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Should obesity be recognised as a disease?

BMJ 2019; 366 doi: https://doi.org/10.1136/bmj.l4258 (Published 17 July 2019) Cite this as: BMJ 2019;366:l4258

Re: Should obesity be recognised as a disease?

Obesity rates are unprecedented in human history and should be regarded as a public health emergency.

The obesity epidemic started in the 1970s, initially in the US and subsequently spreading worldwide.1 Approximately 60-80% of adults, and 20-30% children in most Western countries are now overweight or obese, which is unprecedented in human history.2-4 Should this change be regarded as a consequence of individual choices (on a mass scale) or a disease affecting the population, and a public health emergency?

Obesity is not just a cosmetic or lifestyle problem. In parallel to the obesity epidemic, we have seen an increase of metabolic diseases, such as diabetes, non alcoholic fatty liver disease, not just in adults, but also in children.5 Currently, the global prevalence of diabetes is 8.8% and pre-diabetes is much higher.6 Additional physical complications include osteoarthritis, cardiovascular disease and several cancers.7 Furthermore, the prevalence rate of eating disorders has also been increasing, and is now the highest among those with class III obesity.8 9 A recent population-based Australian study examined the trends from 1995 to 2015 and found significant increases in the prevalence of both obesity (19 to 33%) and binge eating (3 to 11%). The highest increases were in the prevalence of obesity with comorbid binge eating (7.3-fold), or obesity with comorbid very strict dieting/fasting (11.5-fold) 10

Despite intensive research, the causes of the obesity epidemic remain much debated.3 11 The prevailing view has been that this is a question of energy imbalance between input and expenditure. Whilst this may be true in principle, the calorie in and out hypothesis does not explain the reasons for the overconsumption that affects approximately 80% of the population.

The biological and metabolic effects of modern foods have been studied using the ‘cafeteria diet’ model in animals, in which researchers replace standard chow with human cafeteria foods: cookies, cereals, cheese, processed meats, crackers, all high in sugars, vegetable oils and additives. Animals fed on these foods exhibit voluntary hyperphagia, which results in dramatic weight gain. Furthermore, cafeteria diet feeding promotes a prediabetic condition with elevated glucose, insulin, and nonesterified fatty acids, accompanied by decreased insulin tolerance. In addition, chronically inflamed liver and adipose tissues and distorted pancreatic islet architecture develop. 12 13 Furthermore, the cafeteria diet has a profound impact on the gut microbiome, which, may be driving important features of metabolic syndrome14 by influencing host metabolism and can also affect brain function and behaviour through the microbiota-gut-brain axis.15 16

These experimental data mirror the human experience: since the introduction of ultra-processed foods, the majority of the population overeat. Furthermore, the same increase of low grade inflammation is seen in human metabolic disorders, and binge eating disorder.17

A recent, carefully controlled human trial confirmed that participants consumed 500kcal/day in excess when they were placed on an ad libitum, ultra-processed diet, as compared with a minimally processed one, with profound changes in metabolic parameters.18 The appetite-suppressing hormone peptide tyrosine tyrosine (PYY) increased during the unprocessed diet as compared with both the ultra-processed diet and baseline. In contrast, the hunger hormone ghrelin, fasting glucose and insulin levels were increased during the ultra-processed diet. This is a groundbreaking randomised controlled trial, demonstrating that ultra-processed foods lead to overeating in humans through altering multiple endocrine pathways.

The decades of guidelines promoting reduced calorie intake and increased exercise have been ineffective in halting the obesity epidemic,19 despite this message being amplified by the diet and weight loss industries. The ‘eat less and exercise more’ message may have also contributed to the increasing rates of eating disorders, which affect now 4-6% of the population. A recent large study showed since the 1980s BMI has increased for both genetically predisposed and non-predisposed people, confirming that the environment remains the main contributor to the obesity epidemic.11

Recognising obesity as a disease can transform public health policies, and clean up the food environment, which is harming the health of millions of people, and it can be cost effective for the economy by reducing health care costs.20

