essay obesity is a lifestyle disease

• Antioxidants
• Weight Management
• Vitamins & Supplements
• Exercise & Mobility
• Cholesterol
• Hypertension
• Improving Memory
• Give a Gift
• Activate My Web Access
• Customer Service
• Free e-newsletter
• Reset Password

• #7213 (no title)
• Contact the Editor
• Content restricted
• Nutrition 101 – Glossary – J
• Nutrition 101 – Glossary – K
• Nutrition 101 – Glossary – L
• Nutrition 101 – Glossary – M
• Nutrition 101 – Glossary – N
• Nutrition 101 – Glossary – O
• Nutrition 101 – Glossary – P
• Nutrition 101 – Glossary – Q
• Nutrition 101 – Glossary – R
• Nutrition 101 – Glossary – S
• Nutrition 101 – Glossary – T
• Nutrition 101 – Glossary – A
• Nutrition 101 – Glossary – B
• Nutrition 101 – Glossary – C
• Nutrition 101 – Glossary – D
• Nutrition 101 – Glossary – E
• Nutrition 101 – Glossary – F
• Nutrition 101 – Glossary – G
• Nutrition 101 – Glossary – H
• Nutrition 101 – Glossary – I
• Nutrition 101 – Glossary – U
• Nutrition 101 – Glossary – V
• Nutrition 101 – Glossary – W
• Nutrition 101 – Glossary – X
• Nutrition 101 – Glossary – Y
• Nutrition 101 – Glossary – Z
• Manage Email
• Current Issue
• OFIE – Subscriber only
• Online Account Activation
• Privacy Policy
• Registration Complete
• Sample Page
• Subscribe Now
• Tufts & Health Nutrition
• Tufts & Health Nutrition | JH Inforce
• Tufts & Health Nutrition | JHV Employee
• Tufts & Health Nutrition | John Hancock
• Tufts & Health Nutrition | Manulife Asia
• Tufts & Health Nutrition | Manulife Vitality
• Tufts & Health Nutrition | NU101
• Tufts & Health Nutrition | Tufts Employees

100% Fruit Juice Intake Associated with Weight Gain

Dance Can Help with Weight Loss and Body Composition

Spring Veggies

Are You at Risk for 
CKM Syndrome?

Vitamin Supplements: 
Yes, or No?

Dietary Supplements for Sports Performance

Melatonin Supplements

The Truth about “Brain-Boosting” Supplements

Many Herbal Products Found to Have Substantial Quality Issues

Let’s Get Moving!

Even a Little Physical Activity May Lower the Risks of Sedentary…

How to Stick to Those Resolutions!

Activity—of All Kinds—Can Help Lower Blood Pressure

A Large Analysis Clarifies the Concerns About Ultraprocessed Foods

Replace Animal-Based with Plant-Based Foods for Cardiometabolic Health

Where Does Poultry Fit In? 

Hear Ye! Hear Ye!

Healthy (But Not Unhealthy) Plant-Based Diets Associated with Lower Parkinson’s Risk

For Prevention of Cognitive Decline, Reduced Calorie MIND Diet Not Superior…

Consuming Plant Protein in Midlife Can Help Women Age Well

Is Olive Oil the Best Choice?

Making Time for Healthy Behaviors

Even Healthy, Normal-Weight Older Women May Benefit from a Heart-Healthy Lifestyle

• Healthy Eating

Obesity is a Disease: Why it Happens, and Why it Matters

Scientists now understand weight gain is not simply a problem of willpower..

T here has been a pervasive idea in society that obesity is a sign of personal failure—that it is caused exclusively by lack of willpower, laziness, and “gluttony.” The science does not agree. In 1998, the National Institutes of Health declared obesity a disease and the American Medical Association followed suit in 2013.

Let’s look at three key reasons obesity is more a disease then a personal failing, and how this knowledge can help you control your own weight—or be more understanding of others’ struggles.

Human Biology. The prevalence of obesity (a body mass index over 30) among U.S. adults is 42 percent and rising. Although lifestyle choices (like what we eat and how much we move) are important, our natural biology plays a key role in the current obesity epidemic. “Human biology is designed to encourage us to eat when food is there,” says Susan B. Roberts, PhD, a professor at the Friedman School and senior scientist on the Energy Metabolism Team at the Human Nutrtion Research Center on Aging. “This normal biology combines with an unhealthy food environment and food culture to cause weight gain. So-called ‘low willpower’ is normal human behavior, not some defect.”

What to do: Take control of your food environment. Stocking the house with healthy (whole and minimally processed) foods, watching portion sizes, preparing more food at home, and choosing wisely when eating out or ordering in can all help curb the natural tendency to overeat.

Metabolic Adaptation. In addition to storing energy (calories) for future use, fat (adipose tissue) acts as a powerful endocrine organ, secreting hormones and other molecules into the blood. “Many of the hormones released by adipose tissue are involved in regulating appetite, energy expenditure, and fat storage,” says Leon I. Igel, MD, a Tufts alum who is an endocrinologist and chief medical officer for Intellihealth. For example, adipose tissue releases the hormone leptin to signal we’ve had enough to eat. Individuals with obesity can develop a lack of sensitivity to leptin, or leptin resistance. With this condition, one doesn’t get the normal feelings of fullness and satiety and the body starts to burn less calories at rest. Leptin resistance thus contributes to a vicious cycle of obesity.

Many other hormones are released by fat cells, including those involved in glucose tolerance, insulin sensitivity, cell growth, inflammation, and the formation of blood clots in veins and arteries. “As levels of adipose tissue increase,” Igel explains, “multiple metabolic pathways stop working as they should. This leads to the development of a number of medical conditions associated with obesity.” Metabolic changes are also responsible for making it difficult to maintain weight loss.

What to do: Science suggests specific foods have different effects on weight gain. “Eat more minimally processed fruits, vegetables, nuts, beans, whole grains, fish, and yogurt,” says Dariush Mozaffarian, MD, DrPH, dean of policy for the Friedman School and editor-in-chief of this newsletter. “Foods with live probiotics and fermented foods may also help protect against weigh gain. Eat less refined grains, starches, sugars, and red and processed meat. Avoid soda and other highly sweetened drinks. Alcohol is also associated with weight gain—if you drink, do so moderately. Other animal foods, like milk, cheese, poultry, and eggs, appear, in observational studies, to be relatively neutral for long-term weight gain.”

Getting adequate sleep, increasing physical activity, and finding ways to reduce or deal with stress can also help address some of the physiological reasons we gain weight.

Even metabolic adaptations that slow metabolism and make weight loss maintenance difficult may be responsive to dietary intake. “Recent controlled trials show metabolic adaptation is influenced by diet quality and composition,” says Mozaffarian. “This research found that after weight loss resting metabolic rate was best maintained on a high fat, low carb diet (60 percent energy from fat, 20 percent from carbs) compared to a low fat, high carb diet (20 percent energy from fat, 60 percent from carbs), leading to about 300 more calories of energy expenditure a day.” Effects were in between on a moderate fat, moderate carb diet (40 percent energy from each). All the carbohydrates in these diets emphasized fruits, non-starchy vegetables, beans, and whole and minimally processed grains, rather than refined grains and added sugars.

Health Impacts. Obesity is the root cause for many medical diseases, including heart disease, stroke, type 2 diabetes, and certain types of cancer. It is also a risk factor for poor self-esteem, depression, obstructive sleep apnea, osteoarthritis, gout, female infertility, gallstones, pancreatitis, and non-alcoholic fatty liver disease. “This makes obesity its own complex medical disease,” says Igel. “We treat each of these other weight-associated conditions individually, but if we are able to treat obesity itself, we reduce all of these other medical issues at the same time.”

What to do: As with the treatment of other conditions—like high blood pressure, high cholesterol, and diabetes—medication may be necessary if lifestyle modifications are not enough. New medications, in combination with lifestyle changes, can help overcome the body’s metabolic adaptations and assist with weight loss. However, these tend to be expensive and are not yet widely covered by health insurance programs.

It is important to recognize that people with obesity who struggle to lose weight are fighting a real battle with their own bodies. It’s equally important to understand that we are not entirely helpless in the face of our genes, hormones, and metabolism. Lifestyle modification, including diet and physical activity, is still the cornerstone of obesity treatment. Accepting that obesity is a disease will help reduce stigma and discrimination, increase research dollars and insurance coverage, and move us all toward a healthier future.

LEAVE A REPLY Cancel reply

Save my name, email, and website in this browser for the next time I comment.

• Do Not Sell My Personal Information

December 30, 2023

Why Obesity is a Disease

Share this post

The American Medical Association (AMA) designated obesity a disease in 2013. As a result, the idea that obesity is caused by insufficient willpower, lack of discipline, and bad choices began to transform.

The headline, “ AMA Recognizes Obesity as a Disease ” was catapulted across both academic and mainstream media. Obesity was no longer a conversation topic tucked away in a dusty corner but was instead sprinkled across national news for the public to scrutinize. From TED Talks to the New York Times, obesity specialists were asked to weigh in on this groundbreaking and somewhat controversial topic and to answer the question, “is obesity a disease?”

The debate continues today.

Is Obesity a Disease?

New ideas can take a long time to catch on, especially when they have to overcome deep-seated beliefs. Along with those headlines proclaiming the AMA’s 2013 announcement came articles making a counter argument. A Forbes headline promised to explain “Why Labeling Obesity as a Disease is a Big Mistake.” The author argues that smoking became much less common because people changed their behavior in response to health information. Conversely, they argue, labeling obesity a disease removes incentive for behavior change such as eating less or exercising more.

For some, labeling obesity as a disease invalidates the importance of discipline, proper nutrition, and exercise and enables individuals with obesity to escape responsibility. For others, seeing obesity this way is a bridge to additional research, coordination of effective treatment, and increased resources for weight loss.

Another article from that time, this one in The Atlantic , began, “The relationship between health and body weight is not as straightforward as the American Medical Association might have us believe.” This one posits that accepting the “disease” label doesn’t mean that lifestyle change is unnecessary. (And, one could argue, the AMA never said that it was unnecessary.)

Why OMA Says "Yes"

OMA's position is that obesity should be considered a disease.

Our Obesity Algorithm® provides a comprehensive definition. Obesity is a “chronic, relapsing, multi-factorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial health consequences.”

Individuals with obesity have an increased accumulation of fat not always attributable to eating too many calories or lacking physical activity. They experience impaired metabolic pathways along with disordered signaling for hunger, satiety (the feeling of fullness), and fullness (the state of fullness).

For many, efforts to lose weight are met with unyielding resistance or disappointing weight regain. According to the University of Michigan ’s school of medicine, 90% of people who lose weight will regain most of it.

The pathology of obesity is vast and varies based on the cause of weight gain. There is not just one type or cause for obesity. Obesity sub-types include congenital, stress-induced, menopause-related, and MC4R-deficient, to name a few. Obesity is related to genetic, psychological, physical, metabolic, neurological, and hormonal impairments. It is intimately linked to heart disease, sleep apnea, and certain cancers. Obesity is one of the few diseases that can negatively influence social and interpersonal relationships.

Why Some Take Issue with Calling Obesity a Disease

In the U.S. there is a culture of personal responsibility and personal choice when it comes to health. A paper published in 2020 in Perspectives in Psychological Science delved into this phenomenon. It opens, “The United States suffers high rates of preventable lifestyle disease despite widespread calls for people to take responsibility for their health.” The authors link these attitudes to everything from the self-help publishing industry to parks and recreation departments.

The idea that obesity is a disease appears, on the surface, to contradict this reliance on personal responsibility. It should be noted that the debate is not limited to the U.S., as articles like this one in the British Medical Journal illustrate. Consider, however, that a patient with any disease can receive recommendations for diet or lifestyle changes. Nutrition and exercise are no less important, whether we call obesity a disease or not. A doctor may wish to avoid calling obesity a disease if they believe it could give a patient the sense that their choices do not matter to their health.

Cleveland Clinic points out that one hurdle to understanding obesity as a disease is that it is “silent,” meaning it doesn’t have specific symptoms. Instead, it is measured by a person’s weight-to-height ratio, or BMI, which is an imperfect measurement at best. Other measures suggested by some in the profession include waist circumference or hip-to-waist ratio.

Another issue is simply the lack of consensus on how to define disease. Some definitions , in fact, require symptoms, bringing us back to the point above.

Obesity, as we know, is related to a wide range of health conditions and diseases, including diabetes, heart disease, sleep apnea, and cancer.

Wider Implications of Treating Obesity as a Disease

Treating obesity as a disease brings several benefits, which the AMA listed at the time of its designation:

• improved training in obesity at medical schools and residency programs,
• reduced stigma of obesity by the public and physicians,
• improved insurance benefits for obesity-specific treatment, and
• increased research funding for both prevention and treatment strategies .

The rise of new obesity medicines , including strong public interest in GLP-1 receptor agonists, helps to frame it more as a disease. The general public tends to think of a disease as having a corresponding medication to treat it. As more patients come in asking about these medications, it can help to explain to them that this disease warrants a multi-pillared approach, which can mean addressing lifestyle factors too.

Frequently Asked Questions

Is obesity a disease or a disorder.

Obesity is a chronic disease. According to the Centers for Disease Control and Prevention (CDC) , obesity affects 42.8% of middle-age adults. Obesity is closely related to several other chronic diseases , including heart disease, hypertension, type 2 diabetes, sleep apnea, certain cancers, joint diseases, and more.

Is obesity considered a chronic disease?

Yes. Obesity, with its overwhelming prevalence of 1 in 6 adults in the U.S., is now recognized as a chronic disease by several organizations, including the American Medical Association.

The CDC defines “chronic disease” as conditions that last one year or more and require ongoing medical attention or limit activities of daily living, or both. Three leading chronic diseases are heart disease, cancer, and type 2 diabetes.

Obesity is associated with all three of these chronic diseases. The CDC also acknowledges widespread consequences of obesity when compared to normal or healthy weight for many serious health conditions, including all causes of death, hypertension, diabetes mellitus, coronary heart disease, stroke, and many cancers.

Of the $3.3 trillion spent annually on medical care for chronic conditions, obesity alone is associated with $1.4 trillion .

What is the link between obesity and mental health?

Numerous studies support a strong link between obesity and mental health. This relationship appears to be bi-directional; while mental health disorders increase the risk for obesity, having obesity also increases the risk of mental health disorders, especially in certain populations.

Mental health disorders can increase the risk for obesity for several reasons:

• Medications used to treat psychiatric illnesses can cause weight gain and insulin resistance, contributing to obesity.
• Mental illnesses affect behaviors such as decreased sleep, poor eating behaviors, and reduced physical activity, which can contribute to the development of obesity.

Conversely, having obesity increases the risk for depression. This is likely due to numerous complex factors, including poor self-image and depressed mood in response to weight bias and stigma , decreased activity due to joint and back pain associated with excess weight, and biological disruptions caused by chemicals secreted by fat cells when a person has obesity.

The link between obesity and mental health is complex and multi-faceted. It is important that patients with mental health disorders are monitored for weight, and that people with obesity are screened for mental health disorders.

Is Class III obesity a disability?

People with Class III obesity, formerly called morbid obesity, can have disabling health conditions that result from obesity and could qualify them for disability benefits. However, most people who have Class III obesity are quite able to perform their work functions. Having Class III obesity does not automatically qualify someone for benefits.

Hook, C. J., & Rose Markus, H. (2020). Health in the United States: Are Appeals to Choice and Personal Responsibility Making Americans Sick? Perspectives on Psychological Science, 15(3), 643-664. https://doi.org/10.1177/1745691619896252

Rosen H. Is Obesity A Disease or A Behavior Abnormality? Did the AMA Get It Right? Mo Med. 2014 Mar-Apr;111(2):104-108. PMID: 30323513; PMCID: PMC6179496.

