Food and Addiction: The Dopamine Made Me Do It
Research is uncovering a link between our lifestyle, our genes, and a means to overcome the unhealthy connection between food and addiction.
Two human behaviors explain why we’re still here: engaging in sex and consuming food. Both are inextricably linked by dopamine, the neurotransmitter associated with reward and pleasure. It’s what motivates us to read all three volumes of Fifty Shades of Grey or to inhale a plate of mom’s homemade oatmeal raisin cookies. To date, procreative activities have maintained their primal prerogative without too much deviation from nature’s blueprint. Food production and consumption, on the other hand, have fallen prey to psychosocial, cultural and environmental factors that increase our collective girth and make us more vulnerable to disease.
Researchers have recently uncovered a critical clue to help explain this problem—a link between food and addiction.
The Dopamine Connection
“I can’t get off the stuff.” “I need a hit.” “I’ve got to detox.” “Withdrawal is hell.” Fitness, nutrition and health professionals have heard this kind of addiction vernacular for years. However, we’re not talking about drugs, alcohol or cigarettes—this is about food. The big culprits are the hyperpalatables—sugary, starchy, fatty and salty foods. Is there a relationship between food and addiction? Can food products hijack the reward system in much the same way as drugs? Yes, according to newly published data and a growing chorus of scientists.
Central to this burgeoning research is the role of dopamine, the neurotransmitter that
- signals when rewards are present;
- motivates us to seek rewards;
- promotes exploring and learning about rewards; and
- maintains awareness about reward-related cues.
Cocaine and heroin target and hijack this reward system. So do appetite-controlling hormones, leading a growing number of researchers to consider obesity from the standpoint of addiction neuroscience (Dagher 2012).
Dopamine is actually dispersed throughout the brain. Ninety percent of the dopamine neurons in the ventral tegmental area (VTA) become stimulated when we’re about to eat. The VTA reaches out to the rest of the brain via countless axons to stimulate dopamine secretion in several brain regions, including the mesolimbic and mesocortical dopamine systems. The mesolimbic system reaches into the nucleus accumbens (the site of reward, pleasure and addiction), the amygdala (where emotions are processed and remembered) and the hippocampus (a site that converts short-term memory to long-term memory) (Volkow & Wise 2005). In an effort to understand whether certain foods exert the same kind of addictive effect on the reward system as drugs, scientists have turned their attention to the reward centers in normal and overweight humans.
Leading the charge is Nora Volkow, MD, director of the National Institute on Drug Abuse. In 2001, Volkow and her team used PET scans and radioactive chemicals that bind to dopamine receptors (Wang et al. 2001). Their research revealed that obese people had far fewer dopamine receptors in the brain’s striatum, or reward center, and therefore had to eat more to experience the same reward, or “high,” as average-weighted individuals.
Did these people already have fewer receptors—predisposing them to weight gain—or did they once have a normal number of receptors, which through repeated exposure was down-regulated? The answer is both. Animal studies have shown profound down regulation of D2 receptors (dopamine receptors subtype 2) after overconsumption of a hyperpalatable junk food diet (Avena, Bocarsly & Hoebel 2012). Swiss researchers using lab rats discovered that it wasn’t weight gain per se that caused the decrease in receptors, but rather the specific consumption of hyperpalatable foods versus normal rat chow (Alsio et al. 2010).
Volkow then delved into the craving, or “wanting,” question. When people were exposed to their favorite foods but were not allowed to eat them, a tidal wave of dopamine surged through the striatum (Volkow 2002). They said they “hungered” for their food fixes, yet they weren’t hungry at all. This is similar to what occurs in the brains of drug abusers after they watch a video of people using cocaine—or receiving any cue that hearkens back to an addictive pleasure.
Anticipation and Satisfaction
Animal studies have helped us understand this addictive cycle of anticipation and reward. When rats are given free access to a mix of the typical hyperpalatable foods available to humans—chocolate, cheesecake, bacon, sausage and other fat and processed products—the rat’s brain structure changes the same way it would if cocaine were ingested. Yale University researchers used functional MRI (fMRI) studies to prove that both lean and obese women who demonstrate addictive behavior around food show the same pattern of neural activity as a chronic drug abuser: very high levels of anticipation of their drug of choice—in this case, a chocolate milk shake—but very low levels of satisfaction after consumption (Gearhardt et al. 2011).
