Addiction model of obesity | Reverse Diabetes MD

Addiction Neurobehavioral Model of Obesity

April 30, 2019

Reverse Diabetes MD Presentation | Reverse Diabetes MD from Gurpreet Padda on Vimeo. Using an addiction model for obesity may be a more accurate way to view it. Obesity is more complex than the simple calories in, calories out model. Obesity is more than eat less, move more. It is shaped by an underlying response system in the brain and hormones. That system hijacks the endorphin (feel-good) system. The result is a disorder much like substance use. Obesity will not be solved by the “eat less, move more” mantra when the hardwired response is a dopamine reward system. No amount of habit building can steer the patient away from a dopamine rush. This is an itch that demands to be scratched. Treatment requires shutting off cues, providing satiety (the feeling of being full), and for a time swapping in other behaviors. Here is how the problem works. Obesity is not the problem. Obesity is the result of harmful behavior that engineered food keeps reinforcing. Obesity is just the most visible sign of the problems underneath. Food turns on two distinct systems: nutrient set points and the endorphin system. The human brain has set points for how much food and liquid to take in, and they are based on nutrients. Foods packed with nutrients turn on the reward system. That helped early humans survive by storing fat fast. This reward switches on the primitive endorphin system. It works by making dopamine in the nucleus accumbens (the brain’s reward center). That is similar, but not exactly the same, as other addictive substances. Here is the brain science of eating. Some foods (those high in fat, sugar, and salt, when combined with flavor enhancers) have an abuse potential like manufactured, concentrated substances. Think cocaine, alcohol, and opiates. Compulsive overeating is a more classically recognized addiction disorder. Dopamine is the known brain chemical for classic substance abuse disorders. It also governs food reward and the pleasure side of appetite. The classic addiction model does not fully explain obesity, however. We agree with the Nature article that looked at the food addiction model as it relates to obesity. It stated that the model is “misleading”, with supporting evidence described as “inconsistent and weak.” Obesity and the brain: how convincing is the addiction model? Nature Rev. Neurosci. 13, 279–286 (2012). According to the Yale Food Addiction Scale, not all obese people show food addiction. The scale applies the criteria for substance dependence to eating. By those criteria, 25% to 37.5% of obese people qualify. This is 200-300% greater in obese versus lean groups. The rate of food addiction is 500% greater in obese people with binge-eating disorder. Meule, A. How prevalent is “food addiction”? Front. Psychiatry 2, 61 (2011). Davis, C. et al. Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite 57, 711–717 (2011). Gearhardt, A. N. et al. An examination of the food addiction construct in obese patients with binge eating disorder. Int. J. Eat. Disord. 30 Aug 2011 (doi:10.1002/eat.20957). The more likely mechanism is eating too much food. Overeating is like goal‐directed drug-taking. At first the ventral striatal and prefrontal areas of the brain control it. Then it becomes habitual and compulsive, driven mostly by the dorsal striatum, and executive control is lost. Acute (one-time) use of the drug of abuse raises dopamine in the accumbens. Then the mesolimbic dopamine systems become sensitized. That leads to stronger salience (attention), and so to more motivation toward drug‐related cues. Development of addiction is associated with a drop in striatal D2 receptors. This is linked to a reward deficiency syndrome, where more of the drug is taken to get the same reward. Rodents were exposed to high‐sugar diets, high‐fat diets, and a combination of high‐sugar high‐fat diets. They develop behaviors that resemble addiction, such as binge eating, compulsive food‐seeking, and withdrawal symptoms. Sugar addiction models have shown an opiate‐mediated withdrawal syndrome (one run by the body’s opioid system). Compulsive food‐seeking keeps going even against painful foot shocks. Opioid circuits in both the nucleus accumbens and the ventral pallidum control taste reactions to tasty foods. Turning on mu opioid receptors in the ventral striatum and amygdala causes hyperphagia (overeating). It’s the hyperpalatable foods that produce an addiction‐like syndrome. Animals given either high‐sugar or high‐fat diets eat too much. But they do not gain weight, because they make up for it by eating less chow. Only the high fat and sugar combination causes weight gain. We believe the obese patient’s relationship to food is more like a behavioral addiction, such as pathological gambling, than a classic substance addiction. But there is no clear-cut withdrawal mechanism. According to the National Institutes of Health, there is a “harmful use that is maladaptive but does not meet the criteria for dependence.” External cues, anticipation clues, pancreatic training, and loss of fat-burning adaptation drive the refeeding cycle. Specific nutrients do cause endorphin activation and a chemical effect in the brain. Big Food’s push to grow more food results in fewer micronutrients. Megafarms use monocropping (one crop on the same land, year after year). That strips the soil of helpful microelements to maximize production. By 1967, American corn farms were growing nearly three times as much corn as they had thirty years earlier. The surplus from monocropping went to livestock to boost production. The average dairy cow now produces more than 70 pounds of milk per day. The top Holsteins produce two hundred pounds per day. That is a 1,200 percent increase over the 1948 average. In the same way, a typical potato farmer grew about 63 sacks of potatoes for every acre in the 1930s. By the mid-1960s, it was up to two hundred sacks. But fewer micronutrients make food bland. Maximizing food quantity cost nutrient density, and food began to get blander. The fix for bland, high-output food was processing after harvest. Makers added engineered flavoring to fake taste. The field of flavor engineering combines organic chemistry with engineering, neuroscience, psychography, psychophysics, ethnography, demography, molecular biology, finance, botany, economics, and physiology. The goal is flavors that specifically increase cravings. Eating is a behavior driven by an expectation of pleasure. We crave flavors. Food makers design hyperpalatable (tasty), highly processed foods to turn on the reward system and make you eat more. The constant stream of signals promotes grazing. Sadly, fake flavors distort the brain’s read of nutrient value. The patient ends up eating too many manufactured carbs and manufactured fats. That mix is highly obesogenic (it drives obesity). Food palatability (engineering and variety) stirs up appetite. It cuts satiety. It promotes taking in too much energy. More variety and palatability also cause weight gain in animal models. Food combinations high in sugar, fat, and flavor are hyperpalatable. Highly palatable meals were 44% larger than the average meal. That can turn on the brain’s pleasure-seeking pathways. Over time, a highly palatable diet may lead to a weaker reward response in the brain. Processed food contains mostly polyunsaturated fatty acids (PUFA) Omega-6 vegetable oils. The human palate has a hard time tasting rancidity in vegetable oils. So the shelf life of processed foods can be stretched. The standard American diet has a greater than 20:1 ratio of unhealthy Omega-6 to healthy Omega-3. This skewed ratio is associated with many brain and mood problems, including profound anxiety. Restoring a healthy ratio of 4:1 (even by supplementing Omega 3) seems to reduce this profound anxiety. Buydens-Branchey, L., & Branchey, M. (2007). Long-chain n-3 polyunsaturated fatty acids decrease feelings of anger in substance abusers. Psychiatry Research, 157(1-3), 95–104. doi:10.1016/j.psychres.2007.01.004 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2225526/ Sucrose (table sugar) is a disaccharide (a double sugar) made of 50% fructose and 50% glucose. It is broken down mainly in the small intestine, which releases equal parts glucose and fructose. Glucose causes insulin release. Insulin-dependent channels clear it from the blood fast. But fructose does not depend on insulin. The liver takes it up fast in a first-pass effect, and it is preferentially stored as fat. Glucose and fructose have different effects on the addiction centers in the brain. Fructose produced activation in the brain’s ‘reward circuit,’ and increased the desire for food. Glucose, meanwhile, does not directly activate the reward center. American College of Neuropsychopharmacology. “Fructose and glucose: Brain reward circuits respond differently to two kinds of sugar.” ScienceDaily. ScienceDaily, 10 December 2014. www.sciencedaily.com/releases/2014/12/141210080734.htm By contrast, high-fructose corn syrup has a ratio of 55:45 fructose to glucose. High-fructose corn syrup was invented in the early 1970s. It began to replace regular sugar in prepared foods around 1975. The start of the obesity epidemic lines up with the use of HFCS. Today’s sweetened drinks made with HFCS have a fructose-to-glucose ratio of about 60:40. That is 50% more fructose than glucose. According to Science Daily, “Several major brands appear to be produced with HFCS that is 65% fructose. Finally, the sugar profile analyses detected forms of sugar that were inconsistent with what was listed on the food labels.” https://www.ncbi.nlm.nih.gov/pubmed/20948525 University of Southern California – Health Sciences. “Soda consumers may be drinking more fructose than labels reveal.” ScienceDaily. ScienceDaily, 4 June 2014. The deliberate, unlabeled rise in fructose seems strange. Sugar content varied widely from the amounts on labels. On average, the drinks had 18% more fructose than expected. HFCS is supposed to be 55% fructose, compared to the 50% in table sugar. Most foods and drinks are supposed to use HFCS that is 42% fructose. Beverages that contain 65% fructose were Coke, Pepsi, and Sprite. Beverages that contain 60% fructose were Dr. Pepper, Gatorade, and Arizona Iced Tea. http://goranlab.com/pdf/Ventura%20Obesity%202010-sugary%20beverages.pdf Americans drink about 50 gallons of soda every year (with 34 pounds of sugar). But soda drinkers are taking in far more fructose than anyone knew. Fructose specifically turns on the reward center. Could it be that the soda companies know fructose turns on the reward system, which creates more urge to buy? The side effect is too much fat building up in the liver. That feeds our epidemic of NAFLD, Metabolic Syndrome, Prediabetes, Type 2 Diabetes. Could the priming of the opioid epidemic also be associated? Treatment from an addiction approach:

Shutting off the cues that come first
Temporal substitution
Satiety

Effects on the neuroendocrine systems:

Calming neuroinflammation by adding omega-3
Easing insulin resistance by emptying the liver
Time-limited feeding

Frequently asked questions

Is food addiction the same as drug addiction?

Close, but not identical. Hyperpalatable food drives dopamine release in the nucleus accumbens. That is the same reward center that drugs of abuse hit. Rodents fed high-sugar, high-fat diets binge, seek food compulsively and show withdrawal. We see an obese patient’s relationship with food as closer to a behavioral addiction, like pathological gambling, than to a classic substance addiction.

What is the most common food addiction?

Food engineered to combine sugar, fat and salt with flavor enhancers. Sugar alone or fat alone makes animals overeat without gaining weight. The combination of high fat and high sugar causes weight gain. Fructose adds a second hook. It turns on the brain’s reward circuit and raises the desire for food, while glucose does not. Sodas made with high-fructose corn syrup deliver it in bulk.

What causes food addiction?

Engineered food. Megafarms raised yields at the cost of micronutrients, and the food turned bland. Makers fixed the blandness with engineered flavoring built to increase cravings. Hyperpalatable, highly processed foods are designed to turn on the reward system and make you eat more. Synthetic flavors also distort the brain’s read of nutrient value. The result is overeating manufactured carbohydrate and fat.

How do I stop my urge to eat?

Treat it as an addiction, not a willpower problem. Eat less, move more fails against a dopamine reward system. Treatment shuts off the cues that trigger eating. For a time, it swaps in other behaviors. It provides real satiety. On the body side, it adds omega-3 to reduce neuroinflammation (inflammation in the brain and nerves). It empties the liver to improve insulin resistance. And it uses time-limited feeding.