• All Publications
• Priorities Magazine Spring 2018
• The Next Plague and How Science Will Stop It
• Priorities Magazine Winter 2018
• Priorities Magazine Fall 2017
• Little Black Book of Junk Science
• Priorities Magazine Winter 2017
• Should You Worry About Artificial Flavors Or Colors?
• Should You Worry About Artificial Sweeteners?
• Summer Health and Safety Tips
• How Toxic Terrorists Scare You With Science Terms
• Adult Immunization: The Need for Enhanced Utilization
• Should You Worry About Salt?
• Priorities Magazine Spring 2016
• IARC Diesel Exhaust & Lung Cancer: An Analysis
• Teflon and Human Health: Do the Charges Stick?
• Helping Smokers Quit: The Science Behind Tobacco Harm Reduction
• Irradiated Foods
• Foods Are Not Cigarettes: Why Tobacco Lawsuits Are Not a Model for Obesity Lawsuits
• The Prevention and Treatment of Osteoporosis: A Review
• Are "Low Dose" Health Effects of Chemicals Real?
• The Effects of Nicotine on Human Health
• Traditional Holiday Dinner Replete with Natural Carcinogens - Even Organic Thanksgiving Dinners
• A Primer On Dental Care: Quality and Quackery
• Nuclear Energy and Health And the Benefits of Low-Dose Radiation Hormesis
• Priorities in Caring for Your Children: A Primer for Parents
• Endocrine Disrupters: A Scientific Perspective
• Good Stories, Bad Science: A Guide for Journalists to the Health Claims of "Consumer Activist" Groups
• A Comparison of the Health Effects of Alcohol Consumption and Tobacco Use in America
• Moderate Alcohol Consumption and Health
• Irradiated Foods Fifth Edition
• Media/Contact
• Write For Us

Obesity: Lack of Will, Poor Lifestyle Choice, or Disease?

There’s no doubt that obesity is a growing global problem. It lies at one end of the spectrum from its less-discussed – but equally malnourished – polar opposite: hunger. Given that some argue that defining obesity as a disease will change the trajectory of the problem for the better, it’s time for a closer examination.  

What is a disease?

That, of course, is the million-dollar question, and as you have come to learn, it is complicated. We are biological creatures, and to our best understanding, we are in an equilibrium internally and externally. That equipoise, let’s for the minute call it, ease of being, is a dynamic process; we tend to focus on the internal ease of being, but the increasing concern over the socioeconomic determinants of health expresses the ease of being with the external environment. 

In 2013, over the objection of their council of experts, the AMA’s House of Delegates defined obesity as a disease. 

“That our AMA: (1) recognize obesity and overweight as a chronic medical condition (de facto disease state) and urgent public health problem;  (2) recommend that providers receive appropriate financial support and payment from third-party payers, thus ensuring that providers have an incentive to manage the complex diseases associated with obesity; (3) work with third-party payers and governmental agencies to recognize obesity intervention as an essential medical service ;  and (4) establish a comprehensive ICD code for medical services to manage and treat obese and overweight patients.”  [emphasis added]

I added the emphasis because all three of these points address payment for treatment, whether WW (the old Weight Watchers), medications or our current most favored, bariatric surgery. For the cynical amongst us, this might be considered self-serving on the part of physicians.

Report Of The Council On Science And Public Health

A re-reading of the report of those AMA experts demonstrates how little has changed now that obesity is a treatable condition. While we might argue that we can identify obesity when we see it, that is insufficient for those footing the bills – they want quantifiable, objective criteria. The most ubiquitous is the BMI or body mass index. It is a cheap, easily applied (involving only weight and height) screening tool, but as the report notes, 

“Associations between BMI and adiposity (as well as disease risk, described below) vary by age, gender, ethnicity, socioeconomic status, stature, and athletic training. These variations generally reflect population-specific differences in body composition, fat distribution, causes of overweight, and genetic susceptibility. As a screening tool for obesity, BMI demonstrates low sensitivity, particularly at BMIs below 30.”

The gist – BMI is much better at identifying the non-obese. Of course, those standardized cutoff values are subject to revision, just as we continue to lower the criteria for being hypertensive. 

The Council found designating obesity as a disease would bring “greater investments by government and the private sector to develop and reimburse obesity treatments.” That includes medications, surgery, and obesity prevention programs. It might also mean that discrimination based on body weight might be illegal. But more importantly, obesity as a disease would shift societal perceptions. 

“Lack of self-control, laziness, and other detrimental character attributes might be less likely to be associated with obese individuals, and in turn reduce stigmatization.”

On the other hand, obesity as a disease would “medicalize” obesity making the pill or knife the more relied upon alternatives

Public perceptions may shift due to more extensive recognition of obesity as a disease, with a greater appreciation of, and emphasis on, the complex etiology of obesity and the health benefits of achieving and maintaining a healthy weight. Moreover, as BMI became a vital sign, as did pain (which ushered in the era of opioid diversion), the environment might shift away from “healthy eating and physical activity.” Finally, obesity as a disease would result in higher insurance costs. 

Does Obesity Lie Within Our Control?

This is really the concern underlying obesity as a disease. 

"Obesity is a disorder which, like venereal disease, is blamed upon the patient. The finding that treatment doesn't work is ascribed to lack of fortitude."  Edwin Astwood, MD “The suggestion that obesity is not a disease but rather a consequence of a chosen lifestyle exemplified by overeating and/or inactivity is equivalent to suggesting that lung cancer is not a disease because it was brought about by individual choice to smoke cigarettes.”  AMA Resolution

It is tough to think of a way to more dramatically stigmatize an individual than to call them a smoker! Fat and body shaming are culture memes and are stand-ins for lack of control or willpower. The obese remain victims, but now it is less a societal, cultural victimization; they, after all, have a disease. And we don’t shame those with illnesses, do we? To the advocates of obesity as a disease, fat-shaming and employer bias all contribute to increased stress that in turn promotes stress-eating and hesitancy of pursuing exercise in public venues, like gyms. 

We do gain weight as we age, roughly 2 pounds annually, in our middle years. And “during or after weight loss there is a disproportionate increase in the drive to eat and decrease in energy expenditure creating "the perfect storm" for weight regain” – there is biology at work here.  

Obesity, as with many problems, lies within and outside of our control simultaneously. It might be better to think of obesity due to our underlying genetics, our metabolic condition,  and  our lifestyle choices. The relative contribution of each will vary with the individual. I have made some poor lifestyle choices at times, and they have been reflected in my weight. I am trying to make better choices, but that is tough but far easier than another pill, let alone an operation. For the morbidly obese, their metabolic and biological changes are almost insurmountable; a knife or medication can restore a balance between their choices and underlying physiology. 

The Council report to the AMA ends on this note.  

“Thus, rather than trying to determine if obesity meets arguably arbitrary disease criteria, the more relevant question is “would health outcomes be improved if obesity is considered a chronic, medical disease state?”

To the extent that payment for treatment might improve outcomes, the answer is yes. If the goal is now to reduce stigma, then shifting victimization from cultural norms to the “fault of our cells” is not a solution. 

Sources:  " Obesity Is a Disease, Recognize It as Such " Medpage

A.M.A. Recognizes Obesity as a Disease  NY Times

AMA’s Report of the Council on Science and Public Health,  Is Obesity a Disease

View the discussion thread.

By Chuck Dinerstein, MD, MBA

Director of Medicine

Dr. Charles Dinerstein, M.D., MBA, FACS is Director of Medicine at the American Council on Science and Health. He has over 25 years of experience as a vascular surgeon.

Latest from Chuck Dinerstein, MD, MBA :

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

• View all journals
• Explore content
• About the journal
• Publish with us
• Sign up for alerts
• Review Article
• Published: 07 May 2024

Epidemiology and Population Health

Obesity: a 100 year perspective

• George A. Bray   ORCID: orcid.org/0000-0001-9945-8772 1  

International Journal of Obesity ( 2024 ) Cite this article

347 Accesses

23 Altmetric

Metrics details

• Biological techniques
• Health care
• Weight management

This review has examined the scientific basis for our current understanding of obesity that has developed over the past 100 plus years. Obesity was defined as an excess of body fat. Methods of establishing population and individual changes in levels of excess fat are discussed. Fat cells are important storage site for excess nutrients and their size and number affect the response to insulin and other hormones. Obesity as a reflection of a positive fat balance is influenced by a number of genetic and environmental factors and phenotypes of obesity can be developed from several perspectives, some of which have been elaborated here. Food intake is essential for maintenance of human health and for the storage of fat, both in normal amounts and in obesity in excess amounts. Treatment approaches have taken several forms. There have been numerous diets, behavioral approaches, along with the development of medications.. Bariatric/metabolic surgery provides the standard for successful weight loss and has been shown to have important effects on future health. Because so many people are classified with obesity, the problem has taken on important public health dimensions. In addition to the scientific background, obesity through publications and organizations has developed its own identity. While studying the problem of obesity this reviewer developed several aphorisms about the problem that are elaborated in the final section of this paper.

This is a preview of subscription content, access via your institution

Access options

Subscribe to this journal

Receive 12 print issues and online access

251,40 € per year

only 20,95 € per issue

Buy this article

• Purchase on Springer Link
• Instant access to full article PDF

Prices may be subject to local taxes which are calculated during checkout

Similar content being viewed by others

Obesity and the risk of cardiometabolic diseases

Obesity-induced and weight-loss-induced physiological factors affecting weight regain

Normal weight obesity and unaddressed cardiometabolic health risk—a narrative review

Quetelet, Adolphe Sur l’homme et le developpement de ses facultes, ou essai de physique sociale ; Paris: Bachelier, 1835 (Transl of L-A-J. A Treatise on Man and the Development of His Faculties. IN: Bray GA. The Battle of the Bulge: A History of Obesity Research . Pittsburgh: Dorrance Publishing, 2007 pp 423-36.

Bray GA. Quetelet: quantitative medicine. Obes Res. 1994;2:68–71.

Article   CAS   PubMed   Google Scholar  

Bray GA. Beyond BMI. Nutrients. 2023;15:2254.

Article   PubMed   PubMed Central   Google Scholar  

Flegal KM. Use and misuse of BMI categories. AMA J Ethics. 2023;25:E550–8.

Article   PubMed   Google Scholar  

Keys A, Fidanza F, Karvonen MJ, Kimura N, Taylor HL. Indices of relative weight and obesity. J Chr Diseases. 1972;25:329–43.

Article   CAS   Google Scholar  

Bray GA. Definition, measurement, and classification of the syndromes of obesity. Int J Obes. 1978;2:99–112.

CAS   PubMed   Google Scholar  

Garrow JS. Treat Obesity Seriouslv-A Clinical Manual . Edinburgh: Churchill Livingstone; 1981.

Rodgers A, Woodward A, Swinburn B, Dietz WH. Prevalence trends tell us what did not precipitate the US obesity epidemic. Lancet Public Health. 2018;3:e162–3.

Bray GA. Body fat distribution and the distribution of scientific knowledge. Obes Res. 1996;4:189–92.

Janssen I, Katzmarzyk PT, Ross R. Waist circumference and not body mass index explains obesity-related health risk. Am J Clin Nutr. 2004;79:379–84.

Weeks RW. An experiment with the specialized investigation. Actuar Soc Am Trans. 1904;8:17–23.

Google Scholar  

Vague J. La differenciation sexuelle facteur determinant des formes de l’obesite, Presse Medicale. 1947;55:339 340. [Translated. IN: Bray GA. The Battle of the Bulge: A History of Obesity Research . Pittsburgh: Dorrance Publishing, 2007 pp 693–5].

Vague J. The degree of masculine differentiation of obesities: a factor determining predisposition to diabetes, atherosclerosis, gout, and uric calculous disease. Am J Clin Nutr. 1956;4:20–34.

Larsson B, Svardsudd K, Welin L, Wihelmsen L, Bjorntorp P, Tibbllne G. Abdominal adipose tissue distribution, obesity and risk of cardiovascular disease and death: 13 year follow up of participants in the study of 792 men born in 1913. BMJ 1984;288:1401–4.

Article   CAS   PubMed   PubMed Central   Google Scholar  

Bjorntorp P. Visceral obesity: a “civilization syndrome. Obes Res. 1993;1:206–22.

Behnke AR, Feen BG, Welham WC. The specific gravity of healthy men. JAMA 1942;118:495–8.

Article   Google Scholar  

Roentgen WC. Ueber eine neue Art von Strahlen. S.B. Phys-med Ges Wurzburg. 1895;132–41.

Wong MC, Bennett JP, Leong LT, Tian IY, Liu YE, Kelly NN, et al. Monitoring body composition change for intervention studies with advancing 3D optical imaging technology in comparison to dual-energy X-ray absorptiometry. Am J Clin Nutr. 2023:S0002-9165(23)04152-7

Church TS, Thomas DM, Tudor-Locke C, Katzmarzyk PT, Earnest CP, Rodarte RQ, et al. Trends over 5 decades in U.S. occupation-related physical activity and their associations with obesity. PLoS ONE. 2011;6:e19657 https://doi.org/10.1371/journal.pone.0019657 .

Schwann TH; Smith H, Trans. Microsccopical researches into the accordance in the structure and growth of animals and plants . London: Sydenham Society 1847

Hassall A. Observations on the development of the fat vesicle. Lancet. 1849;1:163–4.

Hirsch J, Knittle JL. Cellularity of human obese and nonobese adipose tissue. Fed Proc. 1970;29:1516–21.

Garvey WT. New Horizons. A new paradigm for treating to target with second-generation obesity medications. JCEM. 2022;107:e1339–47.

Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994;372:425–32.

Lavoisier AL, DeLaPlace PS. Memoir on Heat. Read to the Royal Academy of Sciences 28 June 1783 [IN: Bray GA. The Battle of the Bulge: A History of Obesity Research . Pittsburgh: Dorrance Publishing, 2007 pp 498–512].

Bray GA. Lavoisier and Scientific Revolution: The oxygen theory displaces air, fire, earth and water. Obes Res. 1994;2:183–8.

Helmholtz, Hermann von. Uber die Erhaltung der Kraft, ein physikalische Abhandlung, vorgetragen in der Sitzung der physicalischen Gesellschaft zu Berlin am 23sten Juli 1847. Berlin: G. Reimer, 1847.

Bray GA. Commentary on Atwater classic. Obes Res. 1993;1:223–7.

Bray GA. Energy expenditure using doubly labeled water: the unveiling of objective truth. Obes Res. 1997;5:71–7.

Lifson N, Gordon GB, McClintock R. Measurement of total carbon dioxide production by means of D 2 0 18 . J Appl Physiol. 1955;7:704–10.

Lichtman SW, Pisarska K, Berman ER, Pestone M, Dowling H, Offenbacher E, et al. Discrepancy between self-reported and actual caloric intake and exercise in obese subjects. N Engl J Med. 1992;327(Dec):1893–8.

Bray GA. Commentary on classics of obesity 4. Hypothalamic obesity. Obes Res. 1993;1:325–8.

Bruch H. The froehlich syndrome: report of the original case. Am J Dis Child. 1939;58:1281–90.

Babinski JP. Tumeur du corps pituitaire sans acromegalie et arret de development des organs genitaux. Rev Neurol. 1900;8:531–3. [Translation IN: Bray GA. The Battle of the Bulge: A History of Obesity Research . Pittsburgh: Dorrance Publishing, 2007 pp 740–1]

Cushing H. The Pituitary Body and Its Disorders . Philadelphia. PA: JB Lippincott; 1912.