How does the addiction develop? Think of a river during a flood. The water charges over the banks, taking down trees and houses along the way. Something similar happens when dopamine continually floods the brain. The pathway between the VTA and the nucleus accumbens repeatedly floods with dopamine. This results in a down regulation of the total number of dopamine D2 receptors, including those in the limbic system, the site of motivation and emotions. Consequently, greater quantities of hyperpalatables are required to elicit the same level of reward. This launches a vicious cycle: increased ingestion leads only to further down regulation and a relentless, insatiable appetite.
As the D2 receptor population decreases, there is a profound change in the ability of critical brain structures to communicate effectively. In 2008, Volkow and her team found that obese people who have fewer dopamine receptors also have less activity in the prefrontal cortex (Volkow 2008). The prefrontal cortex (PFC) is responsible for handling “executive” functions—including planning, organizing, making choices and being creative—as well as for reining in impulsivity, impatience and irritability. This constitutes double trouble for the food addict. Not only is it necessary to eat more food to experience normal reward and pleasure, but it’s much more difficult to stop after the first bite. This is why stressing “moderation” to a food addict is a moot point.
Hyperpalatables = Heroin?
Is sugar as addictive as heroin or cocaine? Could that cupcake with the mile-high frosting act like crack to a susceptible brain? Animal studies reveal that hyperpalatable diets, and sweet ones in particular, are more rewarding—and potentially more addictive—than intravenous cocaine and heroin (Ahmed 2012).
What about withdrawal from the hyperpalatables in comparison to drugs? Substance abuse researchers note that the brain adaptations that result from regularly eating foods that layer salt, fat and sweet flavors are likely to be more difficult to change than those from cocaine or alcohol because the food-related adaptations involve many more neural pathways. Almost all of the dopamine neurons in the VTA are activated in response to food cues (Wang & Tsien 2011).
An fMRI study found that among women who tested higher for food addiction, just thinking about drinking a chocolate milk shake stimulated greater activation in the anterior cingulate cortex, medial orbitofrontal cortex and amygdala, all areas of the brain involved in emotion, anticipation and decision making (Gearhardt et al. 2011). Rats who received highly palatable food for only 2 weeks showed a decrease in gene expression for enkephalin, a natural painkiller in the nucleus accumbens. The same changes were found in the brains of chronic morphine or heroin addicts (Kelley et al. 2003).
Lab rats with unlimited access to a high-fat, high-carbohydrate diet almost eat themselves to death. They’ll voluntarily walk across an electrified plate and endure painful shocks in order to get their junk food hit. In one study, when rats had access to high-fat, high-carbohydrate food for only 1 hour a day, they consumed 65% of their daily calories in one sitting, continuously gorging until the food was removed. However, when the food disappeared they didn’t simply shrug their rodent shoulders and turn back to regular chow. Instead, they withdrew and curled up into a fetal position, soothing themselves with nervous hand-wringing, and becoming excessively twitchy and easily startled. They were hungry for their fix. Without it, they ended up with “the shakes” (Johnson & Kenny 2010).
Lab rats will quickly develop a tolerance for sugar, eagerly quadrupling their daily sugar consumption in 1 week. If the sugar’s taken away, the hunger for their fix is relentless and leads to withdrawal symptoms. They’ll start fighting with other rats, shaking and getting angry. Once the rats become addicted to sugar, they are far more eager to gobble up amphetamines, alcohol and cocaine in huge quantities—and they become almost instantly addicted to those substances as well. When given the choice between sugar, cocaine and alcohol, those cross-addicted rats will always choose—you guessed it—sugar (Johnson & Kenny 2010).
In humans, there’s clear evidence that habitual consumption of calorie-dense hyperpalatables elicits changes in brain responses that mirror those that occur during drug addiction. And akin to drugs, these same foods are implicated in cravings and in the perception of loss of control (Pelchat 2002). Speaking of cravings, 95% of the foods humans most crave are, not surprisingly, calorie-dense. Why do we favor calorie-dense foods? It’s about survival. When food was scarce, ingesting calorie-dense foods gave us our optimal chance of surviving. That is not the case today.
The Role of Epigenetics
When researchers from the Washington University School of Medicine in St. Louis first did a study of almost 40,000 people in the early 1990s, addictive genes appeared to have no impact on body weight. People were just as likely to be obese whether they came from a family with addiction or not. But when scientists did a follow-up study of 40,000 other people in 2001 and 2002, the picture was very different. Subjects were 30%–40% more likely to be obese if they had addiction in the family. For women, the chance was 50% greater (Finucane et al. 2011).
