↑ Oestrogen
CI, confidence interval; GORD, gastro-oesophageal reflux disease; NAFLD, non-alcoholic fatty liver disease; OR, odds ratio; RR, relative risk.
NAFLD has an estimated prevalence of 25.2% worldwide and 23.7% in Europe, 40 but the true incidence is difficult to characterise due to different diagnostic criteria between studies. The prevalence of NAFLD has increased over the past four decades alongside the increase in obesity. 40 A meta-analysis of 20 studies (12,065 cases, 33,693 controls), 17 from Asian countries and 3 from Western countries, demonstrated that the odds of NAFLD increased by 3–10% per 1 cm increase in WC and 13–38% per 1-unit increase in BMI. 41 Although both BMI and WC were independently associated with NAFLD, markers of abdominal obesity were stronger predictors and remained associated with NAFLD after adjusting for BMI. This may explain why some patients with a normal BMI can develop NAFLD, which is more commonly seen in rural areas of some Asian countries (25–30%) compared with the United States (US) and Europe (10–20%). 41 Therefore, both BMI and WC or WHR should be used to assess NAFLD risk. NAFLD is considered the hepatic manifestation of the metabolic syndrome, 42 whereas longitudinal studies suggest that NAFLD precedes the metabolic syndrome and T2DM. 43 NAFLD increases the risk of T2DM, hypertension, dyslipidaemia and CKD, and it is no surprise that CVD is the leading cause of mortality among this patient group. 10 , 11 Up to one-third of NAFLD patients are at risk of developing non-alcoholic steatohepatitis (NASH), 44 which can progress to liver cirrhosis, hepatocellular carcinoma (HCC), decompensated liver cirrhosis and death. 45 Therefore, individuals with NAFLD require early weight loss intervention to prevent both cardiovascular- and liver-related morbidity and mortality.
Obesity increases the risk of gallbladder disease. A systematic review of 17 prospective studies involving 1,921,103 participants found a RR of 1.63 for a 5-unit increase in BMI and a RR of 1.46 for a 10 cm increase in WC. 46 There was an almost two-fold increased risk of gallbladder disease from the lower to the upper limit of the normal BMI range (18.5–24.9 kg/m 2 ), which suggests that even moderate increases in adiposity increase risk. 46 Hormone changes and gallbladder dysmotility are suggested mechanisms to explain the association between obesity and gallbladder disease ( Table 3 ). 19
Obesity is also associated with oesophageal disorders ( Table 3 ). The prevalence of GORD increases with obesity and meta-analyses report a positive association between BMI and GORD. 47 , 48 Central obesity is an independent predictor of the consequences of GORD (oesphagitis, Barrett’s oesphagus, adenocarcinoma). 49
Obstructive sleep apnoea.
Obesity is the most common risk factor for the development of OSA. Observational data from 2.8 million UK adults found that class I and III obesity were associated with a 5-times and 22-times increased risk of OSA, respectively, 26 which suggests that the risk of OSA increases considerably at a higher BMI. Untreated OSA can cause excessive daytime somnolence, negatively affect work performance, increase the risk of CVD and threaten vehicle licence if driving is affected. 50 , 51 Proposed mechanisms linking obesity to OSA include adipokines, upper airway adiposity and increased neck circumference causing pharyngeal collapse. 50
OHS is defined as a combination of obesity (BMI > 30 kg/m 2 ), daytime hypercapnia (pCO 2 > 6 kpa) and sleep disordered breathing that are not due to other conditions associated with alveolar hypoventilation. 17 OHS has an estimated prevalence of 8.5% in patients with OSA and 19–31% among obese patients. 55 , 56 The pathophysiology of OHS may be related to leptin resistance causing central hypoventilation, impaired compensatory response to hypercapnia and impaired respiratory mechanics due to obesity. 57 The morbidity and mortality of OHS is greater than OSA. The chronic daytime hypoxia and hypercapnia increase the risk of pulmonary hypertension, right-sided heart failure and cor pulmonale. 17 Weight loss is recommended for both OSA and OHS, but adherence to lifestyle interventions can be difficult for this cohort because their exercise capacity is limited due to daytime somnolence, fatigue and chronic hypoxia, whereas poor sleep is associated with increased appetite. 16 Pharmacological therapy has not been proven to be effective in OSA and OHS. 16 Bariatric surgery is an effective treatment for OSA and parameters of sleep quality, 58 but data on OHS is limited due to the associated pulmonary and cardiac complications and therefore weight loss in this group of patients with chronic cardiorespiratory disease can be challenging. 17 Presently, no randomised control data exist to support bariatric surgery as an intervention to treat OHS. 59