Bray GA. Laurence, moon, Bardet Biedl: reflect a syndrome. Obes Res. 1995;3:383–6.

Laurence JZ, Moon RC. Four cases of “Retinitis Pigmentosa,” Occurring in the same family, and accompanied by general imperfections of development. Opthalmol Rev. 1866;2:32–41.

Bardet G. Sur un Syndrome d’Obesity Conginitale avec Polydactylie et Retinite Pigmentaire (Contribution a l’etude des formes clinique de 1 ’Obesite hypophysaire) . Paris: 1920. Thesis [Translation IN: Bray GA. The Battle of the Bulge: A History of Obesity Research . Pittsburgh: Dorrance Publishing, 2007 pp 740–1].

Biedl A. Geschwisterpaar mit adiposo-genitaler Dystrophie. Dtsch Med Woche. 1922;48:1630.

Cuenot L. Pure strains and their combinations in the mouse. Arch Zoot Exptl Gen. 1905;122:123.

Ingalls AM, Dickie MM, Snell GD. Obese, new mutation in the mouse. J Hered. 1950;41:317–8.

Coleman DL. Obesity and diabetes: two mutant genescausing obesity-obesity syndromes in mice. Diabetalogia. 1978;14:141–8.

Zucker TF, Zucker LM. Fat accretion and growth in the rat. J Nutr. 1963;80:6–20.

Schwartz MW, Seeley RJ, Zeltser LM, Drewnowski A, Ravussin E, Redman LM, et al. Obesity pathogenesis: an endocrine society scientific statement. Endocr Rev. 2017;38:267–96.

Oral EA, Simha V, Ruiz E, Andewelt A, Premkumar A, Snell P, et al. Leptin-replacement therapy for lipodystrophy. N Engl J Med. 2002;346:570–8.

Loos RJF, Yeo GSH. The genetics of obesity: from discovery to biology. Nat Rev Genet. 2022;23:120–33.

Blüher M. Metabolically healthy obesity. Endocr Rev. 2020;41:405–20.

Acosta A, Camilleri M, Abu Dayyeh B, Calderon G, Gonzalez D, McRae A, et al. Selection of antiobesity medications based on phenotypes enhances weight loss: a pragmatic trial in an obesity clinic. Obes. 2021;29:662–71.

Bray GA. Commentary on classics in obesity. 6. Science and politics of hunger. Obes Res. 1993;19:489–93.

Cannon WB, Washburn AL. An explanation of hunger. Am J Physiol. 1912;29:441–54.

Carlson AJ. Contributions to the physiology of the stomach -II. the relation between the concentrations of the empty stomach and the sensation of hunger. Am J Physiol. 1912;31:175–92.

Carlson AJ. Control of Hunger in Health and Disease . Chicago, IL: University of Chicago Press; 1916.

Flint A, Raben A, Astrup A, Holst JJ. Glucagon-like peptide 1 promotes satiety and suppresses energy intake in humans. J Clin Invest. 1998;101:515–20.

Bray GA. Eat slowly - From laboratory to clinic; behavioral control of eating. Obes Res. 1996;4:397–400.

Pavlov IP; Thompson WH, trans. The Work of the Digestive Glands . London: Charles Griffin and Co.; 1910.

Skinner BF. Contingencies of Reinforcement: A Theoretical Analysis . New York: Meredith Corporation; 1969.

Ferster CB, Nurenberger JI, Levitt EG. The Control of Eating. J. Math 1964;1:87-109.

Stuart RB. Behavioral control of overeating. Behav Res Ther. 1967;5:357–65. [Also IN: Bray GA. The Battle of the Bulge: A History of Obesity Research . Pittsburgh: Dorrance Publishing, 2007 pp 793–9]

Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM. et a; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346(Feb):393–403.

The Look AHEAD Research Group, Wadden TA, Bantle JP, Blackburn GL, Bolin P, Brancati FL, Bray GA, et al. Eight-year weight losses with an intensive lifestyle intervention: the look AHEAD study. Obesity. 2014;22:5–13.

Bray GA, Suminska M. From Hippocrates to the Obesity Society: A Brief History. IN Handbook of Obesity (Bray GA, Bouchard C, Katzmarzyk P, Kirwan JP, Redman LM, Schauer PL eds). Boca Raton: Taylor & Francis 2024. Vol 2, pp 3–16.

Bray GA. Commentary on Banting Letter. Obes Res. 1993;1:148–52.

Banting W. Letter on Corpulence, Addressed to the Public . London: Harrison and Sons 1863. pp 1–21.

Harvey W. On corpulence in relation to disease” With some remarks of diet . London” Henry Renshaw, 1872.

Schwartz, H. Never Satisfied. A Cultural History of Diets, Fantasies and Fat . 1977.

Foxcroft, Louise. Calories and Corsets. A history of dieting over 2000 years . London: Profile Books, 2011.

Gilman, Sander L. Obesity. The Biography . Oxford: Oxford University Press, 2010.

Linn R Stuart SL. The Last Chance Diet . A Revolutionary New Approach to Weight Loss 1977.

Magendie F. Rapport fait a l’Academie des Sciences au le nom de la Commission diet la gelatine. C.R. Academie Sci (Paris) 1841:237-83.

Bray GA. “The Science of Hunger: Revisiting Two Theories of Feeding. IN Bray GA. The Battle of the Bulge. A History of Obesity Research . Pittsburgh, Dorrance Publishing 1977 p. 238.

Sours HE, Frattalli VP, Brand CD, et al. Sudden death associated with very low calorie weight regimes. Am J Clin Nutr. 1981;34:453–61.

Bray GA. From very-low-energy diets to fasting and back. Obes Res. 1995;3:207–9.

Benedict, F.G. A Study of prolonged fasting . Washington: Carnegie Institution of Washington (Publ No 203), 1915.

Keys A, Brozek J, Henschel A, Mickelsen O,Taylor HL. The biology of human starvation . Minneapolis: University of Minnesota Press, 1950.

Cahill GF Jr, Herrera MG, Morgan AP, Soeldner JS, Steinke J, Levy PL, et al. Hormone-fuel interrelationships during fasting. J Clin Invest. 1966;45:1751–69.

Benedict FG, Miles WR, Roth P, Smith HM. Human vitality and efficiency under prolonged restricted diet. Carnegie Instit Wash, Pub. No. 280. Washington: Carnegie Institution of Washington; 1919.

Evans FA, Strang JM. The treatment of obesity with low-calorie diets. JAMA 1931;97:1063–8.

Bloom WL. Fasting as an introduction to the treatment of obesity. Metabolism 1959;8:2 14–220.

CAS   Google Scholar  

Bray GA, Purnell JQ. An historical review of steps and missteps in the discovery of anti-obesity drugs. IN: Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dhatariya K, Dungan K, et al. editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2022.

Lesses MF, Myerson A. Human autonomic pharmacology. NEJM 1938;218:119-24.

Cohen PA, Goday A, Swann JP. The return of rainbow diet pills. Am J Public Health. 2012;102:1676–86.

Bray GA. Nutrient intake is modulated by peripheral peptide administration. Obes Res. 1995;3:569S–572S.

Kissileff HR, Pi-Sunyer FX, Thornton J, Smith GP. C-terminal octapeptide of cholecystokinin decreases food intake in man. Am J Clin Nutr. 1981;34:154–60.

Wilding JPH, Batterham RL, Calanna S, Davies M, Van Gaal LF, Lingvay I, et al. STEP 1 study group. Once-weekly semaglutide in adults with overweight or obesity. N Engl J Med. 2021;384:989–1002.

Marso SP, Bain SC, Consoli A, Eliaschewitz FG, Jódar E, Leiter LA, et al. SUSTAIN-6 investigators. semaglutide and cardiovascular outcomes in patients with type 2 diabetes. N Engl J Med. 2016;375:1834–44.

Jastreboff AM, Aronne LJ, Ahmad NN, Wharton S, Connery L, Alves B, et al. SURMOUNT-1 investigators. tirzepatide once weekly for the treatment of obesity. N. Engl J Med. 2022;387:205–16.

Jastreboff AM, Kaplan LM, Frías JP, Wu Q, Du Y, Gurbuz S, et al. Retatrutide phase 2 obesity trial investigators. Triple-hormone-receptor agonist retatrutide for obesity - a phase 2 trial. N Engl J Med. 2023;389:514–26.

Bray GA. Obesity and surgery for a chronic disease. Obes Res. 1996;4:301–3.

Kremen AJ, Linner JH, Nelson CH. An experimental evaluation of the nutritional importance of proximal and distal small intestine. Ann Surg. 1954;140:439–48.

Payne JH, DeWind LT, Commons RR. Metabolic observations in patients with jejuno-colic shunts. Am J Surg. 1963;106:273–89.

Payne JH, DeWind LT. Surgical treatment of obesity. Am J Surg. 1969;118:141–6.

Buchwald H, Varco RL. Partial ileal bypass for hypercholesterolemia and atherosclerosis. Surg Gynecol Obstet. 1967;124:1231.

Mason EE, Ito C. Gastric bypass in obesity. Surg Clin North Am. 1967;47:1345–135.

O’Brien PE, MacDonald L, Anderson M, Brennan L, Brown WA. Long-term outcomes after bariatric surgery: fifteen-year follow-up of adjustable gastric banding and a systematic review of the bariatric surgical literature. Ann Surg. 2013;257:87–94.

Arterburn D, Wellman R, Emiliano A, Smith SR, Odegaard AO, Murali S, et al. PCORnet bariatric study collaborative. Comparative effectiveness and safety of bariatric procedures for weight loss: a PCORnet cohort study. Ann Intern Med. 2018;169:741–50.

Picot J, Jones J, Colquitt JL, Gospodarevskaya E, Loveman E, Baxter L, et al. The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation. Health Technol Assess. 2009;13:1–190.

Christou NV, Sampalis JS, Liberman M, et al. Surgery decreases long-term mortality, morbidity, and health care use in morbidly obese patients. Ann Surg. 2004;240:416–23.

Sjöström L. Review of the key results from the Swedish Obese Subjects (SOS) trial - a prospective controlled intervention study of bariatric surgery. J Intern Med. 2013;273:219–34.

Sjöström L. Swedish Obese Subjects, SOS: A review of results from a prospective controlled intervention trial. In: Bray GA, Bochard C, eds. Handbook of Obesity, Volume 2: Clinical Applications. New York: Informa; 2014.

Sjöström L, Narbro K, Sjöström CD, Karason K, Larsson B, Wedel H, et al. Effects of bariatric surgery on mortality in Swedish Obese Subjects. N. Engl J Med. 2007;357:741–52.

Sjöström L, Peltonen M, Jacobson P, Sjöström CD, Karason K, Wedel H, et al. Bariatric surgery and long-term cardiovascular events. JAMA 2012;307:56–65.

Carlsson LM, Peltonen M, Ahlin S, Anveden Å, Bouchard C, Carlsson B, et al. Bariatric surgery and prevention of type 2 diabetes in Swedish Obese Subjects. The New England. J Med. 2012;367:695–704.

Pories WJ, Swanson MS, MacDonald KG, Long SB, Morris PG, Brown BM, et al. Who would have thought it? an operation proves to be the most effective therapy for adult-onset. Diabetes Mellit Ann Surg. 1995;222:339–52.

Bray GA. Life insurance and overweight. Obes Res. 1995;3:97–99.

The Association of Life Insurance Medical Directors and The Actuarial Society of America. Medico- Actuarial Mortality Investigation . New York: The Association of Life Insurance Medical Directors and ‘The Actuarial Society of America; 1913.

Keys A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease . Cambridge, MA: Harvard University Press; 1980.

Dawber TR. The Framingham Study: The Epidemiology of Atherosclerotic Disease . Cambridge, MA: Harvard University Press; 1980.

Bray, G.A. (Ed), Obesity in Perspective . Fogarty International Center Series on Preventive Med. Vol 2, parts 1 and 2, Washington, D.C.: U.S. Govt Prtg Office, 1976, DHEW Publication #75-708.

Fryar CD, Carroll MD, Afful J. Prevalence of overweight, obesity, and severe obesity among adults aged 20 and over: United States, 1960–1962 through 2017–2018. NCHS Health E-Stats. 2020.

Bray GA. Obesity: Historical development of scientific and cultural ideas. Int J Obes. 1990;14:909–26.

Bray GA. The Battle of the Bulge: A History of Obesity Research . Pittsburgh: Dorrance Publishing, 2007 p 30.

Short, T. A Discourse Concerning the Causes and Effects of Corpulency Together with the Method for Its Prevention and Cure , J. Robert, London, 1727.

Flemyng, M. A Discourse on the Nature, Causes and Cure of Corpulency , L Davis and C Reymers, London, 1760.

Wadd, W. Comments on corpulency lineaments of leanness mems on diet and dietetics. London: John Ebers and Co, 1829.

Chambers, TK. Corpulence, or excess fat in the human body. London: Longman, 1850.

Rony HR. Obesity and Leanness . Philadelphia: Lea and Febiger, 1940.

Rynearson EH, Gastineau CF. Obesity . Springfield, IL: Charles C. Thomas, 1949.

Bray, G.A. The Obese Patient. Major Problems in Internal Medicine , Vol 9, Philadelphia, Pa.: W.B. Saunders Company, 1976, pp. 1-450.

Bray G.A. A Guide to Obesity and the Metabolic Syndrome: Origins and Treatment . New York: CRC Press: Taylor and Francis Group. 2011.

Howard AN. The history of the association for the study of obesity. Intern J Obes. 1992;16:S1–8.

Bray GA, Greenwood MRC, Hansen BC. The obesity society is turning 40: a history of the early years. Obesity. 2021;29(Dec):1978–81.

McLean Baird I, Howard AN. Obesity: Medical and Scientific Aspects : Proceedings of the First Symposium of the Obesity Association of Great Britain held in London , October 1968. Edinburgh & London: E. S. Livingston, 1968.

Bray GA, Howard AN. Founding of the international journal of obesity: a journey in medical journalism. Int J Obes. 2015;39:75–9.

Bray G. The founding of obesity research/obesity: a brief history. Obes. 2022;30:2100–2.

Ziman J. The Force of Knowledge. The Scientific Dimension of Society . Cambridge: Cambridge University Press, 1976.

Bray GA, Kim KK, Wilding JPH. Obesity: a chronic relapsing progressive disease process: a position paper of world obesity. Obes Rev. 2017;18:715–23.

Bray GA. Obesity is a chronic, relapsing neurochemical disease. Intern J Obes. 2004;28:34–8.

Allison DB, Downey M, Atkinson RL, Billington CJ, Bray GA, Eckel RH, et al. Obesity as a disease: a white paper on evidence and arguments commissioned by the Council of the Obesity Society. Obes. 2008;16:1161–77.

Garvey WT, Garber AJ, Mechanick JI, Bray GA, Dagogo-Jack S, Einhorn D, et al. American Association of Clinical Endocrinologists and American College of Endocrinology position statement on the 2014 advanced framework for a new diagnosis of obesity as a chronic disease. Endocr Pr. 2014;20:977–89.

Bray GA, Ryan DH. Evidence-based weight loss interventions: individualized treatment options to maximize patient outcomes. Diabetes Obes Metab. 2021;23:50–62.

Ge L, Sadeghirad B, Ball GDC, da Costa BR, Hitchcock CL, Svendrovski A, et al. Comparison of dietary macronutrient patterns of 14 popular named dietary programmes for weight and cardiovascular risk factor reduction in adults: systematic review and network meta-analysis of randomised trials. BMJ 2020;369:m696.