1. Nghiem S, Vu XB, Barnett A. Trends and determinants of weight gains among OECD countries: an ecological study. Public Health 2018;159:31-39. doi: 10.1016/j.puhe.2018.03.004
2. Peralta M, Ramos M, Lipert A, et al. Prevalence and trends of overweight and obesity in older adults from 10 European countries from 2005 to 2013. Scand J Public Health 2018;46(5):522-29. doi: 10.1177/1403494818764810
3. Rodgers A, Woodward A, Swinburn B, et al. Prevalence trends tell us what did not precipitate the US obesity epidemic. Lancet Public Health 2018;3(4):e162-e63. doi: 10.1016/S2468-2667(18)30021-5
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7. Bluher M. Obesity: global epidemiology and pathogenesis. Nat Rev Endocrinol 2019;15(5):288-98. doi: 10.1038/s41574-019-0176-8
8. Nagata JM, Garber AK, Tabler JL, et al. Prevalence and Correlates of Disordered Eating Behaviors Among Young Adults with Overweight or Obesity. J Gen Intern Med 2018;33(8):1337-43. doi: 10.1007/s11606-018-4465-z
9. Duncan AE, Ziobrowski HN, Nicol G. The Prevalence of Past 12-Month and Lifetime DSM-IV Eating Disorders by BMI Category in US Men and Women. Eur Eat Disord Rev 2017;25(3):165-71. doi: 10.1002/erv.2503
10. da Luz FQ, Sainsbury A, Mannan H, et al. Prevalence of obesity and comorbid eating disorder behaviors in South Australia from 1995 to 2015. Int J Obes (Lond) 2017;41(7):1148-53. doi: 10.1038/ijo.2017.79
11. Brandkvist M, Bjorngaard JH, Odegard RA, et al. Quantifying the impact of genes on body mass index during the obesity epidemic: longitudinal findings from the HUNT Study. BMJ 2019;366:l4067. doi: 10.1136/bmj.l4067
12. Sampey BP, Vanhoose AM, Winfield HM, et al. Cafeteria diet is a robust model of human metabolic syndrome with liver and adipose inflammation: comparison to high-fat diet. Obesity (Silver Spring) 2011;19(6):1109-17. doi: 10.1038/oby.2011.18
13. Buyukdere Y, Gulec A, Akyol A. Cafeteria diet increased adiposity in comparison to high fat diet in young male rats. PeerJ 2019;7:e6656. doi: 10.7717/peerj.6656
14. Del Bas JM, Guirro M, Boque N, et al. Alterations in gut microbiota associated with a cafeteria diet and the physiological consequences in the host. Int J Obes (Lond) 2018;42(4):746-54. doi: 10.1038/ijo.2017.284
15. Holder MK, Chassaing B. Impact of food additives on the gut-brain axis. Physiol Behav 2018;192:173-76. doi: 10.1016/j.physbeh.2018.02.025
16. van de Wouw M, Schellekens H, Dinan TG, et al. Microbiota-Gut-Brain Axis: Modulator of Host Metabolism and Appetite. J Nutr 2017;147(5):727-45. doi: 10.3945/jn.116.240481
17. Succurro E, Segura-Garcia C, Ruffo M, et al. Obese Patients With a Binge Eating Disorder Have an Unfavorable Metabolic and Inflammatory Profile. Medicine (Baltimore) 2015;94(52):e2098. doi: 10.1097/MD.0000000000002098
18. Hall KD, Ayuketah A, Brychta R, et al. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab 2019;30(1):67-77 e3. doi: 10.1016/j.cmet.2019.05.008
19. Afshin A, Micha R, Webb M, et al. Effectiveness of Dietary Policies to Reduce Noncommunicable Diseases. In: rd, Prabhakaran D, Anand S, et al., eds. Cardiovascular, Respiratory, and Related Disorders. Washington (DC)2017.
20. Lustig RH. Processed Food-An Experiment That Failed. JAMA Pediatr 2017;171(3):212-14. doi: 10.1001/jamapediatrics.2016.4136

Competing interests: No competing interests

07 August 2019
Agnes Ayton
Consultant psychiatrist
Ali Ibrahim, MBBs, MRCPsych South London and Maudsley NHS foundation trust
Oxford Health NHS Foundation Trust
Oxford Health NHS Trust, Cotswold House Oxford