Obesity increases the risk of asthma in children and adults. Over the past 40 years, there have been parallel increases in childhood obesity and asthma, with asthma prevalence doubling between 1980 and 1994. 52 A meta-analysis of seven prospective epidemiological studies involving 333,102 adult participants found that the prevalence of asthma was 38% in overweight individuals and 92% in obese individuals. 53 Two distinct asthma phenotypes have been described in obese patients; the early-onset allergic form and the late-onset non-allergic form, 54 and weight loss has been associated with improvements in lung function and asthma symptoms among obese patients. 16 The mechanism by which obesity increases asthma risk is unclear but may be related to mechanical, inflammatory and hormonal factors. 52
After smoking, obesity is the second biggest preventable cause of cancer in the UK and maintaining a normal weight could prevent 22,800 annual UK cases. 60 In 2001, the International Agency for Research on Cancer concluded that obesity accounted for 10% of post-menopausal breast cancers and 11% of colon cancers. For kidney, lower oesophageal adenocarcinoma and endometrial cancer, the risks attributed to BMI alone were 25%, 37% and 39%, respectively. 61
A population-based prospective cohort study using data from 5.24 million UK adults concluded that BMI was associated with 17 cancers. 62 Each 5 kg/m 2 increase in BMI was approximately linearly associated with cancer of the uterus, gallbladder, kidney, cervix, thyroid and leukaemia. There was a non-linear but positive association between BMI and liver, colon, ovarian and post-menopausal breast cancer. 62 The authors concluded that the heterogeneity in the effects of BMI on cancer risk suggests that there may be different mechanisms based malignancy type and patient sub-group. 62 Frequently cited mechanisms linking obesity to malignancy include systemic alterations in endogenous hormone metabolism (e.g. insulin, insulin-like growth factor, sex steroids) and chronic inflammation mediated by adipokines. 61
Obesity also impacts cancer prognosis. A meta-analysis of 82 studies involving 213,075 breast cancer patients showed that obesity (BMI > 30 kg/m 2 ) was associated with increased cancer-related mortality. 63 Similarly, the Nurses’ Health Study, which included 5204 patients with non-metastatic breast cancer, showed that weight gain after diagnosis was associated with increased risk of recurrence and breast-cancer specific mortality. 64 Weight loss by diet and physical activity has been shown to reduce the risk of postmenopausal breast cancer; however, evidence for other cancers is less robust. 65
Cardiovascular risk factors such as T2DM, dyslipidaemia and hypertension are well-established complications of obesity that increase the risk of dementia and Alzheimer’s disease. 21 An independent relationship between mid-life obesity and dementia also exists. A meta-analysis of 39 prospective cohort studies analysing data from 1.3 million adults across the US, Europe and Asia found that a high BMI (overweight or obese range) was associated with an increased risk of dementia when BMI was measured 20 years prior to dementia diagnosis, but this relationship was reversed when BMI was measured closer to dementia diagnosis (<10 years). 66 The latter finding could be interpreted as obesity being protective; however, it is likely to be explained by reverse causation and the former finding can be explained by the fact that clinical dementia is preceded by a long (20–30 years) preclinical phase where weight loss is common. 67 , 68
Obesity is an important preventable risk factor for the development CKD because it is associated with major CKD risk factors: diabetes mellitus and hypertension. 69 A large cohort study accruing over 8 million person-years found that a BMI > 25 was an independent predictor for end-stage renal disease. When compared with normal-weight controls (BMI 18.5–24.9 kg/m 2 ) the RR of end-stage renal disease for overweight individuals was 1.87 (95% CI; 1.64–2.14) and 7.07 (95% CI; 5.37–9.31) for those with class III obesity after adjusting for other CKD risk factors. 69 One proposed independent mechanism linking obesity to CKD is hyperfiltration due to the increased metabolic demands of excess body weight. 70