Sjöström L, Rissanen A, Andersen T, Boldrin M, Golay A, Koppeschaar HP, et al. Randomised placebo-controlled trial of orlistat for weight loss and prevention of weight regain in obese patients. European Multicentre Orlistat Study Group. Lancet 1998;352:167–72.

Pi-Sunyer FX, Aronne LJ, Heshmati HM, Devin J, Rosenstock J. Effect of rimonabant, a cannabinoid-1 receptor blocker, on weight and cardiometabolic risk factors in overweight or obese patients: RIO-North America: a randomized controlled trial. JAMA 2006;295:761–75.

Foster GD, Wadden TA, Vogt RA, Brewer G. What is a reasonable weight loss? Patients’ expectations and evaluations of obesity treatment outcomes. J Consult Clin Psychol. 1997;65:79–85.

DiFeliceantonio AG, Coppin G, Rigoux L, Thanarajah ES, Dagher A, Tittgemeyer M, et al. Supra-additive effects of combining fat and carbohydrate on food reward. Cell Metab. 2018;28:33–44.e3.

Thanarajah SE, Backes H, DiFeliceantonio AG, Albus K, Cremer AL, Hanssen R, et al. Food intake recruits orosensory and post-ingestive dopaminergic circuits to affect eating desire in humans. Cell Metab. 2019;29:695–706.e4.

Bray GA. Is sugar addictive? Diabetes 2016;65:1797–9.

Download references

Acknowledgements

The author thanks Dr. Jennifer Lyn Baker for her helpful comments during the early stage of preparing this manuscript.

Author information

Authors and affiliations.

Pennington Biomedical Research Center/LSU, Baton Rouge, LA, 70808, USA

George A. Bray

You can also search for this author in PubMed   Google Scholar

Contributions

All contributions were made by the single author.

Corresponding author

Correspondence to George A. Bray .

Ethics declarations

Competing interests.

The authors declare no competing interests.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

MSS # 2023IJO01171.

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Cite this article.

Bray, G.A. Obesity: a 100 year perspective. Int J Obes (2024). https://doi.org/10.1038/s41366-024-01530-6

Download citation

Received : 13 November 2023

Revised : 23 April 2024

Accepted : 26 April 2024

Published : 07 May 2024

DOI : https://doi.org/10.1038/s41366-024-01530-6

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

Quick links

• Explore articles by subject
• Guide to authors
• Editorial policies

REVIEW article

Obesity: epidemiology, pathophysiology, and therapeutics.

• Department of Endocrinology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China

Obesity is a complex multifactorial disease that accumulated excess body fat leads to negative effects on health. Obesity continues to accelerate resulting in an unprecedented epidemic that shows no significant signs of slowing down any time soon. Raised body mass index (BMI) is a risk factor for noncommunicable diseases such as diabetes, cardiovascular diseases, and musculoskeletal disorders, resulting in dramatic decrease of life quality and expectancy. The main cause of obesity is long-term energy imbalance between consumed calories and expended calories. Here, we explore the biological mechanisms of obesity with the aim of providing actionable treatment strategies to achieve a healthy body weight from nature to nurture. This review summarizes the global trends in obesity with a special focus on the pathogenesis of obesity from genetic factors to epigenetic factors, from social environmental factors to microenvironment factors. Against this background, we discuss several possible intervention strategies to minimize BMI.

There has been a significant global increase in obesity rate during the last 50 years. Obesity is defined as when a person has a body mass index [BMI (kg/m 2 ), dividing a person’s weight by the square of their height] greater than or equal to 30, overweight is defined as a BMI of 25.0-29.9. Being overweight or obesity is linked with more deaths than being underweight and is a more common global occurrence than being underweight. This is a global phenomenon occurring in every region except parts of sub-Saharan Asia and Africa ( 1 ), and also countries with low obesity rates (i.e., Sri Lanka, Indonesia, Sudan, Singapore, Djibouti, etc.) ( 2 ).

Obesity increases the likelihood of various diseases and conditions which are linked to increased mortality. These include Type 2 diabetes mellitus (T2DM), cardiovascular diseases (CVD), metabolic syndrome (MetS), chronic kidney disease (CKD), hyperlipidemia, hypertension, nonalcoholic fatty liver disease (NAFLD), certain types of cancer, obstructive sleep apnea, osteoarthritis, and depression ( 3 ).Treating these conditions can place an additional load on healthcare systems: for example, it is estimated that obese have a 30% higher medical cost than those with a normal BMI ( 4 ). As related total health-care costs double every decade, treating the consequences of obesity poses an expensive challenge for patients ( 5 ).

There are several possible mechanisms leading to obesity. Actually, the traditional view is usually that the main cause is the significantly more excess energy stored than the energy the body used. The excess energy is stored in fat cells, thereby developing the characteristic obesity pathology. The pathologic enlargement of fat cells will alter the nutrient signals responsible for obesity ( 6 ).However, the latest research showed that the food sources and quality of nutrients matter more than their quantities in the diet for weight control, and also for disease prevention ( 7 ). More and more etiologies or defects that lead to obesity can be identified under the background of struggle between nurture and nature, genetic and epigenetic, environmental and microenvironment. We are increasingly understanding how food cravings are upregulated in obesity individuals’ brains, how gut hormones, adipose tissue, or gut microbiota regulate appetite and satiety in the hypothalamus, as well as the roles of gut dysbiosis played in obesity development and how dysfunction of glucose and lipids metabolism causes secondary health problems ( 8 ). In addition, genetic factors are known to play critical roles in determining an individual’s predisposition to weight gain ( 9 ). Recent epigenetic studies have provided very useful tools for understanding the worldwide increase in obesity ( 10 ). Studies have discussed the relationships between genetics, epigenetics, and environment in obesity and explored the roles of epigenetic factors in metabolism regulation and obesity risk as well as its complications ( 11 ).

The field of obesity is rapidly evolving as an abundance of new scientific data continue to emerge. Herein, we discuss the epidemiology of obesity, covering the pathophysiology, pathogenesis, genetics, epigenetics, and environmental (macro and micro) causes that result in obesity. We end by summarizing possible management and prevention strategies.

Epidemiology of Obesity

BMI is used to define and diagnose obesity according to World Health Organization (WHO) guidelines ( 4 ). In adults, WHO defines ‘overweight’ as a BMI of 25.0 to 29.9 and ‘obese’ as a BMI ≥ 30.0. Obesity is further classified into three severity levels: class I (BMI 30.0-34.9), class II (BMI 35.0-39.9) and class III (BMI ≥ 40.0) ( 12 ).However, large individual differences exist in the percent body fat for the given BMI value, which can be attributed to sex, ethnicity and age ( 13 ).Excess fat deposition in the abdominal region is termed ‘abdominal obesity’ and is associated with greater health risks ( 14 ).The definition and measurement guidelines of abdominal obesity differed from WHO, IDF (International Diabetes Federation) to AHA (American Heart Association) ( 15 ). However, there is no international standard suitable for all countries or regions.

The prevalence of excessive weight gain has doubled worldwide since 1980, and about a third of the global population has been determined to be obese or overweight ( 16 ). Obesity rate has dramatically enhanced in both male and female, and across all ages, with proportionally higher prevalence in older persons and women ( 4 ). While this trend is present globally, absolute prevalence rates vary across regions, countries, and ethnicities. The prevalence of obesity also varies with socioeconomic status, with slower rates of BMI increase in high-​income and some middle-income countries. While obesity was once considered a problem of high-income countries, the incidence rates of obese or overweight children in high-​income countries, including the United States, Sweden, Denmark, Norway, France, Australia and Japan, have decreased or plateaued since the early 2000s ( 17 ).

In low- and middle-income countries, rates of overweight and obesity are rising especially in urban areas. In China, one study based on 12,543 participants monitored over 22 years revealed that the prevalence of age-adjusted obesity rose from 2.15% to 13.99% in both sexes, going from 2.78 to 13.22% in female and from 1.46 to 14.99% in male, respectively ( 18 , 19 ). The overweight rate of African children under 5 years old has increased by 24% since 2000. As of 2019, almost half of the Asian children under 5 years old were obese or overweight ( 20 ). WHO datasets from sub-Sarahan Africa reveal that prevalence of overweight and obese in adults and stunting, underweight, and wasting in children are inversely associated ( 21 ).

Pathogenesis of Obesity

The pathogenesis of obesity involves regulation of calorie utilization, appetite, and physical activity, but have complex interactions with availability of health-care systems, the role of socio-economic status, and underlying hereditary and environmental factors.

Food Intake and Energy Balance

The essential causes of obesity remain somewhat controversial. Current health recommendations to manage obesity are based on the underlying physiological property that fat accumulation is driven by an energy imbalance between consumed and expended calories. The obesity epidemic has been fueled in large part by increased energy from greater availability of highly rewarding and energy-dense food. Diet and various social, economic, and environmental factors related to food supply have a significant effect on patient’s ability to achieve the balance ( 22 ). In a 13-year follow-up study on 3,000 young, those who consumed much more fast-food were found to weigh an average of ~6kg more and have larger waist circumferences than those with the lowest fast-food-intake. They were also found to have higher incidences of negative weight-related health issues, such as elevated triglycerides and twice the odds of developing MetS ( 23 ). These issues are compounded in certain individuals that possess a genetic susceptibility to fat accumulation, which may be caused by significant interactions between homeostatic circuits and brain reward. Accumulation of lipid metabolites, inflammatory signaling, or other hypothalamic neuron impairing mechanisms may also lead to obesity, which might explain the biological defense of elevated body fat mass ( 24 ).

Obesogenic marketing to promote beverages or foods that are high in sugar and fat negatively modulates human behavior. Such advertisements may increase preference for energy-​dense foods and beverages ( 25 ). Analysis showed that African American programs had more food advertisements than other general market programs. More food advertisements were for meat, candy, soda, and fast food than for grains, pasta, cereals, vegetables, and fruits. Advertised products were designed to be cheap, have a long shelf-life, and taste ‘irresistible’. This applies particularly to high-fat, high-sugar junk foods that can stimulate the brain reward centers, the same part of the brain that’s stimulated by cocaine, heroin, and other addictive drugs, that is, these products are specifically engineered to be addictive ( 25 ). The brain reward offers a plausible mechanism to explain the elevated body fat mass, however, it seems that only certain individuals present this characteristic according to this theory.

For clinicians, a systematic evaluation of patient health factors affecting energy intake, metabolism, and expenditure is required for effective management of obesity. However, attempting to manage obesity through behavioral alterations aiming at addressing these three factors is more often than not unsuccessful. This suggests that our understanding of energy management and the interactions between intake, metabolism, and expenditure are not yet fully understood ( 26 ).

Family History and Lifestyle

Family history, lifestyle, and psychological factors all function in propensity for obesity. The likelihood of becoming obese can be affected by nature and nurture, enhanced by family genetics (propensity to accumulate fat) ( 27 ) or life style (poor dietary or exercise habits) ( 28 ). A child with one obese parent has a three-time risk to become obese as an adult, while when a child’s parents are both obese, this child has a 10-fold risk of future obesity. A cross-sectional observational study of 260 children (139 female, 121 male, aged 2.4 and 17.2 years) demonstrated that the family history of cardiometabolic diseases and obesity are critical risk factors for severity of obesity in childhood ( 29 ).

A prospective survey of 3148 school boys (aged six to ten years) in Ariana highlighted several child obesity risk factors, including parental obesity of parents, the snacks between meals especially after the dinner, lack of sleep (< 8 hours), and daily consumption of juice, sparkling drink, sweets, and sugary foods ( 30 ). Two studies of mother-child pairs in the United States found that the healthy lifestyle of mothers during the childhood and adolescence of their offspring was closely associated with a significantly reduced risk of obesity in their children ( 31 ). These results underscore the benefits of intervening at the family- or parental-level to reduce the risk of obesity in children ( 31 ).

However, parents are not the sole instigators of childhood obesity. For example, in the United States, physical education was used as a regular part of a public education curriculum ( 32 ). Starting 2011 physical education programs were curtailed such that 25 percent of students could achieve four out of five the national standards of at least 225 minutes weekly at the senior school levels and at least 150 minutes weekly at the primary level ( 33 ). Other factors that may have resulted in the decline of physical activity in children include increasing time spent on video game consoles and mobile devices at a reduction of time spent actively or outdoors. It is hard to argue against technological progress, but based on these studies, such innovations may be taking a toll on children’s health ( 34 ).

Microenvironment and Gut Microbiome

Our knowledge of the intestinal microbiome has grown substantially over recent years, as has our understanding of its intricate relationship to disease. For example, obesity is involved in an altered gut microenvironment that supports more diverse viral species than found in leaner hosts ( 35 ). This environment is more susceptible to the generation of pathogenic variants that can induce more serious disease ( 36 ). Increasing evidence shows that variations of gut microbiome cause alterations in host weight and metabolism. For example, compared with those with normal gut microbiota, germ-free male mice (without gut microflora) had 42% less total body fat, even while consuming 29% more food a day. However, after cecal microbe colonization, the total body fat of these mice increased 57%in, lean body mass decreased 7%, and daily food intake decreased 27% ( 35 ). A follow-up study suggested that these alterations resulted from decreased metabolic rates, with concomitant increased adipose tissue deposition, as capillary density in distal small intestinal villi increased 25% after microflora colonization. Similar results were also observed from female mice ( 37 ).

The human body contains around 3.8 × 10 13 microorganisms and the majority of them occupy the gastrointestinal tract. Over half of the microbial population are bacteria, followed by Archaea and Eukarya ( 38 ). The diversity of healthy gut microbiome allows for functional redundancy, in which multiple microbes can perform similar functions. Normally, gut microbiota have substantial beneficial roles in the host, including involvement in metabolism of carbohydrate and lipid, synthesis of vitamins and amino acids, epithelial cell proliferation, protection against pathogens, and hormone modulation. Gut bacteria can also break down indigestible molecules such as human milk oligosaccharides and plant polysaccharides ( 39 ). Imbalance of microbial populations (‘dysbiosis’) has been show to associate with a wide range of diseases including neurological disorders, inflammatory bowel disease, malnutrition, cancer, diabetes, and obesity ( 40 ). Recent research suggests that caloric restriction can beneficially reshape the gut microbiome and that antibiotic use can negatively harm gut microflora in ways that result in diabetes and obesity. Human studies support findings that microbiome alterations are associated with obesity; however, the exact mechanisms (i.e., ratios and amounts of microflora diversity) are still unknown ( 41 ).

Gut microbiota are central players in the host immune system. Disturbances in gut microflora can lead to inflammation of the intestinal lining ( 42 ). This response has been demonstrated to be mediated by TLRs (toll-like receptors), which identify and attack host microbes. For example, TLR4 recognizes the bacterial LPS (lipopolysaccharides) in the cell walls of Gram-negative bacteria while TLR5 recognizes bacterial flagellin. The body mass of TLR5-knockout mice increased 20% and their epididymal fat pad size increased 100% when compared to the wild-type controls ( 43 ). The dietary fiber and starch fermentation in lower gastrointestinal tract induced by microbiome can also produce SCFAs (Short-chain fatty acids), which can regulate production of gut hormone such as peptide YY (PYY) in the intestinal epithelium and GLP-1, GLP-2 (glucagon-like peptides), and the secretion of gastric inhibitory peptides by K cells ( 44 ). In obese patients, enzymes participated in or glucose signaling pathways are downregulated. It may be that alterations in specific microbial populations are more important than overall phylogenetic ratios, resulting in alterations in enzymes and SCFAs production, which further influence regulation of insulin and glucose, ultimately leading to development of obesity ( 41 ).

