When you want to investigate something using the scientific method, first you create a model that you hope describes a natural phenomenon-- this is called a hypothesis. Then you go about testing that model against reality, under controlled conditions, to see if it has any predictive power. There is rarely a single experiment, or single study, that can demonstrate that a hypothesis is correct. Most important hypotheses require many mutually buttressing lines of evidence from multiple research groups before they're widely accepted. Although it's not necessary, understanding the mechanism by which an effect occurs, and having that mechanism be consistent with the hypothesis, adds substantially to the case.
With that in mind, this post will go into greater detail on the evidence supporting food reward and palatability as major factors in the regulation of food intake and body fatness. There is a large amount of supportive evidence at this point, which is rapidly expanding due to the efforts of many brilliant researchers, however for the sake of clarity and brevity, so far I've only given a "tip of the iceberg" view of it. But there are two types of people who want more detail: (1) the skeptics, and (2) scientifically inclined people who want mechanism. This post is for them. It will get technical at times, as there is no other way to convey the material effectively.
First, some definitions. One of the problems with food reward is it's defined differently by different people, even researchers, and often it isn't defined at all. As defined in previous posts, I use the term food reward to refer specifically to the motivational value of food, i.e. its ability to reinforce behavior. For example, acquiring a taste that causes a person to seek out the food in question more often. This is how some, but not all, researchers define the term. Others use the term "food reward" to refer to both the motivational and the palatability value of food. Palatability refers specifically to the enjoyment derived from a food, also called its hedonic value. Palatability and reward typically travel together, but not always.
The food reward hypothesis of obesity states that the reward (reinforcing, motivational) and hedonic (pleasure, palatability) value of food influence food intake and body fatness, contributing to the development of obesity. Quite a bit is known about the central nervous system (CNS, i.e. brain) circuitry that underlies reward and hedonic processing, and how this circuitry influences food intake and body fatness. Most of the research on reward and hedonic processing began with the study of drug addiction in animals and humans, however these circuits evolved to guide behaviors that enhance fitness in the natural environment such as those relating to food and sex, and research also focuses on these processes.
Although food reward and food palatability typically occur together, they are not the same thing. In the 1990s, Dr. Kent Berridge proposed that behavioral and CNS responses to food can be divided into "wanting", corresponding to the reward/motivational aspects of food, and "liking", corresponding to the hedonic/palatability aspects of food, and this framework has been a good fit for the evidence since then (1). These two elements can be separated from one another experimentally, and sometimes in daily life as well. One example is a person who is addicted to a drug despite no longer deriving pleasure from it. This is a case of strong "wanting" without "liking".
Brain Circuits and Neurotransmitters Underlying Food Reward and Hedonic Processing
The fact that the reward and palatability value of food can be experimentally dissociated implies that they are mediated by distinct CNS circuits. Indeed, although reward and hedonic circuits overlap to some degree and influence one another, each system has its own unique circuitry and suite of chemical neurotransmitters. CNS regions important for reward processing include the orbitofrontal cortex, amygdala, nucleus accumbens, dorsal striatum, ventral tegmental area, substantia nigra and the lateral hypothalamus (2). Dopamine signaling in these areas is a particularly important component of reward, but has little impact on hedonic processes (3). Dopamine isn't so much a pleasure chemical as it is a reward/motivation chemical.
CNS regions important for processing food-related hedonic information include the brainstem, pons, nucleus accumbens, ventral pallidum, amygdala, insula and prefrontal cortex (4). Note that these overlap somewhat with brain regions that process reward information, but in some cases the subregions or neuron sub-populations that mediate these two processes are distinct even within the same general CNS region. Opioid signaling in these regions is a major factor in hedonic processing, but has less impact on reward functions (5, 6). Opioids, in certain parts of the brain, are pleasure chemicals.
Another class of chemical signals worth mentioning is the endocannabinoids. The endocannabinoid receptor CB1 was identified as the brain receptor for delta-9-THC, the primary psychoactive constituent of marijuana, and then the endogenous ligands for the cannabinoid receptors were discovered (7). We now know that the main two endogenous ligands are anandamide and 2-arachidonylglycerol, and the two receptors are CB1 and CB2. Endocannabinoid receptors are expressed in CNS regions related to reward and hedonic processing, and they are known to be involved in both processes.
In addition to these three chemical systems (dopamine, opioids and endocannabinoids), there are other neurotransmitters that are intimately involved such as glutamate and GABA, but these are not specific to reward and hedonic processes since they are the primary excitatory and inhibitory neurotransmitters of the brain, respectively. So their involvement in reward and hedonic processing depends strictly on which neurons they're acting on.
Testing the Food Reward Hypothesis
If the food reward hypothesis is correct, we should expect to observe certain things:
1. Increasing the reward/palatability value of the diet should cause fat gain in animals and humans.
2. Decreasing the reward/palatability of the diet should cause fat loss in animals and humans that carry excess fat.
3. Individual sensitivity to food reward should predict future fat gain.
4. Brain circuitry that controls motivational and hedonic processing should interact with circuits that control food intake and body fatness.
5. Manipulation of reward and hedonic circuits in the brain (e.g., by lesion, drugs or genetic manipulation) should impact food intake and body fatness.
6. Genetic differences that influence reward and/or hedonic circuits should correlate with differences in body fatness.
7. On a cultural level, obesity prevalence should track with changes in the reward/palatability value of prevailing diet patterns.
In the next post, I will explore whether or not the evidence is consistent with these predictions.