This upsurge in obesity was not caused by evolutionary changes to the genome. The basic genetic makeup of humanity cannot change that quickly. No, this explosive weight gain was caused by changes to the environment that switch on individual genes. Enter the exciting, newly emerging science of epigenetics (for more on epigenetics, read “Our Dynamic DNA,” by Charlie Hoolihan, in the May 2012 issue of IDEA Fitness Journal).
Epigenetics (epi meaning “around” and genetics referring to the study of genes) helps us understand how any environmental cue—person, place or thing—can influence how our genes are expressed. If you live and participate in an active social community, with plenty of fresh food and opportunities for exercise, the genes that control your weight operate as nature intended, and you can more easily enjoy a fit and healthy body.
Conversely, here’s a scenario in which gene expression is constantly altered to the detriment of the individual. For example, take someone who starts the day in fight-or-flight overdrive: an argument with a spouse, running out the door, skipping breakfast, driving the 30-mile commute to work, getting to work hungry, dealing with a micromanaging boss and spending hours sitting glued to a computer screen. Levels of acetylcholine and cortisol, stress hormones that trigger fat storage and cravings, go through the roof. To anesthetize the pain of a stressed daily existence, it’s easy to habitually reach for “fixes,” which are often conveniently available at the office vending machine or at drive-throughs. This constant dependence on hyperpalatables not only thickens waistlines and changes brain structures; it also takes its toll on genes, changing their expression to one that supports overeating and addiction. This further reinforces the cycle (Peeke 2012).
What’s the solution? If altering genetic expression facilitates food addiction, can we reverse this messaging to promote healing and recovery? Epigeneticists believe this is possible.
Think of the genome as a book, filled with genes that make up its sentences, paragraphs and chapters. The pages of that book are filled with annotations. Some pages are bookmarked or dog-eared; others are stapled together and inaccessible. The annotations in your genetic book take the form of certain chemicals and molecules that attach themselves to the genes. Because they sit, in a sense, on top of the genome, this collection of annotations is called the epigenome.
Most cells in your body contain the entire genome; a cell in your heart contains not only the genes for a heart cell but also the genes for a liver cell, a nerve cell, a skin cell and every other kind of cell. Yet that heart cell ignores all instructions that aren’t heart cell–related. The epigenome switches certain genes off and certain genes on.
All this switching is the work of special proteins called histones that surround each gene. Histones are genetic referees, scanning every action and choice you make and switching the messages that individual genes deliver to the rest of the body. Eat junk food and your genetic “speech” or expression changes, resulting in a cascade of biological changes, including increased inflammatory processes. Eat an apple and histones order a gene to start a different cascade, resulting in improved immune function. The goals are for histones to script the healthiest messages possible and to maintain happy histones throughout life.
Epigenetics in Action: Agouti Mice
Once born, you cannot alter your genes. What’s exciting about the epigenome is that it adds possibilities. You can change genetic expression, proving that DNA is not destiny. Lifestyle choices powerfully influence genetic expression—and most important, they are passed on to children.
A striking example of this occurs in a breed of lab mouse called agouti. These mice have a unique gene—the agouti gene—that causes them to become obese and also gives them yellow fur. The mice are at high risk for developing heart disease, diabetes and cancer. Scientists have observed that among female agouti mice who have exactly the same genes, one mouse can produce obese pups with the characteristic yellow fur, while the other mother produces pups with brown fur that grow up slim.
How is this possible, and why does it matter? The answer is epigenetics. In one mouse, the agouti gene has been switched off, and so the yellow fur and obesity don’t develop in her pups. The gene is marked “do not read” because a specific molecule, called a methyl group, has been attached to it. The process is called methylation. Researchers simply supplemented this obese, yellow-furred mother’s diet with methyl donors such as vitamin B12, choline, betaine and folic acid or genistein, a phytoestrogen food in soy products. The mouse pups of this agouti mother fed the methylated food were born lean, with brown fur and at no risk for disease (Dolinoy et al. 2007).
This was a groundbreaking experiment and officially established the food–gene connection; it also helped mark the birth of epigenetics.
