Compulsive overeating and sugar addiction are two behaviors that seem to be affecting a significant segment of the population.
Both can result in dangerous weight gain, eating disorders, and health risks including cancer, heart disease, diabetes and metabolic syndrome.
If you can't control the compulsion to eat or modulate your sugar consumption, then the health consequences can be dire.
You may also be exposing your children to these habits, physiologically pre-disposing them to these behaviors, or the home environment may further encouraging expression.
Recent MIT researchers may have unlocked the key to this phenomenon.
A recent study published in the journal, Cell, suggests a singular reward system may be at play.
looked at a single-neural circuit that specifically controls compulsive sugar consumption in mice. This may be manipulated so that the compulsive behavior is limited or intercepted, without affecting the mouse's normal and appropriate feeding behavior.
The MIT lead researcher noted that despite all the therapies currently available to treat type 2 diabetes and obesity, most are not specific to the driving force behind unhealthy eating.
This study offers the possibility of a new treatment angle, namely, selectively limiting the compulsion to overeat, without impairing healthy eating behaviors.
The researchers based their study model on the theory that compulsive overeating is reward driven, similar to drug addiction.
The challenge was to separate normal, health-preserving or life-preserving functions like the normal drive to eat, from an aberration or hyper exaggeration like compulsive overeating or sugar addictive behaviors.
How do you remove the unhealthy compulsion or driver, without affecting the healthy behavior?
The researchers isolated a specific neural pathway that connects the lateral hypothalamus of the brain to the ventral tegmental area, believing it might uniquely play a role in compulsive overeating because it was a pathway already identified in reward-related behaviors, like sexual activity and drug addiction.
The research showed that when the pathway was artificially activated in the mice, it caused well-fed mice to spend more time feeding and to even seek food, despite delivery of shock.
When the researchers inhibited the pathway, the sugar-seeking compulsive behavior was limited, without affecting normal feeding patterns in hungry mice.
We humans were originally set up to forage and store up during warm months, as a preparation for scarcity of foods in colder months.
Clearly, we do not seem to have modified these behaviors now that food is available amply year round, and now that the effort to find food is so much less physical.
If we can't adapt to this new age of sugar lure and availability, then research like this study may help to create new therapies to limit these compulsive behaviors.