Food Addiction: Humans No Longer Eat for Survival

Early humans foraged for and ate food solely for the purposes of survival. Indeed all animals, excepting humans (and laboratory mice and rats), still to this day, consume food solely for the purposes of survival. Modern humans have not eaten solely for survival purposes in hundreds of years. Humans now eat near exclusively, if not exclusively, for hedonistic (self pleasure, indulgence) reasons. Food is little more than a drug which humans consume to satisfy addictive behaviors. We learn to enjoy and get pleasure from certain foods as a consequences of our exposures during early childhood. Eating for pleasure has resulted in the explosion of the obesity, type 2 diabetes, and heart disease rates seen in the industrialized world.

Humans crave both fats and carbohydrates (principally sugars) and although these different foods elicit distinct effects on physiology, brain chemistry, and
behavior, they both share certain neural pathways for reinforcement of behavior. Overall control of feeding behavior is a complex process involving several well deļ¬ned neural circuits. These circuits consist of interactions between the brainstem and the hypothalamus as well as interactions between the gut and the hypothalamus. To read more details of how the neural signals from the gut to the brain and back modulate feeding behavior go to the Gut-Brain Interrelationships page of my website:

http://themedicalbiochemistrypage.org/gut-brain.php

The control of feeding behavior also involves overlapping processes such as motivational drive, satiety and the anticipation of food. A major neurotransmitter involved in the coordination and reinforcement of these reward processes is dopamine. Indeed, every known type of reward, including food, results in increased levels of dopamine in the brain. Although the cell bodies of dopaminergic neurons are confined to only a few areas of the brain, these neurons send projections to numerous areas including those involved in the regulation of feeding behaviors such as the hypothalamus.

Dopamine mediates the motivational and rewarding aspects of food seeking behavior via specific dopaminergic projections from the ventral tegmental area (VTA) to the nucleus acumbens (NAc). The VTA is the origin of the dopaminergic cell bodies and the NAc is a brain region in the basal forebrain that sends projections to the basal ganglia situated at the base of the forebrain. The NAc is involved in reinforced learning, reward, pleasure, addiction, fear, aggression, and impulsivity. The reward pathways involving dopamine are also referred to as the mesolimbic or mesocorticolimbic system which also sends projections to the medial prefrontal cortex, hippocampus and amygdala. Dopamine also mediates food consumption by sending projections from the substantia nigra to the dorsolateral striatum. Studies on the fundamental characteristics of reinforcing stimuli have concluded that mesolimbic dopaminergic signals, acting as positive reinforcers, tend to be preferred and thus, elicit approach, goal-directed, and high demand behaviors characteristic of positive reinforcement.

In other words we eat something that looks, smells, and tastes good and dopamine reward circuits are established so we will repeatedly seek out these reinforcing behaviors.

The most highly addictive foods are those that are high in fats or sugars or both. Do you ever really CRAVE a side of peas? Indeed, brain imaging studies have demonstrated that craving related changes occur in the brain in response to fatty and sweet foods that are nearly identical to those seen during drug craving. Appetite dysfunction, such as seen in binge eating, bulimia, obesity, and anorexia nervosa is associated with alterations in brain dopamine signals as well as in the endocannabinoid pathways. Endocannabinoids are the naturally occurring neurotransmitters that exert effects in the brain and periphery similarly to those seen from the consumption (eating or smoking) of cannabis. Read more about the role of the endocannabinoid system in feeding behaviors in my website:

http://themedicalbiochemistrypage.org/endocannabinoids.php

Although both fatty and sweet foods cause changes in brain chemistry, throughout the reward centers of the brain, that are essentially identical to those seen in response to more classically identified addictive activities, there are some interesting differences. Following sugar bingeing individuals can experience withdrawal symptoms similar to those elicited by opiate withdrawal. However, these types of responses are not seen following fat bingeing. This may be due to one specific difference occurring in the brain in response to fat intake versus sugar intake. Expression of the neuropeptide, galanin, (GAL; go to the Gut-Brain Interrelationships page) is enhanced in response to fat intake but not sugar intake. Receptors for GAL are distributed in the reward centers of the brain. In addition, induction of GAL activity in the hypothalamus (the major feeding behavior control center of the brain) in laboratory mice causes a preference for fat intake over sugar. The synthetic GAL agonist, galnon, can reduce opiate withdrawal in laboratory mice. So, whereas, both fat and sugar are addictive "drugs" there are some differences in the overall form of addiction exerted by the consumption of these foods.

What to do then: Control your access to fat and/or sugar if you find that you crave these foods such that these cravings interfere with your pursuit of a healthy lifestyle. This is no different than what one would do to avoid smoking, or alcohol, or gambling, or any addictive activity: AVOIDANCE 

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