The Road to Recovery: An Integrative Mind-Body Approach
By harnessing the power of epigenetics, it is possible to rein in impulsivity, strengthen PFC function and recover from food addiction for a lifetime. Here are simple, proactive steps to achieve detoxification and sustainable recovery, adapted from The Hunger Fix: The Three-Stage Detox and Recovery Plan for Overeating and Food Addiction (Rodale 2012).
Stress can have a significant impact on PFC function. Studies using fMRI have shown that simply reducing stress can enhance functioning and return it to levels of nonstressed people (Brandon et al. 2010). That’s why radical stress reduction remains a top priority. Meditation is a central focus of successful addiction recovery.
Transcendental Meditation (TM) has been shown to significantly augment PFC function (Hooper 2011). When people engage in regular meditation, they release up to 65% more dopamine in the ventral striatum (Kjaer et al. 2002). One study found that these higher levels of dopamine, along with the continued practice of meditation, reduced people’s impulsiveness (Kjaer et al. 2002).
Meditation also helps prevent relapse. An fMRI study done at the University of California in San Francisco found that people who were least likely to relapse in alcoholic abstinence programs had greater brain volume and thicker cortices. They had a much easier time sticking with their sobriety. When they did fall off the wagon, they experienced less severe relapses (Durazzo et al. 2011).
Another study found that after an 8-week program, previous Mindfulness-Based Stress Reduction (MBSR) novices showed significant gains in brain size, with the most gray matter growing in the posterior cingulate cortex, the temporoparietal junction and the cerebellum. These are brain regions that help us learn and remember, stay calm, critically evaluate our thoughts and understand other people’s perspectives (Hölzel et al. 2011).
The bottom line. The mind plays a crucial role in reclaiming a hijacked reward system and sustaining recovery from food addiction. A strong, well-trained PFC has a better chance of helping an individual remain vigilant, make the right choices, steer clear of hyperpalatables and select fresh, whole, life-promoting foods instead.
The agouti mouse paradigm carries over to humans. The goal is to choose foods that promote health through optimal gene expression. Following are two examples to illustrate how to apply epigenetics through nutrition.
Choline figures prominently in attention and prefrontal cortex function. Studies on rats have shown that supplementing with dietary choline can increase the nerve growth factor in the PFC, improving memory and precision, helping reduce aging deficits and even aiding in recovery from early PFC injury (Sandstrom, Loy & Williams 2002; Tees 1999). Acetylcholine is also credited with strengthening synapses—the connections between neurons—particularly when we’re learning and using our short-term memory (Rasmusson 2000). Although our bodies generate choline, we need food sources to maintain adequate levels.
Omega-3s are used by the brain to form 60% of its fat-based cell structure. These fatty acids ensure that cell membranes will be flexible enough to let in other nutrients. One study (Davis et al. 2010) found that rats fed a diet low in omega-3s had 20% lower levels of the omega-3 docosahexaenoic acid (DHA), which researchers found significantly reduced the density of the D2 dopamine receptors in the ventral striatal section of the brain—an area closely associated with impulsivity.
Another study found that supplementing with fish oil increased serotonin receptor activation and Brain Derived Neurotropic Factor (BDNF) production (Vines 2012). BDNF is a protein that stimulates new neuron growth in the hippocampus, which scientists believe helps improve memory and decrease anxiety and depression.
Perhaps the best way to test how omega-3s can influence our ability to calm down and focus is to look at 8- to 10-year-old boys. One placebo-controlled fMRI study found that supplementing with DHA for 8 weeks increased activity in the boys’ dorsolateral PFC significantly more than taking the placebo. The study also found a “dose response”—the more DHA the boys took, the higher their ability to concentrate, the greater the activity in their PFCs and the faster their reaction times (McNamara et al. 2010).
The bottom line. With every mouthful, an individual alters genetic expression. The stronger the PFC, the more likely the choice will be an apple and not a Twinkie®.
Regular physical activity increases the body’s production of BDNF. This, in turn, can lead to higher PFC functioning. One study in the journal Health Psychology found that kids aged 7–11 who had done more vigorous exercise—40 minutes or more, five times a week, for 3 months—had a net gain of 3.8 additional IQ points. MRIs showed that the kids’ PFC—where decision making, planning, social awareness and complex thought take place—was growing, presumably strengthening their executive function abilities (Davis et al. 2011).