Genetic Factors and Causes

The studies from family and twin studies showed that around 40-70% of the obesity variation in human are resulted from genetic factors ( 45 ). While during the last 20 years, environmental alterations have increased obesity rates, the genetic factors play key roles in development of obesity ( 46 ). GWAS (Genome-wide association scans) approaches have identified over 400 genes associated with T2DM ( 47 , 48 ), however, these genes only predict 5% of obesity risk ( 49 ). The low predictive power may be due to the situation that gene-gene, gene-environment, and epigenetic interactions have not been thoroughly identified using the current methods based on population genetics ( 50 ). Many obesity -associated genes have been identified to be involved in energy homeostasis regulating pathways.

Genetic causes of obesity can be broadly classified as: 1) monogenic causes that result from a single gene mutation, primarily located in the leptin- melanocortin pathway. Many of the genes, such as AgRP (Agouti-related peptide), PYY (orexogenic), or MC4R (the melanocortin-4 receptor), were identified for monogenic obesity disrupt the regulatory system of appetite and weight, hormonal signals (ghrelin, leptin, insulin) are sensed by the receptors located in the arcuate nucleus of the hypothalamus ( 51 ). 2) Syndromic obesity were severe obesity results from neurodevelopmental abnormalities and other organ/system malformations. This may be caused by alterations in a single gene or a larger chromosomal region encompassing several genes ( 52 ). 3) Polygenic obesity is caused by cumulative contribution of many genes. Further, some people with obesity gain excess weight due to the multiple genes they have ( 53 ), and these genes make them to favor food and thereby have a higher caloric intake. The presence of these types of genes can cause increased caloric intake, increased hunger levels, reduced control overeating, reduced satiety, increased tendency to store body fat, and increased tendency to be sedentary ( 54 ).

Rare single-gene defects are associated with high level of hunger and can cause dramatic obesity in young children. Those individuals with severe obesity developed before two years old should consult obesity medicine specialists and consider to be involved in screening for MC4R Deficiency, leptin deficiency, and POMC deficiency ( 55 ). Leptin deficiency can cause diet-induced obesity and metabolic dysregulation. About 50% of female with polymorphism came up with binge eating ( 56 ). The MC4R polymorphism influences the release of ghrelin ( 57 ). The chromosome 2p22 (a region encompassing the POMC gene) has been identified as the site of gene(s) affecting obesity and obesity-related traits ( 58 ). These studies suggest that childhood obesity should be considered in the light of both environmental context and genetic heritage ( 59 ).

There are several genetic, neuroendocrine, and chromosomal precursors that can result in obesity. PWS (Prader-Willi Syndrome) is a neurodevelopmental disorder with hypothalamic dysfunction, due to the deficiency of imprinted genes ( 60 ). Endocrine disorders such as PCOS (Polycystic Ovary Syndrome) can also lead to increased body fat ( 61 ). Chromosomal defects can lead to obesity, including deletion of 16p11.2, 2q37 (brachydactyly mental retardation syndrome; BDMR), 1p36 (monosomy 1p36 syndrome), 9q34 (Kleefstra syndrome), 6q16 (PWS-like syndrome), 17p11.2 (Smith Magenis syndrome; SMS), and 11p13 (WAGR syndrome) ( 62 ). These conditions rely on the conventional current health recommendations that energy imbalance between calories consumed and expended is the key cause of obesity and present circumstances under which traditional weight management methods may not help.

Epigenetic Modification

We have been able to identify some of the genes that contribute to monogenic forms of obesity, but the human genome alterations on timescales that are too long for the genome to be a major player in the current obesity pandemic. Epigenetics, however, may offer a logical explanation for increasing obesity prevalence over the past few decades without necessitating a radical change in the genome ( 63 ). In multicellular organisms, the genetic code is homogenous throughout the body, but the expression of code can vary across cell types. Epigenetics studies showed that the heritable regulatory alterations in the genetic expression do not require alterations in the nucleotide sequence ( 64 ). Epigenetic modifications can be thought of as the differential packaging of the DNA that either allows or silences the expression of certain genes across tissues. Environmental and gut microbiota can influence the epigenetic programming of parental gametes, or programming in later stages of life ( 10 ).

The known epigenetic mechanisms include DNA methylation, histone modifications, and miRNA-mediated regulation. These can be passed from one generation to another meiotically or mitotically. There is evidence showing that the perinatal and embryo-fetal development period plays a critical role in human tissues and organs programming ( 65 ). DNA methylation appears to be the most important epigenetic mechanism for regulating gene expression. Alterations in DNA methylation can be a hallmark of many diseases such as cancers ( 66 ). LEP (Leptin) plays critical roles in adipose tissue regulation. The maternal metabolic status can affect DNA methylation of LEP profile at birth, affecting metabolic remodeling of obesity ( 67 ). The Adiponectin (ADIPOQ) epigenetic status also has relationship with obesity, and association has been reported between LDL-cholesterol levels and DNA methylation of both LEP and ADIPOQ ( 68 ). Paternal obesity has also been associated with inhibited methylation levels in IGF2 (insulin-like growth factor 2) regions, which promote the division and growth of various types of cells ( 69 ). Other genes investigated in the context of metabolism and obesity include: tumor necrosis factor (TNF), hypoxia-inducible factor 3a (HIF3A), neuropeptide Y (NPY), insulin receptor substrate 1 (IRS1), mitochondrial transcription factor A (TFAM), interleukin 6 (IL6), lymphocyte antigen 86 (LY86) and glucose transport 4 (GLUT4) ( 10 , 63 ).

Histones are proteins function in DNA packaging and modifications to histones are associated with epigenetic regulation of adipogenesis and obesity development ( 70 ). Five key regulatory genes in adipogenesis, CCAAT-enhancer-binding protein β (C/EBP β), pre-adipocyte factor-1 (Pref-1), adipocyte protein 2 (aP2), PPARγ, and C/EBPα, are modulated by histone modifications during adipocyte differentiation ( 71 ). The enzymes play roles in histone modification also function in obesity. They also regulate the expression of HDACs (histone deacetylases), which participated in the epigenetic control of gene expression involved in a large amount of environmental factors ( 72 ).

MicroRNAs (miRNAs) are 18 to 25 nucleotides long short noncoding RNA sequences that can regulate gene expression by gene silencing and post-transcriptional alterations. MicroRNAs function in a variety of biological processes, including adipocyte differentiation and proliferation, and are associated with low-grade inflammation and insulin resistance displayed in obese individuals ( 73 ). Increased levels of miRNAs including miR-486-3p, miR-142-3p, miR-486-5p, miR-423-5p and miR-130b were seen in children with high BMI values, among which 10 miRNAs exhibited significant alterations with increasing body weight ( 74 ). Zhao et al. identified miRNA as a signature for weight gain and showed that the individuals with a high-risk score for 8 of these miRNAs had over 3-fold higher odds of weight gain ( 75 ). Alterations in adipocyte-derived exosomal miRNAs is also seen following weight loss and decrease in insulin resistance after gastric bypass ( 76 ). miRNAs have been shown to play a key role in obesity and that the associated metabolic alterations can serve as biomarkers, or potentially therapeutic targets for intervention. Consideration of genetic and epigenetic causes of obesity provide valuable tools for the clinical treatment of obesity.

Therapeutics of Obesity

Lifestyle modifications.

Given the lack of specific pharmacological interventions, ‘lifestyle modification’ remains the cornerstone of obesity management ( 4 ). Individuals with obesity are suggested to lose at least 10% body weight via combination of diet, physical activity, and behavior therapy (or lifestyle modification) ( 77 ). Significant short-term weight loss can be achieved by consumption of portion-controlled diets ( 78 ). Long-term weight control can be achieved via high levels of physical activity and continued patient–practitioner contact. In many cases, lifestyle modification results in dramatic loss of body weight, leading to significant reduction of cardiovascular risk ( 79 ).

Since food choices are mainly determined by peoples’ surroundings, it is imperative that governments improve policies and environment to reduce the availability of unhealthful foods and make healthy foods more accessible. Policies should be changed to increase development of foods with reduced sugar, fat, and salt and decrease availability of obesogenic foods aimed at children ( 80 ). Policy makers and Practitioners must be made aware of the potential impact of food advertisements on human health and behavior and should encourage food manufacturers to create and promote weight-friendly foods. Nutrition educators should help teach how to evaluate food advertisements ( 81 ). Interventions aimed at motivating behavioral alterations (e.g., health promotion, nutrition education, incentives for healthy living, sugar-​sweetened beverage tax, and social marketing) and enforcing actions that reduce causes of obesity (e.g., policy changes, regulations and laws) are likely to have strong impacts on reducing the obesity crisis ( 82 ).

Anti-Obesity Medications

Pharmacotherapy is recommended for those whose BMI ≥30 (or a BMI ≥27 with comorbid conditions) and are unable to lose weight using lifestyle modification alone ( 83 ). The U.S. FDA (Food and Drug Administration) approved some new pharmacotherapy drugs for short-term obesity treatment ( Table 1 ) and since Lorcaserin was withdrawn, there are only four [Naltrexone-Bupropion (Contrave), Orlistat (Xenical, Alli), Liraglutide (Saxenda) and Phentermine-Topiramate (Qsymia)] approved in addition to Gelesis which is now the fifth, have been approved for long-term use ( 84 , 86 , 87 ). The FDA also approved the MC4R agonist-Setmelanotide for use in individuals with severe obesity due to either POMC, PCSK1 (proprotein convertase subtilisin/kexin type 1), or LEPR (leptin receptor) deficiency at the end of 2020 ( 85 ).

Table 1 Prescription medications approved for obesity treatment.

In addition, 11 different components have been identified from 54 families of the plants to have anti-obesity potential. These families include Celastraceae, Zingiberaceae, Theaceae, Magnoliaceae, and Solanaceae ( 88 ). Traditional Chinese medicine delivers unique solutions to treat obesity, such as regulating fat metabolism, enhancing hormone level, regulating intestinal microflora, among other pathways ( 89 ). These findings are helpful for selection of herbal medicine or traditional Chinese medicine for further research.

Bariatric Surgery

For individuals with a BMI > 40 or BMI > 35 with comorbidities who are unable to lose weight by lifestyle modifications or pharmacotherapy bariatric surgery or weight loss surgery is another option ( 83 ). Standard bariatric operations, including BPD (Bilio-pancreatic diversion), SG (sleeve gastrectomy), RYGB (Roux-en-Y gastric bypass), and AGB (adjustable gastric banding), benefits individuals׳ metabolic profiles to varying degrees ( 90 ). Studies reported that the benefits of bariatric surgery go beyond just losing weight. Bariatric surgery reduces chronic inflammation involved in obesity and alters biomarkers, the gut microbiota, and long-term remission for T2DM ( 91 – 93 ). Take RYGB for example, in human subjects, overall gut microbial richness increased after RYGB surgery ( 94 ). Further analysis revealed RYGB contributed to increase of expression of some specific white adipose tissue genes, upregulation of genes central to the transforming growth factor-β signaling pathway, and remarkable downregulation of genes involved in metabolic pathways and inflammatory responses ( 95 ). Decrease of serum leptin levels, which are associated with leaned BMI, typically results from bariatric surgery. Interestingly, those women who had a higher presurgical baseline leptin level were easier to remain the post-procedure weight loss, while those with a lower presurgical baseline level were easier to regain the weight. There is a correlation between the baseline leptin level and alterations in body mass, BMI, as well as total weight loss although the success degree of surgery cannot be predicted by a patient’s serum leptin level ( 96 ).

Fecal Microbiota Transplantation

FMT has attracted considerable research interest recently in the treatment of obesity ( 97 ). There are promising indications that FMT of microbes from healthy individuals into patients with obesity may be affected in weight loss and maintenance. In a groundbreaking key study, Ridaura et al. transplanted fecal slurries from human twins discordant for obesity into germ-free mice ( 98 ). The mice with obese individuals’ microbiota successfully developed obesity, while those with healthy individuals’ microbiota remained lean. The sequencing results of mice post-procedure stool samples showed that the human microbiomes were successfully infused, indicative of the transfer of functions related to the obese or lean microbial communities, respectively ( 98 ). Promising studies in humans are also being attempted: Vrieze et al. were able to improve microbial diversity and insulin sensitivity in obese, diabetic adult males after the transplantation with the taxa from lean donors ( 99 ). An increase was observed in butyrate-producing bacteria and Bacteroidetes, indicative of a shift toward a leaner phenotype related microbial community. While in early stages, FMT may be an option for replacing obesogenic microbial communities ( 100 ).

Summary and Conclusions

The global prevalence of obesity has nearly tripled since 1975 and continues to grow at an exponential rate. Obesity has become the number one lifestyle-related risk factor for premature death. As such, public health policies focused on reducing and treating obesity must be developed ( 17 ). The WHO “Global Action Plan for the Prevention and Control of Noncommunicable Diseases 2013-2020” defines strategies to prevent further increase in obesity prevalence, but progress so far has been slow ( 101 ). However, with the identification of the main obesity causes the modulating factors, the challenge remains is to translate them into effective actions.

Epigenetic modifications and interactions between our genes and environment have strong influences on human health and disease. Increasing evidence is revealing the involvement of epigenetics in obesity prevalence ( 9 ). Propensity for obesity can result from the effects of environmental factors, such as nutrition and lifestyle to the epigenetic remodeling of the early postnatal development, and parental gametes. Epigenetic marks could also significantly affect the obesity risk of the child and thus be transmitted trans-generationally ( 11 ). This epigenetic ‘memory’ may help explain our lack of evidence for genetic heritability in obesity and other diseases. A foundational knowledge of the mechanisms of epigenetic inheritance is of great importance for treating and preventing obesity. Exploration of epigenetic changes is a key for predicting disease trajectories and choosing effective treatment. The reversible characteristic of these modifications makes them ideal targets for epigenetic treatment, and promising “epigenetic drugs” for therapies of obesity are already in the marketplace or in various stages of development ( 102 ). These types of therapies include DNA methyltransferase inhibitors (DNMTis), protein arginine methyltransferase inhibitors (PRMTis), histone acetyltransferase inhibitors (HATi), histone deacetylase inhibitors (HDACi), sirtuin-activating compounds (STACs) and histone demethylating inhibitors (HDMis) ( 103 ).

Microbiome research holds much promise for treating pandemics such as obesity and diabetes. On-going developments in technology and bioinformatics of microbiology are increasingly allowing for the development of a microbiome-manipulating capsule to favor a healthy, lean, and insulin-sensitive profile, but this is still an area of active research ( 8 , 104 ). More targeted therapies will also become possible as we increase our understanding of microbial metabolites, allowing for clinal treatment of inflammation, weight gain and insulin resistance, and ultimately preventing the progression to obesity.

In conclusion, improved understanding of the various dimension of obesity, including propensity to regain lost weight, interindividual differences in pathogenesis, and response to therapy, is needed for developing effective as well as cost-effective interventions. The insights will in turn benefit the related health complications such as incidence of diabetes. More research is required to identify behavioral modification that are effective and available to people from diverse backgrounds. More studies were performed to develop more effective and safer medications to help obese people lose body weight and maintain a healthy weight for long term. Moreover, we must devote greater efforts and resources to the prevention of obesity in children as well as adults. Prevention is a key as treatment alone is not very effective and cannot well reverse the epidemic of obesity for long term.

Author Contributions

HL and XL conceived and wrote the manuscript. All authors contributed to the article and approved the submitted version.

This project was funded by grants from the Zhejiang Provincial Medical Science and Technology Program (2020KY166).

