Perspective: Do Scientists Become Part of the Obesity Problem?

Abstract

Obesity is fundamentally a condition where physiology and behavior of individuals meet the environment, and the emerging global obesity pandemic reflects the contribution of a wide range of cultural, societal, economic and systemic driving forces. Today, different areas of obesity research are relatively separated from each other in discrete silos, with biomedical research determining most of our understanding and solution strategies. This has led to the Y in the road, which means the questionable assumption that effective drug treatment of individual patients is also an effective measure to improve population health. Since human obesity is a condition of population health and planetary impact a better integration of biomedical and public health approaches is based on critical (self-)reflection and communicative understanding of scientists from various research areas who should be on an equal footing.

Introduction

Although population-wide obesity is a public health issue, with implications for planetary sustainability [1], its solution is still widely regarded as a biomedical issue [2]. Accordingly, the wide-spread acceptance of new anti-obesity drugs may suggest that we should accept the epidemic and drug-treat it, not fight it [3]. Presently, there are different perceptions of obesity itself: looking at the same phenomenon, protagonists of biomedicine consider obesity as a disease, where effective therapeutics for obesity management are needed [2–4] whereas public health scientists see increasing fatness as the result of a normal response, by normal people, to an abnormal unhealthy environment, and where structural and political strategies may add to solutions [5]. Since biomedical and the public health experts may have lost sight of each other we feel that they are at risk to become part of the obesity problem.

The Medical Model

Today, obesity is primarily approached using a conceptual framework of endogenous causes, relating to the neurobiology of appetite control and energy balance dysregulation [3]. Consequently, research is directed to pharmacological solutions as an adjunct to lifestyle interventions [2–4], which have led us to the Y of the road suggesting that treatment of patients is a solution of the population-wide obesity issue.

Biomedical research favors personalized strategies of prevention and treatment of obesity which assume that an individual’s unique response to the same diet or to an identical lifestyle change is reproducible. However, as far as human studies are concerned, intraindividual reproducibility of changes in body weight, body composition and metabolism in response to over- and underfeeding have rarely been studied. Recent data suggest that while there is reproducibility with underfeeding, this may not be true for the human response to controlled overfeeding [6]. Replicability and reproducibility are major problems of investigations since many outcomes of biomedical obesity research have only been disclosed on a single occasion.

The Societal Model

Obesity is a condition in which physiology meets the “everyday living environment” that includes the physical as well as the lived environment, collectively dependent on the experience and background of an individual [7]. This interface is mediated by behavior, and the activities of other individuals and entities whose interests shape the obesogenic niche. The “everyday living environment” is not stable or uniform; even in the same built, cultural and social environment, different people interact with different environments (which may drive behaviors and serve as barriers; see Fig. 1) and differ in their “being in the world” [8]. In addition, the behavior of any individual may vary across days and even within any day.

Fig. 1.

The medical model of obesity looks at the endogenous biological causes of obesity. The societal model of obesity is a way of viewing the world, developed by people with obesity suggesting that the society is to blame that obesity is seen as a problem. The model says that people are obese by barriers in society (e.g., by stigma), not by their difference. The global-syndemic model of obesity is an alternative way of viewing the world as structural and social exogenous factors that reinforce each other and precipitate the clustering of obesity, malnutrition, and planetary health.

Addressing Endogenous and Exogenous Causes of Obesity

Today, there still is little consensus about possible molecular causes, their sequence of appearance or how they contribute to the onset of human obesity. In addition, no clinical treatment (counselling, medication or bariatric surgery) can tackle the cultural, societal, and economic drivers of obesity (see ref. [5, 9]). Just as with endogenous causes, the role of exogenous causes could be revealed by carefully controlled scientific studies. The key difference is that the point of intervention should be environmental factors, rather than individuals. For example, recent cluster-randomized intervention studies conducted at the level of the environment have been shown to improve healthy behaviors, reducing BMI and the health risks of individuals [10]. Another example is a randomized social experiment showing that the opportunity to move from a neighborhood with a high level of poverty to one with a lower level of poverty was associated with modest but potentially important reductions in the prevalence of extreme obesity and diabetes [11]. Such studies robustly show therefore that some causes of obesity are located beyond individuals. However, there remains a huge imbalance in the volume of research that targets individual-level versus environment-level causes of obesity. In turn, we argue, this may lead to a misleading notion of the endogenous causes of obesity that are most appropriate for action. The two questions then arise that if we simply treat obesity by drugs, as now seems the dominant view, can we solve the global obesity epidemic and can the planet survive?