Exercise is the best healthy fix because it directly regenerates D2-like dopamine receptors—similar to those linked with food addiction—in the brain, helping to rebuild the damage of past addiction and prevent it in the future (MacRae et al. 1987). And it doesn’t require a gym membership, an elliptical trainer or a set of barbells. It simply requires increasing activities of daily living. In fact, it’s been shown that a 5-minute walk around the block or 30 jumping jacks reduces the intensity of withdrawal symptoms.
One Vanderbilt University study found that 10 (30-minute) sessions of moderate treadmill walking over 2 weeks was enough to cut addicts’ marijuana smoking in half, even though the addicts were not asked to cut down and had, in fact, explicitly said they didn’t want to. Participants cut their original intake by a third even after the study was over (Buchowski et al. 2011).
Researchers believe that exercise altered the reward circuits in the brain to the point where treadmill walking took the place of cannabis. Movement became self-reinforcing, leading the addicts to need less pot to get the same high. Exercise also decreased their cravings, compulsiveness and emotional ups and downs, as well as their desperate focus on marijuana (Buchowski et al. 2011).
Most studies have found that walking is king. Indeed, one randomized controlled fMRI study published in the Proceedings of the National Academy of Sciences found that after a year of taking 40-minute walks three times a week, sedentary older adults grew their hippocampi by 2%—reversing their brains’ aging process by almost 2 years. Those who remained sedentary saw their brains shrink by almost the same amount (Erickson et al. 2011).
The bottom line. Regular physical activity facilitates neurogenesis, augments PFC function and significantly aids in relapse prevention and sustained recovery from addiction.
Beyond Food Addiction
Research on food and addiction is rapidly gathering momentum. World-class scientists are scrutinizing the relationship between the foods we consume and their profound epigenetic effects on our mental and physical health. Kelly Brownell, PhD, director of Yale University’s Rudd Center for Food Policy & Obesity, notes: “Whether food and addiction is a viable concept is scarcely in question. . . . Food can act on the brain as an addictive substance. Certain constituents of food, sugar in particular, may hijack the brain and override will, judgment and personal responsibility. . . . The addictive impact of food may be a contributor to the global health crises created by obesity and diabetes” (Brownell & Gold 2012).
The situation goes further than food and addiction. It’s imperative that we carefully examine the living and working environment that enables overeating and addictive behaviors. What are the persons, places, things and psychosocial stresses that foster our continued overconsumption of calorie-dense hyperpalatable foods? This is required homework that must be done to fully appreciate how to reverse this troubling trend, facilitate long-term recovery and promote a healthier lifestyle for a lifetime.
Ahmed, S. 2012. Is sugar as addictive as cocaine? In K. Brownell & M. Gold (Eds.), Food and Addiction (pp. 231-35). New York: Oxford Press.
Alsio, J., et al. 2010. Dopamine D1 receptor gene expression decreases in the nucleus accumbens upon long-term exposure to palatable food and differs depending on diet-induced obesity phenotype in rats. Neuroscience, 171 (3), 779-87.
Avena, N., Bocarsly, M., & Hoebel, B. 2012. Animal models of sugar and fat bingeing: Relationship to food addiction and increased body weight. Methods in Molecular Biology, 829, 351-65.
Brandon, J., et al. 2010. Self-control at high and low levels of mental construal. Social Psychological and Personality Science, 2, 182.
Brownell, K., & Gold, M. 2012. Food and addiction: Scientific, social, legal and legislative implications. In K. Brownell & M. Gold (Eds.), Food and Addiction (pp. 439-45). New York: Oxford Press.
Buchowski, M., et al. 2011. Aerobic exercise training reduces cannabis craving and use in non-treatment seeking cannabis-dependent adults. PLoS ONE, 6 (3), e17465.
Dagher, A. 2012. Hormones, hunger, and food addiction. In K. Brownell & M. Gold (Eds.), Food and Addiction (pp. 200-203). New York: Oxford Press.
Davis, C., et al. 2011. Exercise improves executive function and achievement and alters brain activation in overweight children: A randomized, controlled trial. Health Psychology, 30 (1), 91-98.
Davis, P.F., et al. 2010. Dopamine receptor alterations in female rats with diet-induced decreased brain docosahexaenoic acid (DHA): Interactions with reproductive status. Nutritional Neuroscience, 13 (4), 161-69.
Dolinoy, D.C., et al. 2007. Metastable epialleles, imprinting, and the fetal origins of adult diseases. Pediatric Research, 61, 30R-37R.
