Experimental biology can inform our understanding of food insecurity

Abstract

Food insecurity is a major public health issue. Millions of households worldwide have intermittent and unpredictable access to food and this experience is associated with greater risk for a host of negative health outcomes. While food insecurity is a contemporary concern, we can understand its effects better if we acknowledge that there are ancient biological programs that evolved to respond to the experience of food scarcity and uncertainty, and they may be particularly sensitive to food insecurity during development. Support for this conjecture comes from common findings in several recent animal studies that have modeled insecurity by manipulating predictability of food access in various ways. Using different experimental paradigms in different species, these studies have shown that experience of insecure access to food can lead to changes in weight, motivation and cognition. Some of these studies account for changes in weight through changes in metabolism, while others observe increases in feeding and motivation to work for food. It has been proposed that weight gain is an adaptive response to the experience of food insecurity as 'insurance' in an uncertain future, while changes in motivation and cognition may reflect strategic adjustments in foraging behavior. Animal studies also offer the opportunity to make in-depth controlled studies of mechanisms and behavior. So far, there is evidence that the experience of food insecurity can impact metabolic efficiency, reproductive capacity and dopamine neuron synapses. Further work on behavior, the central and peripheral nervous system, the gut and liver, along with variation in age of exposure, will be needed to better understand the full body impacts of food insecurity at different stages of development.

Keywords: Adaptive; Cognition; Food insecurity; Metabolism; Stress; Uncertainty.

Fig. 1.

Mechanisms by which experience of food insecurity impacts the brain. Environmental signals: an animal (once independent from parental care) can detect scarcity and uncertainty in the feeding environment by monitoring its foraging success. We posit that prediction errors in the dopamine system are likely to be larger and more frequent in animals experiencing food insecurity than in their more securely fed conspecifics (Lin et al., 2020). For younger animals (not shown) parental care quantity and quality may also reflect external conditions. Internal signals: the brain also receives input about stressors from corticosterone released from the adrenal glands and body condition through leptin signaling from adipose tissue. These signals may contribute to programming homeostatic systems in the brain which may be particularly sensitive to these changes during development. Circuitry: zooming in on the ventral portion of the brain, which has access to the circulating hormones, shows circuits that are implicated in the behavior and physiological outcomes of food insecurity. These include the ventral tegmental area (VTA) dopamine neurons, which send projections to the ventral striatum nucleus accumbens (NAc), and the hypothalamic arcuate nucleus (ARC) melanocortin neurons, which project to the paraventricular nucleus (PVH). The schematic diagram shows that leptin and ghrelin receptors are present in these systems, and studies of food insecurity and food scarcity have shown dysfunctional signals within them. These hypothalamus circuits may be particularly sensitive to food-related signals during gestation and the perinatal period, and striatal-dopamine circuits may be sensitive during the late juvenile/early adolescent period. By changing how these neurons function, experience of food insecurity can impact metabolic homeostasis and a wide range of behaviors. Figure made using BioRender.