Estimating the effect of calorie menu labeling on calories purchased in a large restaurant franchise in the southern United States: quasi-experimental study

The calorie in, calorie out hypothesis is fundamentally flawed and calorie labelling is at best ineffective, or at worst harmful

We would like to congratulate Petimar and colleagues for their innovative study on the effects of calorie labelling on food consumption.[1] In contrast with the Kaur and Brigg editorial,[2] we regard the paper an important nail in the coffin of the ‘calorie in and calorie out’ hypothesis.

The calorie was first introduced as a unit of heat energy by Clément in the 1820s, but it remained a scientific measure until the first dietary guidelines in 1977,[3 ] which introduced calorie counting for the population as a tool for monitoring dietary intake and weight control. It has failed spectacularly. Since then, we have seen an explosion of the obesity epidemic to levels unprecedented in human history, [4-7] leading to an increase of metabolic diseases, such as diabetes, non alcoholic fatty liver disease, and eating disorders not just in adults, but also in children.[8]

The various public health interventions to stop the obesity epidemic have repeatedly reinforced the message to restrict calories, and move more. For example, Public Health England actively promotes calorie reduction[9] by advocating calorie counting from a very young age, including advocating 100 kcal snacks for children (https://www.nhs.uk/change4life/food-facts/healthier-snacks-for-kids/100-...), and 400+600+600 kcal meals for adults (https://publichealthmatters.blog.gov.uk/2018/03/06/why-we-are-working-to...).

While we welcome efforts to address the obesity epidemic, it is important to dispel misunderstandings that may have inadvertently contributed to the issue, as continued use of these failed strategies and ideas could contribute to making the situation worse. The participants in Petimar’s study reduced the calories per purchase by a small amount in the first year, but calorie intake actually increased in the second year and we do not know what happened thereafter. The real question is whether the small reduction in calories per purchase translates into change of total dietary intake, as well as meaningful and sustained weight loss or improvements in metabolic health.

There are multiple problems with the calorie in, calorie out hypothesis and promoting calorie counting. In addition to implying that obesity is a result of individual failure in the context of widely available hyper-palatable foods, the calorie in, calorie out hypothesis disregards the parallel roles of multiple neuro-endocrine systems, which directly impact both appetite regulation and metabolism and are influenced by types of food eaten and where these calories are derived from. The human body is not a bomb calorimeter. It has different metabolic pathways for different nutrients, such as fats, carbohydrates and protein, with separate pathways to the brain to regulate food intake.[10] Not all calories are equal, have the same impact or are used by the body in the same way. Additionally, uncoupling proteins found in brown adipose tissue, muscles and other cells convert calories into heat. Individuals have different amounts of brown adipose tissue, muscle mass, and uncoupling proteins, and this means a calorie cannot be predicted to have the same impact between different individuals. Once you add the multiple mechanisms involved (some of which we know about and possibly many others science is yet to discover), calculating calorific intake, and reducing it, becomes a highly unreliable way of addressing obesity.

We are today surrounded by low fat and calorie counted products. They are promoted and seen as healthier options by the population. The sports industry and smart phone applications measure our activity, calculate calorie intake and expenditure. Not only has there been a parallel continued increase in obesity despite these changes to our food and sophisticated monitoring techniques, they have also contributed to the increased rates of dieting and disordered eating.[11] It it clear that these interventions used to address the problem have indeed contributed to worsening the situation. Is it not time to stop, take stock and re-evaluate this strategy, as it has clearly been ineffective to halt the obesity epidemic?