Durazzo, T., et al. 2011. Cortical thickness, surface area, and volume of the brain reward system in alcohol dependence: Relationships to relapse and extended abstinence. Alcoholism: Clinical and Experimental Research. doi:10.1111/j.1530-0277.2011.001452.x.
Erickson, K., et al. 2011. Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of Sciences of the USA. doi: 10.1073/pnas.1015950108.
Finucane, M., et al. 2011. National, regional, and global trends in body-mass index since 1980: Systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9.1 million participants. Lancet, 377 (9765), 557-67.
Gearhardt, A., et al. 2011. Neural correlates of food addiction. Archives of General ÔÇ¿Psychiatry, 68 (8), 808-16.
H├Âlzel, B., et al. 2011. Mindfulness practice leads to increases in regional brain gray matter density. Psychiatry Research, 191 (1), 36-43.
Hooper, J. 2011. Meditation nation. www.details.com/ culture-trends/critical-eye/201109/transcendental-meditation-pure-consciousness; retrieved July 2012.
Johnson, P., & Kenny, P. 2010. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience, 13 (5), 635-41.
Kelley, A., et al. 2003. Restricted daily consumption of a highly palatable food alters striatal enkephalin gene expression. European Journal of Neuroscience, 18 (9), 2592-98.
Kjaer, T., et al. 2002. Increased dopamine tone during meditation-induced change of consciousness. Cognitive Brain Research, 13 (2), 255-59.
MacRae, P., et al. 1987. Endurance training effects on striatal D2 dopamine receptor binding and striatal dopamine metabolites in presenescent older rats. Psychopharmacology, 92 (2), 236-40.
McNamara, R., et al. 2010. Docosahexaenoic acid supplementation increases prefrontal cortex activation during sustained attention in healthy boys: A placebo-controlled, dose-ranging, functional magnetic resonance imaging study. American Journal of Clinical Nutrition, 91 (4), 1060-67.
Peeke, P. 2012. The Hunger Fix: The 3 Stage Detox and Recovery Plan for Overeating and Food Addiction. New York: Rodale.
Pelchat, M. 2002. Of human bondage: food craving, obsession, compulsion, and addiction. Physiology & Behavior, 76 (3), 347-52.
Rasmusson, D. 2000. The role of acetylcholine in cortical synaptic plasticity. Behavioural Brain Research, 115 (2), 205-18.
Sandstrom, N., Loy, R., & Williams, C. 2002. Prenatal choline supplementation increases NGF levels in the hippocampus and frontal cortex of young and adult rats. Brain Research, 947, 9-16.
Tees, R. 1999. The influences of rearing environment and neonatal choline dietary supplementation on spatial learning and memory in adult rats. Behavioural Brain ÔÇ¿Research, 105 (2), 173-88.
Vines, A. 2012. The role of 5-HTÔéüA receptors in fish oil-mediated increased BDN expression in the rat hippocampus and cortex: A possible antidepressant mechanism. Neuropharmacology, 62 (1), 184-91.
Volkow, N. 2002. ÔÇÿNonhedonic’ food motivation in humans involves dopamine in the ÔÇ¿dorsal striatum and methylphenidate amplifies this effect. Synapse, 44 (3), 175-80.
Volkow, N. 2008. Inverse association between BMI and prefrontal metabolic activity in healthy adults. Obesity, 17 (1), 60-65.
Volkow, N., & Wise, R. 2005. How can drug addiction help us understand obesity? Nature Neuroscience, 8 (5), 555-60.
Wang, D., & Tsien, J. 2011 Convergent processing of both positive and negative ÔÇ¿motivational signals by the VTA dopamine neuronal populations. PLoS ONE, 6 ÔÇ¿ (2), e17047.
To find out more about food addiction, the dopamine connection and epigenetics, read The Hunger Fix: The Three-Stage Detox and Recovery Plan for Overeating and Food Addiction by Pam Peeke, MD, MPH, FACP (Rodale 2012).
The following quiz is adapted from the Yale Food Addiction Scale (Peeke 2012).
Please respond to statements 1 through 7 using these numerical options:
1: once per month
2: 2–4 times per month
1. I find myself consuming certain foods even when I am no longer hungry. _____
2. I worry about cutting down on certain foods. _____
3. I feel sluggish or fatigued from overeating. _____
4. I spend time dealing with negative feelings from overeating certain foods instead of sharing time with family or friends, working or doin
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