Between 1986 and 2000, there was a 10-fold increase in obesity-related glomerulopathy, which is characterised by proteinuria, glomerulomegaly, progressive glomerulosclerosis and renal function decline. 71 Short-term improvement is achieved with renin-angiotensin-aldosterone blockade, whereas weight loss through low-calorie dieting or bariatric surgery is associated with improvements in proteinuria and kidney function. 72 A prospective randomised control trial observed that 3 months of endurance and endurance-strength exercise among obese women (BMI 35 kg/m 2 ) was associated with an 10 ml/min/1.73 m 2 improvements in estimated glomerular filtration rate. 73
Obesity can increase the risk of kidney stones, 74 and roux-en-y gastric bypass, an operation used to treat obesity, can also increase the risk of hyperoxaluric kidney stones due to increased enteral oxalate absorption. 75 General and central obesity are both associated with urinary incontinence in men and women, overactive bladder syndrome in women and benign prostatic hyperplasia in men. 76 , 77
Obesity is a well-recognised risk factor for the development and progression of osteoarthritis in weight-bearing joints, especially the knee. 18 There is a 36% increased risk of knee osteoarthritis with every 2 unit increase in BMI and patients with obesity suffer more severe joint degeneration. 78 Both obesity and osteoarthritis can reduce mobility, which can increase the risk of weight gain. In patients with osteoarthritis, weight loss of 10% has been associated with an improvement in joint symptoms, physical function and health related quality of life. 18
Osteoarthritis. Obesity is also associated with osteoarthritis in non-weight bearing joints such as the hands, which is linked to increased levels of adipokines. 79 Similarly, inflammatory markers observed in obesity are also associated with pre-clinical rheumatoid arthritis. 80 Prospective cohort data from the Nurses’ Health Study accruing more than 4,500,000 person-years of follow up showed that excess body weight (BMI > 24.9 kg/m 2 ) was associated with a 40–70% increased risk of rheumatoid arthritis in women, with the highest risk observed in overweight or obese women aged 18 years old. 80 Therefore, interventions that combat childhood obesity may reduce the incidence of adult rheumatoid arthritis.
Obesity has been independently associated with gout. A longitudinal community-based cohort study involving 15,533 men and women demonstrated that the relative risk of gout was almost doubled in those with a BMI > 30 kg/m 2 , and that obesity was associated with earlier onset of the disease. 81 Both gout and obesity are associated with elevated levels of serum uric acid and weight loss has been associated with reduced incidence of hyperuricaemia and gout attacks. 82
Individuals with obesity are often stigmatised in education, health and employment settings. This results in obesity discrimination, 83 which has increased by 66% over the past decade with prevalence rates comparable with those of race-based discrimination. 84 Discrimination can result in low self-esteem and poor body image, which can negatively impact engagement in physical activity. 85 Obesity is also associated with psychiatric comorbidity. A cross-sectional US epidemiological survey showed that obesity (BMI > 30 kg/m 2 ) was associated with an approximately 25% increased odds of mood and anxiety disorders. 86 Similarly, another US epidemiological study involving 41,654 respondents in the National Epidemiologic Survey on Alcohol and Related Conditions showed that obesity was associated with an increased odds of alcohol use and mood, anxiety, and personality disorders, with odds ratio ranging from 1.28 to 2.08. 87 Increased BMI is also associated with an increased risk of suicidal ideation in women but not in men. 88 , 89
Obesity has a complex aetiology that requires a multifaceted strategy for prevention and treatment at a population and individual level. 90 The social ecological model can provide a framework to help identify the personal and environmental determinants of obesity which can facilitate the development of interventions. 91 Indeed, primary and secondary prevention of obesity requires input and collaboration from multiple bodies, such as the government, policy makers, legislative powers and healthcare system. Figure 1 provides an overview of selected interventions, superimposed onto a modified social ecological model, that have been implemented in different countries. No country has yet implemented a successful population-level strategy to reverse the rising trends of obesity. 1
Examples of selected interventions used by different countries to prevent and treat obesity displayed on a modified social ecological model.
UK, United Kingdom; US, United States.