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

1. Al Kibria GM. Prevalence and Factors Affecting Underweight, Overweight and Obesity Using Asian and World Health Organization Cutoffs Among Adults in Nepal: Analysis of the Demographic and Health Survey 2016. Obes Res Clin Pract (2019) 13(2):129–36. doi: 10.1016/j.orcp.2019.01.006

PubMed Abstract | CrossRef Full Text | Google Scholar

2. Mbogori T, Kimmel K, Zhang M, Kandiah J, Wang Y. Nutrition Transition and Double Burden of Malnutrition in Africa: A Case Study of Four Selected Countries With Different Social Economic Development. AIMS Public Health (2020) 7:425–39. doi: 10.3934/publichealth.2020035

3. Swinburn BA, Sacks G, Hall KD, McPherson K, Finegood DT, Moodie ML, et al. The Global Obesity Pandemic: Shaped by Global Drivers and Local Environments. Lancet (2011) 378(9793):804–14. doi: 10.1016/S0140-6736(11)60813-1

4. WHO Consultation on Obesity (‎1999: Geneva, Switzerland) & World Health Organization. Obesity: Preventing and Managing the Global Epidemic. Report of a WHO Consultation. World Health Organ Tech Rep Ser (2000) 894:i–xii, 1-253.

PubMed Abstract | Google Scholar

5. Bray GA, Kim KK, Wilding J, World Obesity Federation. Obesity: A Chronic Relapsing Progressive Disease Process. A Position Statement of the World Obesity Federation. Obes Rev (2017) 18(7):715–23.doi: 10.1111/obr.12551

6. Lee SJ, Shin SW. Mechanisms, Pathophysiology, and Management of Obesity. N Engl J Med (2017) 376(15):1491–2. doi: 10.1056/NEJMc1701944

7. Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD, et al. Comparison of Weight-Loss Diets With Different Compositions of Fat, Protein, and Carbohydrates. N Engl J Med (2009) 360(9):859–73. doi: 10.1056/NEJMoa0804748

8. Singer-Englar T, Barlow G, Mathur R. Obesity, Diabetes, and the Gut Microbiome: An Updated Review. Expert Rev Gastroenterol Hepatol (2019) 13(1):3–15. doi: 10.1080/17474124.2019.1543023

9. Singh RK, Kumar P, Mahalingam K. Molecular Genetics of Human Obesity: A Comprehensive Review. C R Biol (2017) 340(2):87–108. doi: 10.1016/j.crvi.2016.11.007

10. Lopomo A, Burgio E, Migliore L. Epigenetics of Obesity. Prog Mol Biol Transl Sci (2016) 140:151–84. doi: 10.1016/bs.pmbts.2016.02.002

11. Dubern B. Genetics and Epigenetics of Obesity: Keys to Understand. Rev Prat (2019) 69(9):1016–9.

12. Poirier P, Giles TD, Bray GA, Hong Y, Stern JS, Pi-Sunyer FX, et al. Obesity and Cardiovascular Disease: Pathophysiology, Evaluation, and Effect of Weight Loss. Arterioscler Thromb Vasc Biol (2006) 26(5):968–76. doi: 10.1161/01.ATV.0000216787.85457.f3

13. Kok P, Seidell JC, Meinders AE. [The Value and Limitations of the Body Mass Index (BMI) in the Assessment of the Health Risks of Overweight and Obesity]. Ned Tijdschr Geneeskd (2004) 148(48):2379–82.

14. Løvsletten O, Jacobsen BK, Grimsgaard S, Njølstad I, Wilsgaard T, Løchen ML, et al. Prevalence of General and Abdominal Obesity in 2015-2016 and 8-Year Longitudinal Weight and Waist Circumference Changes in Adults and Elderly: The Tromsø Study. BMJ Open (2020) 10(11):e038465. doi: 10.1136/bmjopen-2020-038465

15. Paley CA, Johnson MI. Abdominal Obesity and Metabolic Syndrome: Exercise as Medicine. BMC Sports Sci Med Rehabil (2018) 10:7. doi: 10.1186/s13102-018-0097-1

16. Ataey A, Jafarvand E, Adham D, Moradi-Asl E. The Relationship Between Obesity, Overweight, and the Human Development Index in World Health Organization Eastern Mediterranean Region Countries. J Prev Med Public Health (2020) 53(2):98–105. doi: 10.3961/jpmph.19.100

17. NCD Risk Factor Collaboration (NCD-RisC). 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 (2017) 390(10113):2627–42. doi: 10.1016/S0140-6736(17)32129-3

18. Chen Y, Peng Q, Yang Y, Zheng S, Wang Y, Lu W. The Prevalence and Increasing Trends of Overweight, General Obesity, and Abdominal Obesity Among Chinese Adults: A Repeated Cross-Sectional Study. BMC Public Health (2019) 19(1):1293. doi: 10.1186/s12889-019-7633-0

19. Jia W. Obesity in China: Its Characteristics, Diagnostic Criteria, and Implications. Front Med (2015) 9(2):129–33. doi: 10.1007/s11684-015-0387-x

20. Wariri O, Alhassan J, Mark G, Adesiyan O, Hanson L. Trends in Obesity by Socioeconomic Status Among non-Pregnant Women Aged 15-49 Y: A Cross-Sectional, Multi-Dimensional Equity Analysis of Demographic and Health Surveys in 11 Sub-Saharan Africa Countries, 1994-2015. Int Health (2020) 0:1–10. doi: 10.1093/inthealth/ihaa093

CrossRef Full Text | Google Scholar

21. Tydeman-Edwards R, Van Rooyen FC, Walsh CM. Obesity, Undernutrition and the Double Burden of Malnutrition in the Urban and Rural Southern Free State, South Africa. Heliyon (2018) 4(12):e00983. doi: 10.1016/j.heliyon.2018.e00983

22. Yoo S. Dynamic Energy Balance and Obesity Prevention. J Obes Metab Syndr (2018) 27(4):203–12. doi: 10.7570/jomes.2018.27.4.203

23. Duffey KJ, Gordon-Larsen P, Jacobs DR Jr, Williams OD, Popkin BM. Differential Associations of Fast Food and Restaurant Food Consumption With 3-Y Change in Body Mass Index: The Coronary Artery Risk Development in Young Adults Study. Am J Clin Nutr (2007) 85(1):201–8. doi: 10.1093/ajcn/85.1.201

24. Obri A, Claret M. The Role of Epigenetics in Hypothalamic Energy Balance Control: Implications for Obesity. Cell Stress (2019) 3(7):208–20. doi: 10.15698/cst2019.07.191

25. Sadeghirad B, Duhaney T, Motaghipisheh S, Campbell NR, Johnston BC. Influence of Unhealthy Food and Beverage Marketing on Children's Dietary Intake and Preference: A Systematic Review and Meta-Analysis of Randomized Trials. Obes Rev (2016) 17(10):945–59. doi: 10.1111/obr.12445

26. Willett WC, Leibel RL. Dietary Fat Is Not a Major Determinant of Body Fat. Am J Med (2002) 113(Suppl 9B):47S–59S. doi: 10.1016/S0002-9343(01)00992-5

27. Fitzgerald MP, Hennigan K, O'Gorman CS, McCarron L. Obesity, Diet and Lifestyle in 9-Year-Old Children With Parentally Reported Chronic Diseases: Findings From the Growing Up in Ireland Longitudinal Child Cohort Study. Ir J Med Sci (2019) 188(1):29–34. doi: 10.1007/s11845-018-1814-1

28. Romero-Ibarguengoitia ME, Vadillo-Ortega F, Caballero AE, Ibarra-González I, Herrera-Rosas A, Serratos-Canales MF, et al. Family History and Obesity in Youth, Their Effect on Acylcarnitine/Aminoacids Metabolomics and Non-Alcoholic Fatty Liver Disease (NAFLD). Structural Equation Modeling Approach. PloS One (2018) 13(2):e0193138. doi: 10.1371/journal.pone.0193138

29. Corica D, Aversa T, Valenzise M, Messina MF, Alibrandi A, De Luca F, et al. Does Family History of Obesity, Cardiovascular, and Metabolic Diseases Influence Onset and Severity of Childhood Obesity. Front Endocrinol (Lausanne) (2018) 9:187. doi: 10.3389/fendo.2018.00187

30. Ben Slama F, Achour A, Belhadj O, Hsairi M, Oueslati M, Achour N. [Obesity and Life Style in a Population of Male School Children Aged 6 to 10 Years in Ariana (Tunisia)]. Tunis Med (2002) 80(9):542–7.

31. Dhana K, Haines J, Liu G, Zhang C, Wang X, Field AE, et al. Association Between Maternal Adherence to Healthy Lifestyle Practices and Risk of Obesity in Offspring: Results From Two Prospective Cohort Studies of Mother-Child Pairs in the United States. BMJ (2018) 362:k2486. doi: 10.1136/bmj.k2486

32. Mulligan EP, Rauh MJ, Heiderscheit B, Jenkins WL. Sports Physical Therapy Education in the United States: Where Do We Go From Here? A Survey of American Academy of Sports Physical Therapy Members. J Allied Health (2020) 49:e79–79e87.

33. Beets MW, Wallner M, Beighle A. Defining Standards and Policies for Promoting Physical Activity in Afterschool Programs. J Sch Health (2010) 80:411–7. doi: 10.1111/j.1746-1561.2010.00521.x

34. Salam RA, Padhani ZA, Das JK, Shaikh AY, Hoodbhoy Z, Jeelani S, et al. Effects of Lifestyle Modification Interventions to Prevent and Manage Child and Adolescent Obesity: A Systematic Review and Meta-Analysis. Nutrients (2020) 12(8):2208. doi: 10.3390/nu12082208

35. Bäckhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, et al. The Gut Microbiota as an Environmental Factor That Regulates Fat Storage. Proc Natl Acad Sci USA (2004) 101(44):15718–23. doi: 10.1073/pnas.0407076101

36. Honce R, Karlsson EA, Wohlgemuth N, Estrada LD, Meliopoulos VA, Yao J, et al. Obesity-Related Microenvironment Promotes Emergence of Virulent Influenza Virus Strains. mBio (2020) 11(2):e03341–19. doi: 10.1128/mBio.03341-19

37. Stappenbeck TS, Hooper LV, Gordon JI. Developmental Regulation of Intestinal Angiogenesis by Indigenous Microbes via Paneth Cells. Proc Natl Acad Sci USA (2002) 99(24):15451–5. doi: 10.1073/pnas.202604299

38. Sender R, Fuchs S, Milo R. Revised Estimates for the Number of Human and Bacteria Cells in the Body. PloS Biol (2016) 14(8):e1002533. doi: 10.1371/journal.pbio.1002533

39. Jandhyala SM, Talukdar R, Subramanyam C, Vuyyuru H, Sasikala M, Nageshwar Reddy D. Role of the Normal Gut Microbiota. World J Gastroenterol (2015) 21(29):8787–803. doi: 10.3748/wjg.v21.i29.8787

40. DeGruttola AK, Low D, Mizoguchi A, Mizoguchi E. Current Understanding of Dysbiosis in Disease in Human and Animal Models. Inflammation Bowel Dis (2016) 22(5):1137–50. doi: 10.1097/MIB.0000000000000750

41. Gao R, Zhu C, Li H, Yin M, Pan C, Huang L, et al. Dysbiosis Signatures of Gut Microbiota Along the Sequence From Healthy, Young Patients to Those With Overweight and Obesity. Obes (Silver Spring) (2018) 26(2):351–61. doi: 10.1002/oby.22088

42. Chassaing B, Raja SM, Lewis JD, Srinivasan S, Gewirtz AT. Colonic Microbiota Encroachment Correlates With Dysglycemia in Humans. Cell Mol Gastroenterol Hepatol (2017) 4(2):205–21. doi: 10.1016/j.jcmgh.2017.04.001

43. Vijay-Kumar M, Aitken JD, Carvalho FA, Cullender TC, Mwangi S, Srinivasan S, et al. Metabolic Syndrome and Altered Gut Microbiota in Mice Lacking Toll-Like Receptor 5. Science (2010) 328(5975):228–31. doi: 10.1126/science.1179721

44. Gill PA, van Zelm MC, Muir JG, Gibson PR. Review Article: Short Chain Fatty Acids as Potential Therapeutic Agents in Human Gastrointestinal and Inflammatory Disorders. Aliment Pharmacol Ther (2018) 48(1):15–34. doi: 10.1111/apt.14689

45. Wu Y, Duan H, Tian X, Xu C, Wang W, Jiang W, et al. Genetics of Obesity Traits: A Bivariate Genome-Wide Association Analysis. Front Genet (2018) 9:179. doi: 10.3389/fgene.2018.00179

46. Kasuga M. [Genetic Factor for Diabetes and Obesity]. Nihon Rinsho (2010) 68(Suppl 8):359–63.

47. Srinivasan S, Chen L, Todd J, Divers J, Gidding S, Chernausek S, et al. The First Genome-Wide Association Study for Type 2 Diabetes in Youth: The Progress in Diabetes Genetics in Youth (ProDiGY) Consortium. Diabetes (2021) 70:996–1005. doi: 10.2337/db20-0443

48. Chen J, Sun M, Adeyemo A, Pirie F, Carstensen T, Pomilla C, et al. Genome-Wide Association Study of Type 2 Diabetes in Africa. Diabetologia (2019) 62:1204–11. doi: 10.1007/s00125-019-4880-7

49. Bogardus C. Missing Heritability and GWAS Utility. Obes (Silver Spring) (2009) 17(2):209–10. doi: 10.1038/oby.2008.613

50. Wang T, Xu M, Bi Y, Ning G. Interplay Between Diet and Genetic Susceptibility in Obesity and Related Traits. Front Med (2018) 12(6):601–7. doi: 10.1007/s11684-018-0648-6

51. Thaker VV. Genetic And Epigenetic Causes Of Obesity. Adolesc Med State Art Rev (2017) 28(2):379–405.

52. Huvenne H, Dubern B, Clément K, Poitou C. Rare Genetic Forms of Obesity: Clinical Approach and Current Treatments in 2016. Obes Facts (2016) 9(3):158–73. doi: 10.1159/000445061

53. Czajkowski P, Adamska-Patruno E, Bauer W, Fiedorczuk J, Krasowska U, Moroz M, et al. The Impact of FTO Genetic Variants on Obesity and Its Metabolic Consequences Is Dependent on Daily Macronutrient Intake. Nutrients (2020) 12(11):3255. doi: 10.3390/nu12113255

54. Koochakpour G, Esfandiar Z, Hosseini-Esfahani F, Mirmiran P, Daneshpour MS, Sedaghati-Khayat B, et al. Evaluating the Interaction of Common FTO Genetic Variants, Added Sugar, and Trans-Fatty Acid Intakes in Altering Obesity Phenotypes. Nutr Metab Cardiovasc Dis (2019) 29(5):474–80. doi: 10.1016/j.numecd.2019.01.005

55. Martins MC, Trujillo J, Freitas-Vilela AA, Farias DR, Rosado EL, Struchiner CJ, et al. Associations Between Obesity Candidate Gene Polymorphisms (Fat Mass and Obesity-Associated (FTO), Melanocortin-4 Receptor (MC4R), Leptin (LEP) and Leptin Receptor (LEPR)) and Dietary Intake in Pregnant Women. Br J Nutr (2018) 120(4):454–63. doi: 10.1017/S0007114518001423

56. Yupanqui-Lozno H, Bastarrachea RA, Yupanqui-Velazco ME, Alvarez-Jaramillo M, Medina-Méndez E, Giraldo-Peña AP, et al. Congenital Leptin Deficiency and Leptin Gene Missense Mutation Found in Two Colombian Sisters With Severe Obesity. Genes (Basel) (2019) 10(5):342. doi: 10.3390/genes10050342

