novo mutation affecting human TrkB associated with severe obesity and developmental delay. Nat. Neurosci. 7 , 1187–1189 (2004).

Thorleifsson, G. et al. Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity. Nat. Genet. 41 , 18–24 (2009).

Finucane, H. K. et al. Heritability enrichment of specifically expressed genes identifies disease-relevant tissues and cell types. Nat. Genet. 50 , 621–629 (2018).

Ndiaye, F. K. et al. The expression of genes in top obesity-associated loci is enriched in insula and substantia nigra brain regions involved in addiction and reward. Int. J. Obes. 44 , 539–543 (2020).

Loos, R. J. & Yeo, G. S. The bigger picture of FTO: the first GWAS-identified obesity gene. Nat. Rev. Endocrinol. 10 , 51–61 (2014).

Church, C. et al. Overexpression of Fto leads to increased food intake and results in obesity. Nat. Genet. 42 , 1086–1092 (2010).

Fischer, J. et al. Inactivation of the Fto gene protects from obesity. Nature 458 , 894–898 (2009).

Cheung, M. K., Gulati, P., O’Rahilly, S. & Yeo, G. S. FTO expression is regulated by availability of essential amino acids. Int. J. Obes. 37 , 744–747 (2013).

Gulati, P. et al. Role for the obesity-related FTO gene in the cellular sensing of amino acids. Proc. Natl Acad. Sci. USA 110 , 2557–2562 (2013).

Karra, E. et al. A link between FTO, ghrelin, and impaired brain food-cue responsivity. J. Clin. Invest. 123 , 3539–3551 (2013).

Hess, M. E. et al. The fat mass and obesity associated gene (Fto) regulates activity of the dopaminergic midbrain circuitry. Nat. Neurosci. 16 , 1042–1048 (2013).

Ruud, J. et al. The fat mass and obesity-associated protein (FTO) regulates locomotor responses to novelty via D2R medium spiny neurons. Cell Rep. 27 , 3182–3198.e9 (2019).

Stratigopoulos, G., LeDuc, C. A., Cremona, M. L., Chung, W. K. & Leibel, R. L. Cut-like homeobox 1 (CUX1) regulates expression of the fat mass and obesity-associated and retinitis pigmentosa GTPase regulator-interacting protein-1-like (RPGRIP1L) genes and coordinates leptin receptor signaling. J. Biol. Chem. 286 , 2155–2170 (2011).

Stratigopoulos, G. et al. Hypomorphism for RPGRIP1L, a ciliary gene vicinal to the FTO locus, causes increased adiposity in mice. Cell Metab. 19 , 767–779 (2014).

Stratigopoulos, G. et al. Hypomorphism of Fto and Rpgrip1l causes obesity in mice. J. Clin. Invest. 126 , 1897–1910 (2016).

Smemo, S. et al. Obesity-associated variants within FTO form long-range functional connections with IRX3. Nature 507 , 371–375 (2014).

Claussnitzer, M. et al. FTO obesity variant circuitry and adipocyte browning in humans. N. Engl. J. Med. 373 , 895–907 (2015).

O’Rahilly, S., Coll, A. P. & Yeo, G. S. FTO obesity variant and adipocyte browning in humans. N. Engl. J. Med. 374 , 191 (2016).

PubMed   Google Scholar  

Sobreira, D. R. et al. Extensive pleiotropism and allelic heterogeneity mediate metabolic effects of IRX3 and IRX5. Science 372 , 1085–1091 (2021).

Almen, M. S. et al. The obesity gene, TMEM18, is of ancient origin, found in majority of neuronal cells in all major brain regions and associated with obesity in severely obese children. BMC Med. Genet. 11 , 58 (2010).

Larder, R. et al. Obesity-associated gene TMEM18 has a role in the central control of appetite and body weight regulation. Proc. Natl Acad. Sci. USA 114 , 9421–9426 (2017). Aside from the efforts at characterizing the FTO locus, this paper establishes a plausible role for yet another GWAS-identified candidate gene, TMEM18 , in energy homeostasis .

Wiemerslage, L. et al. The Drosophila ortholog of TMEM18 regulates insulin and glucagon-like signaling. J. Endocrinol. 229 , 233–243 (2016).