The environment is obesogenic. Healthful messages from policy makers are often undermined by advertisements that promote large portions of highly palatable energy-dense processed foods and sugar-sweetened beverages, 92 which are key drivers of obesity. 93 The availability of fast-food outlets around schools may be associated with an increased risk of unhealthy eating patterns and childhood obesity, especially in deprived areas. 94 , 95 This could be curtailed by governments granting local authorities’ the power to restrict take-away outlets, especially close to schools. Furthermore, fast-foods are more readily available to both children and adults at any time of day through ordering via mobile phone applications; however, the implications of this on eating behaviour and childhood obesity remain to be elucidated. Policy makers should strongly consider implementing legislation regarding the age at which take-away foods can be purchased, and responsibility must be shared by local providers of fast-foods to enforce this legislation. 96 , 97 Clearly, labelling the calorie content of takeaway foods may also help consumers opt for more sensible food choices. 93
Obesity impacts the poorest in society. A UK study of 119,669 individuals aged 37–73 found a strong association between higher BMI and lower socioeconomic status, especially in women. 98 Similarly, a US study reported that overweight women are more likely to work in lower paying-jobs than non-overweight women and all men. 99 This health inequality is further compounded by the fact that fast-food availability is greater in areas of higher deprivation. 100 Taxation of unhealthy foods may be one strategy to limit the availability of fast-foods. Indeed, a tax on sugary-sweetened drinks in Mexico led to an average reduction of 7.6% in purchases of these beverages, 101 whilst a 21% reduction in consumption was observed amongst low-income neighbourhoods in California. 102 In the UK, the soft drinks levy has raised money from taxation to invest into physical activity and healthy eating in UK schools, 103 but whether any of these changes will prevent obesity remains to be seen.
Individuals with obesity face a pervasive form of social stigma due to their weight that subjects them to discrimination in employment, education and healthcare. In the workplace, there is a lack of legislation that protects the vast majority of individuals with obesity who experience discrimination. The UK Equality Act (2010) does not specifically prohibit discrimination against obesity 104 and in 2014, the European Court of Justice ruled that being severely overweight could be considered a disability yet obesity per se is not specified as a disabling condition in European Union (EU) employment law. 105 However, some US states have recently introduced legislation that protects against height and weight discrimination, 106 and legislation is a key step to tackling the stigma associated with obesity.
Recognising obesity as a disease rather than a lifestyle choice will address the fallacy that obesity is the fault of the individual due to laziness or gluttony and replace it with scientific knowledge that body weight is maintained within a relatively narrow individualised range by a precise subconscious homeostatic mechanism. 105 , 107 Changing this narrative is fundamental so that patients with obesity receive appropriate treatment because there is evidence that patients with obesity are not receiving appropriate referral to specialist services. Worldwide, 0.1–2% of eligible obese patients undergo bariatric or metabolic surgery. 108 In the UK, access to specialist weight management centres is variable in some areas and absent in others. Only 1% of patients who fulfil the National Institute of Clinical Excellence (NICE) eligibility for bariatric surgery are able to access this service in the UK. 109 Greater awareness of the efficacy and cost-effectiveness of surgical interventions for obesity and morbid obesity as well as pathways to access this service should be easily available for local clinicians so that their patients can receive appropriate treatment. 110 , 111
In 2012, the US Preventative Services Task Force recommended that all adults be screened for obesity and those with a BMI > 30 kg/m 2 should be offered referral for an intensive multicomponent behavioural intervention. 112 Screening may be one way to increase referral to specialist weight management centres and there is good evidence that treating patients with obesity early in their disease course, especially those with T2DM, can prevent or delay complications. 93
Patients with obesity can be challenging to manage because the causes and complications of the disease are patient specific and this requires bespoke management at a specialist multidisciplinary weight management centre. Behavioural interventions are fundamental to lifelong weight management, and unique strategies are required for weight loss, maintenance of weight loss and avoiding weight regain, all of which require motivation and commitment from patients. 93 This can be challenging because patients with obesity often have psychological, psychiatric and medical comorbidities that can negatively impact long-term adherence to behavioural interventions. 93 Data from two large randomised control trials of lifestyle interventions, the Diabetes Prevention Programme and the Look AHEAD trial, 113 , 114 suggest that frequency of patient contact, individualising patient care and face-to-face interventions were important predictors of weight loss. In a separate study, patients who attended group sessions every other week for 1 year after weight loss maintained 13 kg of their initial 13.2 kg weight loss, 115 which suggests that regular group sessions may prevent weight regain. However, implementing behavioural interventions can be difficult due to a lack of resources and time. Remotely delivered behavioural programmes via telephone or the internet are alternative approaches that may be more easily accessible and affordable. Patients who received 20 weight loss intervention phone calls over 6 months lost an average of 4.9 kg; those who received 10 calls lost 3.2 kg and those who were self-directed lost 2.3 kg. 116 In another study, patients who received 24 weekly bespoke weight loss sessions via email in addition to internet resources lost 4.4 kg after 1 year when compared with a group receiving internet resources only who lost 2.0 kg. 117 Despite their popularity, little is known about the effectiveness of smart-phone applications for weight management and therefore more research is needed.