57. Magno F, Guaraná HC, da Fonseca A, Pedrosa AP, Zembrzuski VM, Cabello PH, et al. Association of the MC4R Rs17782313 Polymorphism With Plasma Ghrelin, Leptin, IL6 and Tnfα Concentrations, Food Intake and Eating Behaviors in Morbidly Obese Women. Eat Weight Disord (2020) 26(4):1079–87. doi: 10.1007/s40519-020-01003-5

58. Yu H, Chhabra KH, Thompson Z, Jones GL, Kiran S, Shangguan G, et al. Hypothalamic POMC Deficiency Increases Circulating Adiponectin Despite Obesity. Mol Metab (2020) 35:100957. doi: 10.1016/j.molmet.2020.01.021

59. Cunha M, Aparício G, Duarte J, Pereira A, Albuquerque C, Oliveira A. Genetic Heritage as a Risk Factor Enabling Chilhood Obesity. Aten Primaria (2013) 45(Suppl 2):201–7. doi: 10.1016/S0212-6567(13)70023-4

60. Gupta N, Jain V. Prader Willi Syndrome - A Common Epigenetic Cause of Syndromic Obesity. Indian J Pediatr (2017) 84:809–10. doi: 10.1007/s12098-017-2512-0

61. Cena H, Chiovato L, Nappi RE. Obesity, Polycystic Ovary Syndrome, and Infertility: A New Avenue for GLP-1 Receptor Agonists. J Clin Endocrinol Metab (2020) 105(8):e2695–709. doi: 10.1210/clinem/dgaa285

62. D'Angelo CS, Koiffmann CP. Copy Number Variants in Obesity-Related Syndromes: Review and Perspectives on Novel Molecular Approaches. J Obes (2012) 2012:845480. doi: 10.1155/2012/845480

63. Rosen ED, Kaestner KH, Natarajan R, Patti ME, Sallari R, Sander M, et al. Epigenetics and Epigenomics: Implications for Diabetes and Obesity. Diabetes (2018) 67(10):1923–31. doi: 10.2337/db18-0537

64. Jaenisch R, Bird A. Epigenetic Regulation of Gene Expression: How the Genome Integrates Intrinsic and Environmental Signals. Nat Genet (2003) 33(Suppl):245–54. doi: 10.1038/ng1089

65. Holmes D. Epigenetics: On-Off Switch for Obesity. Nat Rev Endocrinol (2016) 12(3):125. doi: 10.1038/nrendo.2016.18

66. Burgio E, Lopomo A, Migliore L. Obesity and Diabetes: From Genetics to Epigenetics. Mol Biol Rep (2015) 42(4):799–818. doi: 10.1007/s11033-014-3751-z

67. Sherwood WB, Bion V, Lockett GA, Ziyab AH, Soto-Ramírez N, Mukherjee N, et al. Duration of Breastfeeding Is Associated With Leptin (LEP) DNA Methylation Profiles and BMI in 10-Year-Old Children. Clin Epigenet (2019) 11(1):128. doi: 10.1186/s13148-019-0727-9

68. Houde AA, Légaré C, Biron S, Lescelleur O, Biertho L, Marceau S, et al. Leptin and Adiponectin DNA Methylation Levels in Adipose Tissues and Blood Cells are Associated With BMI, Waist Girth and LDL-Cholesterol Levels in Severely Obese Men and Women. BMC Med Genet (2015) 16:29. doi: 10.1186/s12881-015-0174-1

69. Soubry A, Schildkraut JM, Murtha A, Wang F, Huang Z, Bernal A, et al. Paternal Obesity is Associated With IGF2 Hypomethylation in Newborns: Results From a Newborn Epigenetics Study (NEST) Cohort. BMC Med (2013) 11:29. doi: 10.1186/1741-7015-11-29

70. Bannister AJ, Kouzarides T. Regulation of Chromatin by Histone Modifications. Cell Res (2011) 21(3):381–95. doi: 10.1038/cr.2011.22

71. Zhang Q, Ramlee MK, Brunmeir R, Villanueva CJ, Halperin D, Xu F. Dynamic and Distinct Histone Modifications Modulate the Expression of Key Adipogenesis Regulatory Genes. Cell Cycle (2012) 11(23):4310–22. doi: 10.4161/cc.22224

72. Funato H, Oda S, Yokofujita J, Igarashi H, Kuroda M. Fasting and High-Fat Diet Alter Histone Deacetylase Expression in the Medial Hypothalamus. PloS One (2011) 6(4):e18950. doi: 10.1371/journal.pone.0018950

73. Pasquinelli AE. MicroRNAs and Their Targets: Recognition, Regulation and an Emerging Reciprocal Relationship. Nat Rev Genet (2012) 13(4):271–82. doi: 10.1038/nrg3162

74. Cruz K, de Oliveira A, Morais J, Severo JS, Marreiro D. Role of microRNAs on Adipogenesis, Chronic Low-Grade Inflammation, and Insulin Resistance in Obesity. Nutrition (2017) 35:28–35. doi: 10.1016/j.nut.2016.10.003

75. Zhao H, Shen J, Daniel-MacDougall C, Wu X, Chow WH. Plasma MicroRNA Signature Predicting Weight Gain Among Mexican-American Women. Obes (Silver Spring) (2017) 25(5):958–64. doi: 10.1002/oby.21824

76. Hubal MJ, Nadler EP, Ferrante SC, Barberio MD, Suh JH, Wang J, et al. Circulating Adipocyte-Derived Exosomal MicroRNAs Associated With Decreased Insulin Resistance After Gastric Bypass. Obes (Silver Spring) (2017) 25(1):102–10. doi: 10.1002/oby.21709

77. Guidelines (2013) for Managing Overweight and Obesity in Adults. Preface to the Expert Panel Report (Comprehensive Version Which Includes Systematic Evidence Review, Evidence Statements, and Recommendations). Obes (Silver Spring) (2014) 22 Suppl 2:S40. doi: 10.1002/oby.20822

78. Lee EY, Yoon KH. Epidemic Obesity in Children and Adolescents: Risk Factors and Prevention. Front Med (2018) 12(6):658–66. doi: 10.1007/s11684-018-0640-1

79. Nguyen B, Clements J. Obesity Management Among Patients With Type 2 Diabetes and Prediabetes: A Focus on Lifestyle Modifications and Evidence of Antiobesity Medications. Expert Rev Endocrinol Metab (2017) 12(5):303–13. doi: 10.1080/17446651.2017.1367285

80. Mozaffarian D, Hao T, Rimm EB, Willett WC, Hu FB. Changes in Diet and Lifestyle and Long-Term Weight Gain in Women and Men. N Engl J Med (2011) 364(25):2392–404. doi: 10.1056/NEJMoa1014296

81. Struben J, Chan D, Dubé L. Policy Insights From the Nutritional Food Market Transformation Model: The Case of Obesity Prevention. Ann N Y Acad Sci (2014) 1331:57–75. doi: 10.1111/nyas.12381

82. Lal A, Mantilla-Herrera AM, Veerman L, Backholer K, Sacks G, Moodie M, et al. Correction: Modelled Health Benefits of a Sugar-Sweetened Beverage Tax Across Different Socioeconomic Groups in Australia: A Cost-Effectiveness and Equity Analysis. PloS Med (2020) 17(7):e1003310. doi: 10.1371/journal.pmed.1003310

83. Telles S, Gangadhar BN, Chandwani KD. Lifestyle Modification in the Prevention and Management of Obesity. J Obes (2016) 2016:5818601. doi: 10.1155/2016/5818601

84. Greenway FL, Aronne LJ, Raben A, Astrup A, Apovian CM, Hill JO, et al. A Randomized, Double-Blind, Placebo-Controlled Study of Gelesis100: A Novel Nonsystemic Oral Hydrogel for Weight Loss. Obes (Silver Spring) (2019) 27:205–16. doi: 10.1002/oby.22347

85. Yeo G, Chao D, Siegert AM, Koerperich ZM, Ericson MD, Simonds SE, et al. The Melanocortin Pathway and Energy Homeostasis: From Discovery to Obesity Therapy. Mol Metab (2021) 48:101206. doi: 10.1016/j.molmet.2021.101206

86. Gomez G, Stanford FC. US Health Policy and Prescription Drug Coverage of FDA-Approved Medications for the Treatment of Obesity. Int J Obes (Lond) (2018) 42(3):495–500. doi: 10.1038/ijo.2017.287

87. Rebello CJ, Greenway FL. Obesity Medications in Development. Expert Opin Investig Drugs (2020) 29:63–71. doi: 10.1080/13543784.2020.1705277

88. Karri S, Sharma S, Hatware K, Patil K. Natural Anti-Obesity Agents and Their Therapeutic Role in Management of Obesity: A Future Trend Perspective. BioMed Pharmacother (2019) 110:224–38. doi: 10.1016/j.biopha.2018.11.076

89. Gong S, Ye T, Wang M, Wang M, Li Y, Ma L, et al. Traditional Chinese Medicine Formula Kang Shuai Lao Pian Improves Obesity, Gut Dysbiosis, and Fecal Metabolic Disorders in High-Fat Diet-Fed Mice. Front Pharmacol (2020) 11:297. doi: 10.3389/fphar.2020.00297

90. Aminian A, Zelisko A, Kirwan JP, Brethauer SA, Schauer PR. Exploring the Impact of Bariatric Surgery on High Density Lipoprotein. Surg Obes Relat Dis (2015) 11:238–47. doi: 10.1016/j.soard.2014.07.017

91. Osto M, Abegg K, Bueter M, le Roux CW, Cani PD, Lutz TA. Roux-En-Y Gastric Bypass Surgery in Rats Alters Gut Microbiota Profile Along the Intestine. Physiol Behav (2013) 119:92–6. doi: 10.1016/j.physbeh.2013.06.008

92. Al-Rubaye H, McGlone ER, Farzaneh B, Mustafa L, Johnson M, Kayal A, et al. Roux-En-Y Gastric Bypass or Sleeve Gastrectomy for Obstructive Sleep Apnea: A Systematic Review and Meta-Analysis. Laparoscopic Endoscopic Robotic Surg (2019) 2(3):53–8. doi: 10.1016/j.lers.2019.05.002

93. Kops NL, Vivan MA, Fülber ER, Fleuri M, Fagundes J, Friedman R. Preoperative Binge Eating and Weight Loss After Bariatric Surgery: A Systematic Review and Meta-Analysis. Obes Surg (2020) 31(3):1239–48. doi: 10.1007/s11695-020-05124-9

94. Kong LC, Tap J, Aron-Wisnewsky J, Pelloux V, Basdevant A, Bouillot JL, et al. Gut Microbiota After Gastric Bypass in Human Obesity: Increased Richness and Associations of Bacterial Genera With Adipose Tissue Genes. Am J Clin Nutr (2013) 98(1):16–24. doi: 10.3945/ajcn.113.058743

95. Zhang H, DiBaise JK, Zuccolo A, Kudrna D, Braidotti M, Yu Y, et al. Human Gut Microbiota in Obesity and After Gastric Bypass. Proc Natl Acad Sci USA (2009) 106(7):2365–70. doi: 10.1073/pnas.0812600106

96. van Leiden HA, Dekker JM, Moll AC, Nijpels G, Heine RJ, Bouter LM, et al. Blood Pressure, Lipids, and Obesity are Associated With Retinopathy: The Hoorn Study. Diabetes Care (2002) 25(8):1320–5. doi: 10.2337/diacare.25.8.1320

97. Yu EW, Gao L, Stastka P, Cheney MC, Mahabamunuge J, Torres Soto M, et al. Fecal Microbiota Transplantation for the Improvement of Metabolism in Obesity: The FMT-TRIM Double-Blind Placebo-Controlled Pilot Trial. PloS Med (2020) 17(3):e1003051. doi: 10.1371/journal.pmed.1003051

98. Ridaura VK, Faith JJ, Rey FE, Cheng J, Duncan AE, Kau AL, et al. Gut Microbiota From Twins Discordant for Obesity Modulate Metabolism in Mice. Science (2013) 341(6150):1241214. doi: 10.1126/science.1241214

99. Vrieze A, Van Nood E, Holleman F, Salojärvi J, Kootte RS, Bartelsman JF, et al. Transfer of Intestinal Microbiota From Lean Donors Increases Insulin Sensitivity in Individuals With Metabolic Syndrome. Gastroenterology (2012) 143(4):913–6.e7. doi: 10.1053/j.gastro.2012.06.031

100. Zhang Z, Mocanu V, Cai C, Dang J, Slater L, Deehan EC, et al. Impact of Fecal Microbiota Transplantation on Obesity and Metabolic Syndrome-A Systematic Review. Nutrients (2019) 11(10):2291. doi: 10.3390/nu11102291

101. Phan HD, Nguyen T, Bui PL, Pham TT, Doan TV, Nguyen, et al. Overweight and Obesity Among Vietnamese School-Aged Children: National Prevalence Estimates Based on the World Health Organization and International Obesity Task Force Definition. PloS One (2020) 15(10):e0240459. doi: 10.1371/journal.pone.0240459

102. Epigenetic Drugs. Nat Biotechnol (2020) 38(5):558. doi: 10.1038/s41587-020-0523-2

103. Arguelles AO, Meruvu S, Bowman JD, Choudhury M. Are Epigenetic Drugs for Diabetes and Obesity at Our Door Step. Drug Discov Today (2016) 21(3):499–509. doi: 10.1016/j.drudis.2015.12.001

104. Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial Ecology: Human Gut Microbes Associated With Obesity. Nature (2006) 444(7122):1022–3. doi: 10.1038/4441022a

Keywords: obesity, epidemiology, pathophysiology, genetics, epigenetics, microenvironment

Citation: Lin X and Li H (2021) Obesity: Epidemiology, Pathophysiology, and Therapeutics. Front. Endocrinol. 12:706978. doi: 10.3389/fendo.2021.706978

Received: 08 May 2021; Accepted: 10 August 2021; Published: 06 September 2021.

Reviewed by:

Copyright © 2021 Lin and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Hong Li, [email protected]

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Causes and Effects of Obesity Essay

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

Bibliography

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.

• Chicago (A-D)
• Chicago (N-B)

IvyPanda. (2023, October 28). Causes and Effects of Obesity Essay. https://ivypanda.com/essays/effects-of-obesity/

"Causes and Effects of Obesity Essay." IvyPanda , 28 Oct. 2023, ivypanda.com/essays/effects-of-obesity/.

IvyPanda . (2023) 'Causes and Effects of Obesity Essay'. 28 October.

IvyPanda . 2023. "Causes and Effects of Obesity Essay." October 28, 2023. https://ivypanda.com/essays/effects-of-obesity/.

1. IvyPanda . "Causes and Effects of Obesity Essay." October 28, 2023. https://ivypanda.com/essays/effects-of-obesity/.

IvyPanda . "Causes and Effects of Obesity Essay." October 28, 2023. https://ivypanda.com/essays/effects-of-obesity/.

• Public Health. Epidemiology of Obesity
• Recreation Hub as a Way to Combat Sedentary Lifestyle
• Parental Education on Overweight and Obese Children
• Eating Disorders: Assessment & Misconceptions
• Human Digestion
• Definitions of Obesity and Criteria for Diagnosing It
• Obesity Could Be Catching
• White Wines vs. Red Wines

• About Project
• Testimonials

Business Management Ideas

Essay on Obesity

List of essays on obesity, essay on obesity – short essay (essay 1 – 150 words), essay on obesity (essay 2 – 250 words), essay on obesity – written in english (essay 3 – 300 words), essay on obesity – for school students (class 5, 6, 7, 8, 9, 10, 11 and 12 standard) (essay 4 – 400 words), essay on obesity – for college students (essay 5 – 500 words), essay on obesity – with causes and treatment (essay 6 – 600 words), essay on obesity – for science students (essay 7 – 750 words), essay on obesity – long essay for medical students (essay 8 – 1000 words).

