T HE R ELATIONSHIP BETWEEN C ARBOHYDRATES AND E NDOGENOUS O PIOIDS

13.2.2 T HE R ELATIONSHIP BETWEEN C ARBOHYDRATES AND E NDOGENOUS O PIOIDS

Opioids comprise families of peptides, including the endorphins, enkephalins, dynor- phins, and many nociceptins, and a variety of receptor subtypes. These peptides are found in a variety of networks in the brain, especially in areas that are involved in regulating emotions, responses to pain and stress, endocrine regulation, and food

intake. 35 Because of this extensive distribution of opioids throughout the brain and the regions they innervate, it has been hypothesized that these peptides play a role in many biological and psychological processes, such as food intake, reinforcement, pain modulation, affect and emotion, and response to stress. 35,36

I will focus on the effect that endogenous opioids exert on food intake and affect. Considerable evidence has accumulated revealing that endogenous opioids influence food intake. In general, it has consistently been demonstrated that endog- enous aPD antagonists decrease food intake, whereas agonists increase food intake

(see Mercer and Holder 37 for a review). Although there is considerable agreement that opioids are involved in food intake, the precise nature of the relationship has not been determined. However, there is increasing evidence and agreement that

opioids regulate the palatability or hedonic value of food, 36 or what Berridge 38 has called the liking value of food. The suggestion that endogenous opioids mediate the reward value or liking of food 38 is based on studies demonstrating that aPD antagonists selectively decrease and aPD agonists selectively increase the palat- ability of sweet-tasting food. 35–38 For example, Fantino et al. 39 has demonstrated that the aPD antagonist naltrexone reduces subjective ratings of sweetness. Drewnowski et al. 40 revealed that the aPD antagonist naloxone reduced hedonic preference for sugar–fat mixtures among female binge eaters and controls, but did not affect perceived hunger. Similarly, it has been demonstrated that animals show

a decrease in the palatability of sweet substances following the administration of an aPD antagonist and an increase in the palatability of sweet foods following administration of an aPD agonist. 35–37

If opioids mediate the liking or palatability of food, then the consumption of palatable foods should activate the aPD systems. There are several lines of evidence to suggest that this effect does occur. Studies (see Mercer and Holder 37 for a review) have revealed that consumption of sweet high-fat foods results in the release of beta- endorphins in the hypothalamus and alters pain perception in both rats and humans. For example, sucrose reduces infants’ crying that is provoked by some standard painful hospital procedures. Additionally, electrical stimulation of areas of the brain that are involved in reward are also those brain areas that are involved in feeding. Electrical stimulation of the lateral hypothalamus, for example, is not only rewarding, but also induces feeding. However, aPD antagonists inhibit the electrical induced feeding, probably by reducing the ability of the electrical stimulation to enhance the

reward value of the food consumed (see Carr 41 for a review). The research provides strong evidence indicating that endogenous opioids exert

a powerful affective state that is summarized by the terms palatability or liking. This positive state is strong enough to entice animals to engage in learning to obtain intravenous opiates, suggesting that opiates play an important role in brain

Dietary Carbohydrates as Mood and Performance Modulators

reinforcement. 35,36 Because food palatability or the liking component of food is mediated by aPD activity, several investigators 37,40,42 have hypothesized that endog- enous aPD peptides mediate behaviors such as food cravings and binge eating. While it may seem logical that a brain substrate that modulates our liking for food would induce cravings and binge eating, there are apparently two components involved in the seeking out and consumption of food. Food reward includes both

liking and wanting. 38 The liking component is mediated by endogenous opioids and represents the affective reaction to the consumption of food. It is the reaction to having consumed a food. The wanting component refers to the craving or incentive to seek out and obtain the food. These are two different components and are primarily controlled by different brain substrates.

While the liking or affective component of food reward is determined by endog- enous opioids, the wanting component seems to be affected by dopaminergic neural systems, as these systems play a role specific to motivation because massive deple- tion of dopamine does not influence the affective reaction to food — only the appetite for or the motivation to attain the food. Similarly, neither dopamine agonists or antagonists alter the affective or liking response to food. Rather, these drugs seem to alter the wanting or motivation to seek out and eat the available food (see

Berridge 38 for a review). Therefore, the dopaminergic neural system influences the wanting or motivation to eat specific foods and the aPD peptide system influences

the hedonic response to the consumption of the food. The dopaminergic neural system thus seems to be the brain substrate that accounts for the desire or cravings

for specific foods. 39 Endogenous opioids therefore mediate the liking for or palat- ability of a food, and the dopaminergic neural systems mediate the wanting or desire

for a specific food. These two systems would seem to work together and represent the neural substrate explaining our desire for certain foods and our hedonic reaction

to or liking for the food consumed.