Food Addiction? Debate of the validity of “food addiction” Is it based on the environment? Strength of willpower? New research has started to show evidence for a biological basis of addictions to high fat and sugary foods Similar neurological changes occurred in rats that were addicted to substances of abuse, such as opiates and cocaine
Sugar Addiction One study done by Avena et al., 2008 deprived rats of all food for 12 hours and then allowed them to have access to both regular chow food and a sugar solution for 12 hours This created an intermittent availability of sugar intake and it was continued for 1 month The rats started to show similar signs of addiction and withdrawal during periods of sugar abstinence: “Bingeing” – the rats started to drink excessive amounts of the sugar solution, especially when it first became available during the day Similar to drug addiction when users build and tolerance and escalate their use to continue feeling the same euphoric effects When compared to rats who had 24 hour access to sugar, the rats with intermittent access ate the same amount of sugar within a shorter timeframe, consisting of larger, but fewer meals
Sugar Addiction Opiate-like “withdrawal” – when the rats were deprived of sugar, they displayed similar signs of opiate withdrawal, such as: Somatic signs – teeth chattering, forepaw tremor, head shakes Behavioral anxiety – spending less time than control rats in an open and exposed arm of a maze Behavioral depression – decreased escape efforts and more passive floating in a forced-swim test “Craving” – the rats showed an enhanced motivation to obtain the sugar by: Pressing a lever 23% more after a 2 week period of sugar abstinence compared to when the experiment was first over Suggests that the motivational impact of sugar persists and enhances even during periods of abstinence
Sugar Addiction “Cross-sensitization” – rats showed different behaviors when exposed to other drugs of abuse: Hyperactivity – when given low doses of amphetamine (0.5 mg/kg that have no effect on naïve rats), the rats that were fed intermittent sugar showed hyperactive behaviors and locomotor cross-sensitization Similar effect s when given cocaine, suggesting similar pathways in the mesolimbic dopaminergic neurotransmission and could be an explanation for poly-substance abuse Increased intake of another drug – rats that were fed intermittent sugar and then forced to abstain showed a 9% increase intake of alcohol Similar results have been found with an increase in self- administration of cocaine compared to control groups and could be an explanation for the “gateway effect”
Neurobiological Changes The researchers also found significant changes within the brain during and after intermittent sugar intake: Increase in release of dopamine in the nucleus accumbens during sugar intake After continued use, increase in D1 receptor binding and decrease in D2 receptor binding similar to results found in cocaine abuse Changes within the opioid system, showing a decrease in enkephalin mRNA expression in the nucleus accumbens (thought to lead to a decrease in the release of dopamine through mu and delta receptors) similar results in human subjects that were cocaine- dependent During abstinence, there was a decrease in extracellular dopamine, followed by release of acetylcholine mimics the response that occurs during morphine, nicotine, and alcohol withdrawal Impact on dopaminergic, cholinergic and opioid systems, with similarities to other drugs of abuse
Fat Addiction? Similar studies have been done with high fat diets, which showed rats bingeing on the food, but did NOT display the same signs of opiate-like “withdrawal” that were seen with sugar In addition, rats on the high sugar diet tended to compensate for their bingeing by decreasing their intake of normal chow food, and had normal weights Rats placed on high fat, or high sugar and fat combination diets tended to gain weight Could this explain our obesity epidemic? Much of the American diet is a combination of fat and sugar, such as fried doughnuts and cupcakes Could the sugar be accounting for the addiction and fat be accounting for the weight gain?
Neurofunctional Imaging Studies PET studies have shown a decrease in the number of dopamine D2 receptors in obese patients as well as those addicted to cocaine, methamphetamine, alcohol, and heroine Inverse relationship between obese BMI (42- 60) and the amount of dopamine D2 receptors, but not in control group plays a larger role in obese subjects
Gastric Banding Surgery Places an inflatable band around the stomach to restrict food intake Size of stomach can be adjusted easily Lowest mortality rate Least invasive Weight loss does not come as fast and is not as permanent as other options
Roux en-Y gastric bypass A small pouch is created from the top portion of the stomach, which is then connected to the jejunum A majority of the stomach and duodenum are bypassed Faster and longer lasting weight loss More complications such as ulcers, internal hernias, and malabsorption
Oprah Show Clip http://www.youtube.com/watch?v=oAo2VRr1cIY
Post-Surgery Findings Studies have found a change in alcohol metabolism after bariatric surgery Patients get intoxicated faster and take longer to become sober Another study found an increased percent in alcoholism in bariatric surgery patients 6-10 years after the surgery Possibly because food and drugs compete for the same reinforcement sites in the brain through the mesolimbic dopaminergic pathway If a patient undergoes bariatric surgery and can no longer satisfy their cravings by bingeing on high fat and sugary foods, they may turn to other substances to activate the same pathway addiction transfer?
Addiction Transfer Some professionals have started to coin this term for when a person replaces one compulsive behavior for another We see the concept occurring after bariatric surgery, as substance abuse is not commonly found in the obese population, but there is an increase after bariatric surgery Also seen in some recovering alcoholics who develop a dependence on nicotine or caffeine – same phenomenon? Not an accepted clinical or scientific term Not a common outcome of bariatric surgery, but increased risk of problematic substance abuse
Addiction Transfer Patients have lost the weight, but still have not dealt with their emotions that caused them to turn to food for comfort in the first place Feel a “void”, so turn to another substance for the comfort that food used to provide “The weight loss surgery didn’t cause me to be an alcoholic. I’m born an addict” – bariatric patient One study found that cognitive-behavioral group therapy was helpful for patients post-surgery, but they also thought that individualized therapy would be helpful as well More studies need to be conducted on the most effective therapy for bariatric patients
Conclusion Significant neurobiological and behavioral changes occur when given excessive, intermittent high fat and sugar diets These parallel the changes found in those with drug addictions, such as cocaine, amphetamines, and heroine Patients who undergo bariatric surgery may have an increased risk of developing another addiction or compulsive behavior “Addiction transfer” is not a clinical term, but the theory is supported by many clinicians and can be seen across different groups of people