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.

Health , Obesity

Get FREE Work-at-Home Job Leads Delivered Weekly!

Join more than 50,000 subscribers receiving regular updates! Plus, get a FREE copy of How to Make Money Blogging!

Message from Sophia!

Like this post? Don’t forget to share it!

Here are a few recommended articles for you to read next:

• Essay on Cleanliness
• Essay on Cancer
• Essay on AIDS
• Essay on Health and Fitness

No comments yet.

Leave a reply click here to cancel reply..

You must be logged in to post a comment.

Billionaires

• Donald Trump
• Warren Buffett
• Email Address
• Free Stock Photos
• Keyword Research Tools
• URL Shortener Tools
• WordPress Theme

Book Summaries

• How To Win Friends
• Rich Dad Poor Dad
• The Code of the Extraordinary Mind
• The Luck Factor
• The Millionaire Fastlane
• The ONE Thing
• Think and Grow Rich
• 100 Million Dollar Business
• Business Ideas

Digital Marketing

• Mobile Addiction
• Social Media Addiction
• Computer Addiction
• Drug Addiction
• Internet Addiction
• TV Addiction
• Healthy Habits
• Morning Rituals
• Wake up Early
• Cholesterol
• Reducing Cholesterol
• Fat Loss Diet Plan
• Reducing Hair Fall
• Sleep Apnea
• Weight Loss

Internet Marketing

• Email Marketing

Law of Attraction

• Subconscious Mind
• Vision Board
• Visualization

Law of Vibration

• Professional Life

Motivational Speakers

• Bob Proctor
• Robert Kiyosaki
• Vivek Bindra
• Inner Peace

Productivity

• Not To-do List
• Project Management Software
• Negative Energies

Relationship

• Getting Back Your Ex

Self-help 21 and 14 Days Course

Self-improvement.

• Body Language
• Complainers
• Emotional Intelligence
• Personality

Social Media

• Project Management
• Anik Singal
• Baba Ramdev
• Dwayne Johnson
• Jackie Chan
• Leonardo DiCaprio
• Narendra Modi
• Nikola Tesla
• Sachin Tendulkar
• Sandeep Maheshwari
• Shaqir Hussyin

Website Development

Wisdom post, worlds most.

• Expensive Cars

Our Portals: Gulf Canada USA Italy Gulf UK

Privacy Overview

Home — Essay Samples — Nursing & Health — Public Health Issues — Obesity

Essay Examples on Obesity

Hook examples for obesity essays, "the silent epidemic among us" hook.

"Obesity silently creeps into our lives, affecting millions. Explore the hidden health crisis, its causes, and its far-reaching consequences on individuals and society."

"From Childhood to Adulthood: Battling Obesity" Hook

"Childhood obesity often follows us into adulthood. Share stories of individuals who have embarked on journeys of transformation and discuss the challenges they face."

"Obesity's Toll on Public Health" Hook

"Obesity is a public health crisis with wide-ranging effects. Investigate the strain on healthcare systems, the rise of related diseases, and the economic impact of obesity."

"The Cultural Shift: Food, Technology, and Sedentary Lifestyles" Hook

"Examine how cultural factors, including dietary habits, technology use, and sedentary lifestyles, have contributed to the obesity epidemic. What can we learn from these trends?"

"Breaking the Cycle: Strategies for Prevention" Hook

"Prevention is key to combating obesity. Discuss effective strategies for preventing obesity in children and adults, from education to policy changes."

"The Psychological Battle: Obesity and Mental Health" Hook

"Obesity often intersects with mental health challenges. Explore the complex relationship between obesity and mental well-being, as well as the stigma attached to it."

"Shifting Perspectives: Celebrating Body Positivity" Hook

"In the midst of the obesity crisis, the body positivity movement is gaining ground. Discuss the importance of promoting self-acceptance and diverse body images."

Obesity: a Satirical Look at a Growing Epidemic

The study, diagnosis, and prevention of obesity, made-to-order essay as fast as you need it.

Each essay is customized to cater to your unique preferences

+ experts online

The Rise of Fast Food: Causes and Effects

The issue of obesity and way of its prevention, a worldwide epidemic of obesity and ways to handle it, the most common causes of obesity, let us write you an essay from scratch.

• 450+ experts on 30 subjects ready to help
• Custom essay delivered in as few as 3 hours

The Problem of Obesity and The Unhealthy Lifestyle Among The Us Citizens

Obesity in america: causes, effects, and ways to combat, an increasing in obesity both in adults and children in united states, the issues of the obesity and the american problem, get a personalized essay in under 3 hours.

Expert-written essays crafted with your exact needs in mind

Obesity in The United States and Ways to Avoid It

Obesity as a stigma or a threat to health, why obesity should be classified a disease, don’t blame the eater': the issue of america’s growing weight, childhood obesity, obesity and its effects in the united kingdom, analysis of the theme of fast food and obesity in the article "don’t blame the eater", the main causes of obesity in america, careless consuming and lazy living: obesity in america, the effect of obesity on depression, analysis of the causes of obesity, the role of food companies in rising rate of obesity in america, the causes for the obesity epidemic in america, obesity as one of the most important social problems in america, the problem of obesity among college students and solutions to combat it, age and socio economic issues as risk factors of obesity, childhood obesity: prevention & treatment, the need for healthier lifestyle campaigns to prevent the issue of overweight and obesity in singapore, obesity epidemic in america and the factors contributing to it, the factors of the problem of obesity in america.

Obesity is a condition in which excess body fat has accumulated to such an extent that it may have a negative effect on health. Medical organizations tend to classify people as obese based on body mass index (BMI) – a ratio of a person's weight in kilograms to the square of their height in meters.

There are three types of obesity: Class 1 (low-risk) obesity, if BMI is 30.0 to 34.9; Class 2 (moderate-risk) obesity, if BMI is 35.0 to 39.9; Class 3 (high-risk) obesity, if BMI is equal to or greater than 40.0.

The major contributors to obesity are: diet, sedentary lifestyle, genetics, other illnesses, social determinants, gut bacteria, and other factors.

Excessive body weight has a strong link to many diseases and conditions, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, osteoarthritis, and asthma. As a result, obesity has been found to reduce life expectancy.

Most of the world's population live in countries where overweight and obesity kills more people than underweight. 39 million children under the age of 5 were overweight or obese in 2020. Worldwide obesity has nearly tripled since 1975. From 1999-2000 through 2017-March 2020, US obesity prevalence increased from 30.5% to 41.9%.

Relevant topics

• Eating Disorders
• Drug Addiction
• Mental Health

By clicking “Check Writers’ Offers”, you agree to our terms of service and privacy policy . We’ll occasionally send you promo and account related email

No need to pay just yet!

Bibliography

We use cookies to personalyze your web-site experience. By continuing we’ll assume you board with our cookie policy .

• Instructions Followed To The Letter
• Deadlines Met At Every Stage
• Unique And Plagiarism Free

• Chronicle Conversations
• Article archives
• Issue archives
• Join our mailing list

LIFESTYLE DISEASES: An Economic Burden on the Health Services

About the author, fatma al-maskari.

Lifestyle diseases share risk factors similar to prolonged exposure to three modifiable lifestyle behaviours -- smoking, unhealthy diet, and physical inactivity -- and result in the development of chronic diseases, specifically heart disease, stroke, diabetes, obesity, metabolic syndrome, chronic obstructive pulmonary disease, and some types of cancer. These illnesses used to be considered the diseases of industrialized countries, so-called "Western diseases" or "diseases of affluence"; however, internationally they are known as non-communicable and chronic diseases, part of the degenerative diseases group. Chronic disease can result in loss of independence, years of disability, or death, and impose a considerable economic burden on health services. Today, chronic diseases are a major public health problem worldwide. In 2005, the World Health Organization (WHO) estimated that 61 per cent of all deaths -- 35 million -- and 49 per cent of the global burden of disease were attributable to chronic diseases. By 2030, the proportion of total global deaths due to chronic diseases is expected to increase to 70 per cent and the global burden of disease to 56 per cent. The greatest increase is anticipated in the African and Eastern Mediterranean regions. The World Health Assembly adopted a resolution in 2000 on the prevention and control of chronic diseases. It called on its Member States to develop national policy frameworks, taking into account healthy public policies as well as fiscal and taxation measures towards healthy and unhealthy goods and services. The resolution also asked to establish programmes for the prevention and control of chronic diseases; assess and monitor mortality and the proportion of sickness in an area due to chronic diseases; promote effective secondary and tertiary prevention; and develop guidelines for cost-effective screening, diagnosis, and treatment of chronic diseases, with special emphasis in developing countries. The combination of four healthy lifestyle factors -- maintaining a healthy weight, exercising regularly, following a healthy diet, and not smoking -- seem to be associated with as much as an 80 per cent reduction in the risk of developing the most common and deadly chronic diseases. This reinforces the current public health recommendations for the observance of healthy lifestyle habits, and because the roots of these habits often originate during the formative stages of life, it is especially important to start early in teaching important lessons concerning healthy living. However, despite the well known benefits of a healthy lifestyle, only a small proportion of adults follow such a routine; in fact, the numbers are declining. Unfortunately, there is very little public awareness of the association between health and lifestyle. Many are unaware that a change in lifestyle is an important factor in the emergence of chronic diseases as causes of increased morbidity and mortality. Lifestyle is -generally considered a personal issue. However, lifestyles are social practices and ways of living adopted by individuals that reflect personal, group, and socio-economic identities. Modest but achievable adjustments to lifestyle behaviours are likely to have a considerable impact at the individual and population level. Health professionals and the media now repeatedly carry the message that to remain healthy, people need to adopt healthy behaviours. Physical activity, cessation of tobacco consumption, eating a high-fibre, low-fat diet, controlling body weight, and learning to cope with stress reduce the risk of cardiovascular disease, cancer, and premature mortality. A comprehensive public health approach to tobacco control effectively inhibits the beginning of tobacco use and promotes its cessation, through a range of measures including tax and price policy, restriction on tobacco advertising, promotion and sponsorship, packing and labelling requirements, educational campaigns, restrictions on smoking in public places, and cessation support services. A comprehensive approach must include young people to reach the entire population. National policy measures known to have the biggest impact on individual levels of consumption, cessation rates, and initiation rates require sustained political will and engagement and, above all, effective and well-enforced legislation. Furthermore, effective public health measures are urgently needed to promote physical activity and improve health around the world. The challenge of promoting physical activity is as much the responsibility of governments, as of the people. However, individual action for physical activity is influenced by the environment, sports and recreational facilities, and national policy. It requires coordination among many sectors, such as health, sports, education and culture policy, media and information, transport, urban planning, local governments, and financial and economic planning. Towards this end, the World Health Organization is supporting its member States by providing nationwide evidence-based advocacy on the health, social, and economic benefits of healthy lifestyles.

Centers for Disease Control and Prevention, Merck Institute of Aging & Health. The State of Aging and Health in America 2004. (Washington, DC: Merck Institute of Aging & Health, 2004). Ford, Earl S; Bergmann, Manuela M; Kroger, Janine; Schienkiewitz, Anja; Weikert, Cornelia; Boeing, Heiner. "Healthy Living Is the Best Revenge: Findings From the European Prospective Investigation Into Cancer and Nutrition-Potsdam Study", Arch Intern Med, 169 (15) (2009): 1355-1362. King D.E, Mainous A.G 3rd, Carnemolla M, Everett C.J. "Adherence to Healthy Lifestyle Habits in US Adults, 1988-2006", Am J Med. 122(6) (June 2009): 528-34. Kvaavik, Elisabeth; Batty, G. David; Ursin, Giske; Huxley, Rachel; Gale, Catharine R. "Influence of Individual and Combined Health Behaviors on Total and Cause-Specific Mortality in Men and Women: The United Kingdom Health and Lifestyle Survey", Arch Intern Med, 2010; 170 (8): 711-718. Murray, C.J.L & Lopez, A.D. "The global burden of disease: a comprehensive assessment of Mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020". Cambridge, MA: Harvard School of Public Health, 1996. WHO. Neglected Global Epidemics: three growing threats. The World Health Report, 2003. WHO. Projections of mortality and burden of disease to 2030 (Geneva: 2007).

The UN Chronicle  is not an official record. It is privileged to host senior United Nations officials as well as distinguished contributors from outside the United Nations system whose views are not necessarily those of the United Nations. Similarly, the boundaries and names shown, and the designations used, in maps or articles do not necessarily imply endorsement or acceptance by the United Nations.

Thirty Years On, Leaders Need to Recommit to the International Conference on Population and Development Agenda

With the gains from the Cairo conference now in peril, the population and development framework is more relevant than ever. At the end of April 2024, countries will convene to review the progress made on the ICPD agenda during the annual session of the Commission on Population and Development.

The LDC Future Forum: Accelerating the Attainment of the Sustainable Development Goals in the Least Developed Countries

The desired outcome of the LDC Future Forums is the dissemination of practical and evidence-based case studies, solutions and policy recommendations for achieving sustainable development.

From Local Moments to Global Movement: Reparation Mechanisms and a Development Framework

For two centuries, emancipated Black people have been calling for reparations for the crimes committed against them. 

Documents and publications

• Yearbook of the United Nations 
• Basic Facts About the United Nations
• Journal of the United Nations
• Meetings Coverage and Press Releases
• United Nations Official Document System (ODS)
• Africa Renewal

Libraries and Archives

• Dag Hammarskjöld Library
• UN Audiovisual Library
• UN Archives and Records Management 
• Audiovisual Library of International Law
• UN iLibrary 

News and media

• UN News Centre 
• UN Chronicle on Twitter
• UN Chronicle on Facebook

The UN at Work

• 17 Goals to Transform Our World
• Official observances
• United Nations Academic Impact (UNAI)
• Protecting Human Rights
• Maintaining International Peace and Security
• The Office of the Secretary-General’s Envoy on Youth
• United Nations Careers

The critical role of gut microbiota in obesity

Affiliation.

• 1 Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
• PMID: 36339448
• PMCID: PMC9630587
• DOI: 10.3389/fendo.2022.1025706

Obesity is a global epidemic characterized by energy disequilibrium, metabolic disorder, fat mass development, and chronic low-grade inflammation, which significantly affects the health state of individuals of all ages and strains the socioeconomic system. The prevalence of obesity is rising at alarming rates and its etiology involves complicated interplay of diet, genetic, and environmental factors. The gut microbiota, as an important constituent of environmental factors, has been confirmed to correlate with the onset and progression of obesity. However, the specific relationship between obesity and the gut microbiota, and its associated mechanisms, have not been fully elucidated. In this review, we have summarized that the microbial diversity was significantly decreased and the Firmicutes/Bacteroidetes ratio was significantly increased in obesity. The altered gut microbiota and associated metabolites contributed to the progression of the disease by disrupting energy homeostasis, promoting lipid synthesis and storage, modulating central appetite and feeding behavior, as well as triggering chronic inflammation, and that the intentional manipulation of gut microbiota held promise as novel therapies for obesity, including probiotics, prebiotics, and fecal microbiota transplantation.

Keywords: SCFAs; bile acids; energy homeostasis; gut microbiota; obesity.

Copyright © 2022 Cheng, Zhang, Yang and Chu.

Publication types

• Research Support, Non-U.S. Gov't
• Fecal Microbiota Transplantation / adverse effects
• Gastrointestinal Microbiome*
• Inflammation / complications
• Obesity / metabolism