Obesity is a multisystem disease that increases the risk of the most common non-communicable chronic diseases of the 21st century. 21 , 57 The population is developing obesity at a younger age and it is likely that these individuals will suffer morbidity for longer. 2 , 118 This will be challenging for clinicians because the symptom and disease burden from multi-organ impairment can become irreversible without timely intervention. Early identification of individuals with obesity through simple anthropometric measurements should be a priority for prompt interventions to prevent morbidity and the associated healthcare and economic costs. 119
Tackling obesity requires a whole systems approach. Governments and policy makers, rather than individuals, have the ability to change the food environment through regulation, taxation and restricting the availability of high-calorie processed foods to adults and children. Patients with obesity who face weight-based discrimination deserve policies and legislation that aim to prevent weight-based inequality. This will help change the current narrative that patients with obesity are to blame for their disease, which fuels a pervasive form of social stigma. Replacing this fallacy with scientific knowledge can prevent discrimination and facilitate referral to specialist weight management centres where a multidisciplinary team can provide bespoke patient care.
Author contribution(s): Saleem Ansari: Conceptualization; Writing-original draft; Writing-review & editing.
Nadim Haboubi: Conceptualization; Formal analysis; Supervision; Visualization; Writing-review & editing.
Conflict of interest statement: The authors declare that there is no conflict of interest.
Funding: The authors received no financial support for the research, authorship, and/or publication of this article.
Saleem Ansari, Clinical Biochemistry, King’s College Hospital, Denmark Hill, London, England SE5 9RS, UK.
Hasan Haboubi, Department of Gastroenterology, Guy’s & St Thomas’ Foundation trust, London, England, UK.
Nadim Haboubi, Consultant Physician, University of South Wales, Pontypridd, Rhondda Cynon Taff, UK.
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Nature Reviews Endocrinology volume 15 , pages 288–298 ( 2019 ) Cite this article
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The prevalence of obesity has increased worldwide in the past ~50 years, reaching pandemic levels. Obesity represents a major health challenge because it substantially increases the risk of diseases such as type 2 diabetes mellitus, fatty liver disease, hypertension, myocardial infarction, stroke, dementia, osteoarthritis, obstructive sleep apnoea and several cancers, thereby contributing to a decline in both quality of life and life expectancy. Obesity is also associated with unemployment, social disadvantages and reduced socio-economic productivity, thus increasingly creating an economic burden. Thus far, obesity prevention and treatment strategies — both at the individual and population level — have not been successful in the long term. Lifestyle and behavioural interventions aimed at reducing calorie intake and increasing energy expenditure have limited effectiveness because complex and persistent hormonal, metabolic and neurochemical adaptations defend against weight loss and promote weight regain. Reducing the obesity burden requires approaches that combine individual interventions with changes in the environment and society. Therefore, a better understanding of the remarkable regional differences in obesity prevalence and trends might help to identify societal causes of obesity and provide guidance on which are the most promising intervention strategies.
Obesity prevalence has increased in pandemic dimensions over the past 50 years.
Obesity is a disease that can cause premature disability and death by increasing the risk of cardiometabolic diseases, osteoarthritis, dementia, depression and some types of cancers.
Obesity prevention and treatments frequently fail in the long term (for example, behavioural interventions aiming at reducing energy intake and increasing energy expenditure) or are not available or suitable (bariatric surgery) for the majority of people affected.
Although obesity prevalence increased in every single country in the world, regional differences exist in both obesity prevalence and trends; understanding the drivers of these regional differences might help to provide guidance for the most promising intervention strategies.
Changes in the global food system together with increased sedentary behaviour seem to be the main drivers of the obesity pandemic.
The major challenge is to translate our knowledge of the main causes of increased obesity prevalence into effective actions; such actions might include policy changes that facilitate individual choices for foods that have reduced fat, sugar and salt content.
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Blüher, M. Obesity: global epidemiology and pathogenesis. Nat Rev Endocrinol 15 , 288–298 (2019). https://doi.org/10.1038/s41574-019-0176-8
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