The Global-Syndemic Model

The global obesity epidemic reflects the influence of changes in cultural, societal, built, economic, and ecological environments that foster behaviors that promote weight gain, as well as a failure to develop successful strategies at scientific, cultural, societal, and policy levels to tackle these trends [1, 5, 7, 9]; (Fig. 1). Although it is widely held that, for individual health as well as for cost-efficacy, prevention is better than cure, prevention of obesity is rarely given the highest priority. Obesity prevention requires fundamental insights into its systemic drivers as well as power of persuasion, consensus, public engagement, and political will, which can only emerge from a broad perspective of obesity [1, 7]. Thus, to effectively address the global health issue, rigorous and transformative scientific approaches must be applied to mechanisms of social, ecological, and economic development driving population-wide obesity. The obesity pandemic was and is associated with “nutrition transition,” characterized by the integrated globalization and expansion of industrial food systems, resulting in high productivity (e.g., of ultra-processed foods), food security, increased market penetration [1, 12]. On this basis, the obesity pandemic may be seen as a symptom, resulting from a culture and economic strategies that restrict autonomous action of individuals and thus, actively promote overconsumption and underactivity as well as a stressful life to “drive” economic growth [1, 7, 9]. Besides its physiological basis, population-wide obesity may be seen as a “wicked” problem where obesity is advantageously perceived as a system in which some interest groups gain payoffs [9, 12].

Research and Solutions of the Population-Wide Obesity Issue

Unsustainable solutions to the public health issue of obesity are frequently attributed to a complex interplay of genetic, metabolic, behavioral, and environmental factors [2, 4]. However, some simplifications may impact this interpretation, such as characterizing the phenotype of adult obesity using a single dichotomous BMI threshold or the degree of excess fat that causes deleterious health effects [13]. In addition, our current research strategies and academic systems tend to favor subject-specific expertise and narrow specialisms [14], where academic research is under the dictates of productivity, effectiveness, and performance promoting a new habitus of scientists as well as a success-oriented appreciation in the culture of science [15]. Taking this point of view biomedical research rather than public health research promises chances of success and economic profits.

Going beyond the Horizon

It is a challenging and provocative hypothesis that taking a public health and global perspective modern biomedical research on human obesity may not add much to population-wide solutions of the problem. The same economic processes are currently endangering the health of people as well as planetary health [1]. Even if we could neutralize the health impacts of obesity with pharmacological treatments, we would still have to care about its high impact on social inequalities and on planetary health. The multifactorial etiology of obesity requires crossing disciplinary boundaries and establishing think-tanks that can synthesize interdisciplinary knowledge and provide new concepts and strategies for solution-oriented obesity research (Fig. 1), e.g., a scientific approach addressing food systems is required to find shared solutions of the issues of obesity, NCD, and planetary health [1, 7, 9, 12, 16].

Conclusions

Future science about human obesity should conduct complementary research on both, the endogenous and exogenous causes of obesity. Presently, obesity researchers need to engage with the Y in the road and realize that drug treatment is another silo. If we miss that discussion, scientists may become part of the obesity problem itself. Following the great philosopher Jürgen Habermas, a solution is based on an appropriate use of rationality (to deal appropriately with criticism) and communicative understanding [17].

Acknowledgments

The authors wish to thank Prof. John Blundell (Leeds) who had contributed to the discussion of a very 1st version of the manuscript.

Conflict of Interest Statement

The authors have no conflicts of interest.

Funding Sources

There was no funding.

Author Contributions

M.J.M. conceived the manuscript and wrote the first draft version. All authors (M.J.M., A.-B.W., J.C.K.W.) equally contributed to the discussion and writing of the final version; they all have read and approved the final manuscript.

Funding Statement

There was no funding.