Elsevier

Physiology & Behavior

Volume 162, 1 August 2016, Pages 88-92
Physiology & Behavior

Review
The food-insecurity obesity paradox: A resource scarcity hypothesis

https://doi.org/10.1016/j.physbeh.2016.04.025Get rights and content

Highlights

  • Mechanistic hypotheses explaining the food insecurity-obesity paradox do not exist.

  • A resource scarcity hypothesis is proposed to explain this paradox.

  • Implications of this theory for research and intervention are discussed.

Abstract

Food insecurity is paradoxically associated with obesity in the United States. Current hypotheses to explain this phenomenon are descriptive regarding the low food security population's dietary and physical activity habits, but are not mechanistic. Herein it is proposed that a resource scarcity hypothesis may explain this paradox, such that fattening is a physiologically regulated response to threatened food supply that occurs specifically in low social status individuals. Evidence that this may be occurring, the implications for addressing the food insecurity-obesity paradox, and future areas of research, are reviewed and discussed.

Introduction

Low food security is associated with obesity in some circumstances (reviewed in [1], [2]). Low food security, defined as, “reports of reduced quality, variety, or desirability of diet. Little or no indication of reduced food intake,” by the USDA, does not involve hunger, whereas very low food security, defined as, “Reports of multiple indications of disrupted eating patterns and reduced food intake,” is accompanied by hunger [3]. The prevalence of low food security has risen in the United States in the last 15 years, and was 10.7% of households in 2001, and peaked at 14.9% in 2011 following a spike during the Great Recession [4]. It is not well understood if low food security plays a causative role in the development of obesity, and if it does, what the mechanisms may be.

There are two predominant, related hypotheses that have been proposed to explain this link in the literature:

  • 1.

    Low food security is associated with obesity because of the high calorie, palatable food consumed by low food secure populations [5], [6].

  • 2.

    Low food security is associated with obesity because of the limited knowledge, time, and resources that low food-secure populations experience to engage in healthful eating and exercise.

Both hypotheses are descriptive, but not probative or mechanistic in nature, as an explanation for the relationship between low food security and obesity. For substantial weight gain to occur, energy intake must be greater than energy expenditure on a long-term, chronic basis. There is a physiologically regulated, adaptable system that is designed to resist weight change.

Therefore, although documenting increased intake of high-energy, palatable foods or reduced physical activity in low food secure populations may document crucial parts of a mechanism, neither is a probative mechanistic explanation. Concluding that the intake of high calorie foods is sufficient to explain weight gain in low food secure populations is similar to concluding that individuals with Prader-Willi Syndrome gain weight because of the food they eat.

Though it is true that Prader-Willi Syndrome patients do consume more food than they require, this does not explain how this occurs on a chronic basis. The presence of food and the intake of food is a permissive, but not causative factor in their weight gain. The neurobiological mechanisms that cause increased food intake and weight gain are becoming well understood [7] so that therapeutics can be developed. Similarly, although an abundance of high calorie, palatable food may be a crucial permissive factor in the development of obesity in low food secure populations, its presence alone does not explain how low food security may drive the development of chronic positive energy balance. It is crucial to understand why and how low food secure populations gain weight, and what about low food security may be a fundamental driver of a net, chronic shift in the homeostatic regulation of energy balance. Such a mechanistic explanation may lead to more effective, cause-specific interventions.

The need for a more probative mechanism to explain the link between low food secure populations and obesity is clear from the lack of results from interventions that focus on food, resources, and knowledge to reduce weight gain. For example, when exercise facilities are made available to low SES populations, they are often not utilized [8]. Similarly, providing monetary resources or food caused weight gain in a low SES population in rural Mexico [9]. In another study, increasing food stamp funds to $2000/year had no effect on social BMI disparities [10]. It is plausible that such interventions are ineffective because they are not addressing the root mechanisms behind low food security's association with weight gain and obesity.

A probative, mechanistic explanation for the relationship between low food security and obesity can be proposed from intersections in findings from the fields of evolutionary biology, ecology, and obesity (Fig. 1). This “Resource Scarcity Hypothesis” suggests that perceived food insecurity, in a permissive environment where there is access to high calorie foods, may cause positive energy balance specifically in low social status individuals, but not in high social status individuals. Evidence suggesting this may be the case is reviewed in the following sections.

Section snippets

Social status and metabolic efficiency

Social status may be associated with low energy expenditure and metabolic efficiency. Since low food security tends to be associated with low social status, the role of social status in determining metabolic efficiency may contribute to the development of obesity in this population. Both animal and human studies suggest that low social status organisms may be more metabolically efficient.

For example, dominant mice have higher energy expenditure compared to subordinate mice, and are more obesity

Social status and excess food intake

Some evidence suggests that social rank may not only influence energy expenditure and metabolic efficiency, but energy intake as well. In animals, several experiments suggest social hierarchy has a causative influence on energy intake. Subordinate primates consistently consume more energy than dominant primates, regardless of diet type available (high or low-fat) [14]. This effect seems to be enhanced in the presence of a palatable, high fat diet. While both dominant and subordinate primates

Evidence that low food security influences body fat stores selectively in low social status individuals

In animals, an unpredictable or threatened food supply, in comparison to a predictable and secure food supply, has an influence on body weight and body fat stores, and the effect may be pronounced in low social status organisms in particular. For example, when female rats undergo just 5% energy restriction, they respond paradoxically by increasing fat stores [25]. In animals, experimental manipulation or natural circumstances that threaten the perception of food security increase body fat in

Potential physiological mechanisms linking low food security and social status with weight gain

Cortisol metabolism may mediate weight gain in response to low food security in low social status individuals. Low social status is associated higher basal cortisol levels, lower cortisol reactivity to acute stress, and a lack of cortisol habituation [34], [35], [36]. Impaired cortisol habituation is hypothesized to be a robust indicator of cumulative exposure to elevated cortisol that may accompany repeated exposure to stress [37]. Thus, higher basal cortisol, and lower cortisol habituation

Implications of the resource scarcity hypothesis in addressing the food insecurity-obesity paradox

If fat gain is a physiologically regulated, strategic response to low food security to ensure survival and reproduction, this would have several implications. First, interventions that seek to educate low food security populations about reducing energy intake and increasing energy expenditure may be insufficient to address the underlying problem, and therefore be unproductive. A lack of effect of such interventions is reflected in the literature [8], [9], [10].

On the other hand, the “Moving to

Acknowledgements

I would like to thank Drs. David Allison, Kathryn Kaiser, Gregory Pavela, and Michelle Cardel, as conversations with each of them have contributed in some way to the ideas presented in this paper. Also, this work was supported by Award Number P30DK056336 from the National Institute of Diabetes and Digestive and Kidney Diseases. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Diabetes and Digestive and

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