Biederer, T. et al. SynCAM, a synaptic adhesion molecule that drives synapse assembly. Science 297 , 1525–1531 (2002).

Yan, X. et al. Cadm2 regulates body weight and energy homeostasis in mice. Mol. Metab. 8 , 180–188 (2018).

Rathjen, T. et al. Regulation of body weight and energy homeostasis by neuronal cell adhesion molecule 1. Nat. Neurosci. 20 , 1096–1103 (2017).

Wheeler, E. et al. Genome-wide SNP and CNV analysis identifies common and low-frequency variants associated with severe early-onset obesity. Nat. Genet. 45 , 513–517 (2013).

Schafer, M., Brauer, A. U., Savaskan, N. E., Rathjen, F. G. & Brummendorf, T. Neurotractin/kilon promotes neurite outgrowth and is expressed on reactive astrocytes after entorhinal cortex lesion. Mol. Cell. Neurosci. 29 , 580–590 (2005).

Matikainen-Ankney, B. A. & Kravitz, A. V. Persistent effects of obesity: a neuroplasticity hypothesis. Ann. N. Y. Acad. Sci. 1428 , 221–239 (2018).

Lee, A. W. et al. Functional inactivation of the genome-wide association study obesity gene neuronal growth regulator 1 in mice causes a body mass phenotype. PLoS ONE 7 , e41537 (2012).

Joo, Y., Kim, H., Lee, S. & Lee, S. Neuronal growth regulator 1-deficient mice show increased adiposity and decreased muscle mass. Int. J. Obes. 43 , 1769–1782 (2019).

Boender, A. J., van Gestel, M. A., Garner, K. M., Luijendijk, M. C. & Adan, R. A. The obesity-associated gene Negr1 regulates aspects of energy balance in rat hypothalamic areas. Physiol. Rep. 2 , e12083 (2014).

Singh, K. et al. Neuronal growth and behavioral alterations in mice deficient for the psychiatric disease-associated negr1 gene. Front. Mol. Neurosci. 11 , 30 (2018).

Szczurkowska, J. et al. NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice. Brain 141 , 2772–2794 (2018).

PubMed   PubMed Central   Google Scholar  

Noh, K. et al. Negr1 controls adult hippocampal neurogenesis and affective behaviors. Mol. Psychiatry 24 , 1189–1205 (2019).

Cano-Gamez, E. & Trynka, G. From GWAS to function: using functional genomics to identify the mechanisms underlying complex diseases. Front. Genet. 11 , 424 (2020).

Loos, R. J. et al. Common variants near MC4R are associated with fat mass, weight and risk of obesity. Nat. Genet. 40 , 768–775 (2008).

Chambers, J. C. et al. Common genetic variation near MC4R is associated with waist circumference and insulin resistance. Nat. Genet. 40 , 716–718 (2008).

Yaghootkar, H. et al. Genetic studies of leptin concentrations implicate leptin in the regulation of early adiposity. Diabetes 69 , 2806–2818 (2020).

Kichaev, G. et al. Leveraging polygenic functional enrichment to improve GWAS power. Am. J. Hum. Genet. 104 , 65–75 (2019).

Pulit, S. L. et al. Meta-analysis of genome-wide association studies for body fat distribution in 694 649 individuals of European ancestry. Hum. Mol. Genet. 28 , 166–174 (2019).

Wang, Y. et al. Melanocortin 4 receptor signals at the neuronal primary cilium to control food intake and body weight. J. Clin. Invest. 131 , e142064 (2021).

Article   CAS   PubMed Central   Google Scholar  

Farooqi, I. S. et al. Effects of recombinant leptin therapy in a child with congenital leptin deficiency. N. Engl. J. Med. 341 , 879–884 (1999). This paper is the first description of the treatment of leptin deficiency using leptin replacement therapy .

Farooqi, I. S. & O’Rahilly, S. 20 years of leptin: human disorders of leptin action. J. Endocrinol. 223 , T63–T70 (2014).

Yeo, G. S. H. et al. The melanocortin pathway and energy homeostasis: from discovery to obesity therapy. Mol. Metab. 48 , 101206 (2021).

