In an earlier post The Sugar Made Me Do It, I covered recent research by de Araujo, Oliveira-Maia et al. on how food, specifically sucrose, can reinforce eating by activating mid-brain dopamine circuitry, even in the absence of taste. In the accompanying editorial essay by Andrews and Horvath, this great graphic appeared, representing what is known about how eating can act on the hypothalamus and on the mesolimbic dopamine system (ventral tegmental area, nucleus accumbens, and prefrontal cortex).

Here is a much more convincing link to how eating can become appetite-driven, which previous posts on Genetics and Obesity and On the Causes of Obesity had raised as an important issue in the obesity problem.

Just one more note on the graphic: in terms of how taste can affect dopamine function, see some thoughts in the post on the neuropeptide orexin.

Figure 1. Schematic Illustration Depicting Some of the Major Findings of de Araujo and Oliveira-Maia et al

Taste alone (noncaloric sweetener), taste with caloric value (sucrose solution), or caloric value only (in the absence of taste receptors) can all equally activate the midbrain reward circuitry. To date, major emphasis has been placed on the hypothalamus and its various circuits, including orexin (ORX/Hcrt)- and melanin concentrating hormone (MCH)-producing neurons in the lateral hypothalamus as well as neuropeptide Y (NPY)/agouti-related protein (AgRP)- and -melanocyte-stimulating hormone (-MSH)-producing neurons in the arcuate nucleus, as a homeostatic center for feeding, responding to various peripheral metabolic hormones and fuels. The mesencephalic dopamine system is also targeted by peripheral hormones that affect and alter behavioral (and potentially endocrine) components of energy homeostasis. The results by de Araujo and Oliveira-Maia et al. highlight, however, that without classical hedonic signaling associated with reward-seeking behavior, the midbrain dopamine system can be entrained by caloric value arising from the periphery. While the precise signaling modality that mediates caloric value on dopamine neuronal activity remains to be deciphered, overall it is reasonable to suggest that distinction between hedonic and homeostatic regulation of feeding is redundant. DA, dopamine; GABA, γ-aminobutyric acid; Glut, glutamate.

Neuroscientifically Challenged had a great post awhile back, Every Sweet Hath Its Sour, reporting on research that basically equates modern, processed food with drugs.

Why? As the Duke Health news release tells us, “Researchers at Duke University Medical Center have discovered that the brain can respond to the calorie content of food, even in the absence of taste.” An even better title summarizing this research is “Tasteless Food Reward.”

This March 2008 Neuron paper “Food Reward in the Absence of Taste Receptor Signaling” by Ivan de Araujo, Albino Oliveira-Maia and colleagues shows that high-calorie food can directly reinforce the mesolimbic dopamine system. This result overturns that common assumption that what we eat relies on conditioned preference, pairing taste with the ingestion of a particular substance, say, cops and their donuts. This assumption has been used to great effect in evolutionary medicine research—we evolved in a fat-, sugar- and salt-limited environment, and today our evolved tastes drive our excessive consumptions of fast food in the modern world.

Now the modern situation appears even more dire, for calories alone can also reinforce food consumption, at least in mice “which lack the cellular machinery required for sweet taste transduction.” The Tasteless Food Reward editorial by Zane Andrews and Tamas Horvath tells us that “de Araujo et al. show that mice lacking functional ‘sweet’ taste receptors (trpm5−/−) develop a preference for sucrose by activating the mesolimbic dopamine-accumbal pathway, solely based on calorie load.”

Continue reading “The Sugar Made Me Do It”