Alternative models used to understand the obesity epidemic include the carbohydrate-insulin model,[12] which focuses on the endocrine and metabolic effects of food. It is based on the role of the anabolic hormone insulin as an important factor. Insulin is secreted in response to carbohydrates and sugar and plays multiple roles that include stimulating glucose up-take into tissues, suppressing release of fatty acids from adipose tissue, inhibiting production of ketones in the liver, and promoting fat and glycogen deposition. Increased insulin is associated with increased appetite and weight gain.[13] This model provides a framework for understanding how the modern food environment with its ultra-processed foods, heavily loaded with carbohydrates, results in hormonal changes that promote calorie deposition in adipose tissue, and exacerbate hunger. [14] In traditional societies, access to high sugary foods was limited to fruit or honey, and these were seasonal in most latitudes. The consumption of refined sugars only became widespread from the 19th century onwards. Furthermore, different types of sugars have been shown to have different effects on hunger, satiety and the interpretation of food cues by the brain, as demonstrated by recent FMRI studies.[15] It has been suggested that glucose could be more satiating as compared with fructose, which results in increasing the brain reactivity to food cues.[16] Large amounts of fructose overwhelm the normal mechanism of intestinal fructose absorption, resulting in fructose reaching both the liver and colonic microbiota, initiating the processes leading to metabolic disease, fatty liver disease and insulin resistance, and obesity.[17] This was not an issue in the human diet until recently, when fructose became available in endless quantities all year round compared to the seasonal consumption humans had previously been adapted to. This mechanism of dealing with short periods of excess fructose may have had an evolutionary advantage by increasing fat storage in preparation for winter shortages.[18] The modern diet, however, abuses this ancient mechanism by the constant stream of high amounts of fructose, which contribute to metabolic disorders and obesity. Despite this, current dietary guidelines recommend 45-65% of energy intake from carbohydrates. We should be asking serious questions as to whether current guidelines and our food environment are addressing the problem of obesity, or indeed contributing to it.

Public health interventions need to move away from attempting to reduce calories to consider the effects of the modern food environment on eating behaviours and appetite.

1. Petimar J, Zhang F, Cleveland LP, et al. Estimating the effect of calorie menu labeling on calories purchased in a large restaurant franchise in the southern United States: quasi-experimental study. BMJ 2019;367:l5837. doi: 10.1136/bmj.l5837
2. Kaur A, researcher, Briggs ADM, et al. Calorie labelling to reduce obesity. BMJ 2019;367:l6119. doi: 10.1136/bmj.l6119
3. USDA. Dietary Guidelines Advisory Committee Report. Appendix 5: History of the Dietary Guidelines for Americans, 2005.
4. 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
5. 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
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8. Rodriguez LA, Madsen KA, Cotterman C, et al. Added sugar intake and metabolic syndrome in US adolescents: cross-sectional analysis of the National Health and Nutrition Examination Survey 2005-2012. Public Health Nutr 2016;19(13):2424-34. doi: 10.1017/S1368980016000057
9. Public Health England. Calorie reduction: The scope and ambition for action. London, UK, 2018.
10. Small DM, DiFeliceantonio AG. Processed foods and food reward. Science 2019;363(6425):346-47. doi: 10.1126/science.aav0556
11. Eikey EV, Reddy MC, Booth KM, et al. Desire to Be Underweight: Exploratory Study on a Weight Loss App Community and User Perceptions of the Impact on Disordered Eating Behaviors. JMIR Mhealth Uhealth 2017;5(10):e150. doi: 10.2196/mhealth.6683
12. Ludwig DS, Ebbeling CB. The Carbohydrate-Insulin Model of Obesity: Beyond "Calories In, Calories Out". JAMA Intern Med 2018 doi: 10.1001/jamainternmed.2018.2933
13. Astley CM, Todd JN, Salem RM, et al. Genetic Evidence That Carbohydrate-Stimulated Insulin Secretion Leads to Obesity. Clin Chem 2018;64(1):192-200. doi: 10.1373/clinchem.2017.280727
14. Juul F, Martinez-Steele E, Parekh N, et al. Ultra-processed food consumption and excess weight among US adults. Br J Nutr 2018;120(1):90-100. doi: 10.1017/S0007114518001046
15. Jastreboff AM, Sinha R, Arora J, et al. Altered Brain Response to Drinking Glucose and Fructose in Obese Adolescents. Diabetes 2016;65(7):1929-39. doi: 10.2337/db15-1216
16. van Opstal AM, Kaal I, van den Berg-Huysmans AA, et al. Dietary sugars and non-caloric sweeteners elicit different homeostatic and hedonic responses in the brain. Nutrition 2018;60:80-86. doi: 10.1016/j.nut.2018.09.004
17. Kroemer G, Lopez-Otin C, Madeo F, et al. Carbotoxicity-Noxious Effects of Carbohydrates. Cell 2018;175(3):605-14. doi: 10.1016/j.cell.2018.07.044
18. Johnson RJ, Andrews P, Benner SA, et al. Theodore E. Woodward award. The evolution of obesity: insights from the mid-Miocene. Trans Am Clin Climatol Assoc 2010;121:295-305; discussion 05-8.