Kuhnen, P. et al. Proopiomelanocortin deficiency treated with a melanocortin-4 receptor agonist. N. Engl. J. Med. 375 , 240–246 (2016). This paper is the first to demonstrate that the melanocortin pathway is a relevant and, so far, safe therapeutic target for the treatment of at least rare genetic causes of obesity .

Clement, K. et al. MC4R agonism promotes durable weight loss in patients with leptin receptor deficiency. Nat. Med. 24 , 551–555 (2018).

Clement, K. et al. Efficacy and safety of setmelanotide, an MC4R agonist, in individuals with severe obesity due to LEPR or POMC deficiency: single-arm, open-label, multicentre, phase 3 trials. Lancet Diabetes Endocrinol. 8 , 960–970 (2020).

Ayers, K. L. et al. Melanocortin 4 receptor pathway dysfunction in obesity: patient stratification aimed at MC4R agonist treatment. J. Clin. Endocrinol. Metab. 103 , 2601–2612 (2018).

Heymsfield, S. B. et al. Recombinant leptin for weight loss in obese and lean adults: a randomized, controlled, dose-escalation trial. JAMA 282 , 1568–1575 (1999).

Collet, T. H. et al. Evaluation of a melanocortin-4 receptor (MC4R) agonist (setmelanotide) in MC4R deficiency. Mol. Metab. 6 , 1321–1329 (2017).

Khera, A. V. et al. Polygenic prediction of weight and obesity trajectories from birth to adulthood. Cell 177 , 587–596.e9 (2019). This study describes a comprehensive PGS and its association with BMI throughout the life course .

Loos, R. J. F. 15 years of genome-wide association studies and no signs of slowing down. Nat. Commun. 11 , 5900 (2020).

Pearce, L. R. et al. KSR2 mutations are associated with obesity, insulin resistance, and impaired cellular fuel oxidation. Cell 155 , 765–777 (2013).

Greenfield, J. R. et al. Modulation of blood pressure by central melanocortinergic pathways. N. Engl. J. Med. 360 , 44–52 (2009).

Torkamani, A. & Topol, E. Polygenic risk scores expand to obesity. Cell 177 , 518–520 (2019).

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Acknowledgements

R.J.F.L. is supported by funding from Novo Nordisk Foundation (NNF Laureate Award) and the US National Institutes of Health (R01DK110113; R01DK107786; R01HL142302; R01 DK124097). G.S.H.Y. is supported by the Medical Research Council (MRC Metabolic Diseases Unit (MC_UU_00014/1)). The authors thank M. Guindo Martinez for her help with creating data for Fig. 3 and Supplementary Tables 1 and 2.

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Supplementary information

Supplementary information.

An environment that promotes weight gain.

A severe, early-onset form of obesity, caused by a single-gene mutation, with little or no influence of the environment.

A common multifactorial form of obesity, resulting from an interaction between the obesogenic environment and hundreds of genetic variants.

An approach used to understand the function of a gene by analysing the consequences of genetically manipulating specific sequences within the gene.

A hypothesis-driven approach to study the effect of a given gene (chosen based on the current understanding of its biology and pathophysiology) on susceptibility to the phenotype under study.

A method that relies on the relatedness of study participants to test whether certain chromosomal regions co-segregate with a disease or trait across generations.

(GWAS). A hypothesis-generating approach that screens whole genomes for associations between genetic variants and a phenotype of interest at much higher resolution than is possible for genome-wide linkage studies, and is thus better able to narrow down the associated locus.

(PGS). A measure used to assess an individual’s genetic susceptibility to disease, calculated by summing the number of disease-increasing alleles, weighted by each variant’s effect size observed in a genome-wide association study.

(AUC ROC ). A metric used to assess the ability of a predictor to discriminate between individuals with and without a disease. The AUC ranges from 0.50 (equal to tossing a coin) to 1.0 (perfect prediction).

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Loos, R.J.F., Yeo, G.S.H. The genetics of obesity: from discovery to biology. Nat Rev Genet 23 , 120–133 (2022). https://doi.org/10.1038/s41576-021-00414-z

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DOI : https://doi.org/10.1038/s41576-021-00414-z

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