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:
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). Leir 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). Ley said they “hungered” for their food fixes, yet they weren’t hungry at all. Lis 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. Lis 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. Lis 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. Lis 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 handwringing, and becoming excessively twitchy and easily startled. Ley 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 waist- lines 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 dis- ease, 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.
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).
Mind
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 non-stressed people (Brandon et al. 2010). Lat’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. Ley 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. Lese 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.
Mouth
Le 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. Lese 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®.
Muscle
Regular physical activity increases the body’s production of BDNF. Lis, 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 sub- stance. 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 over-consumption 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.
Pamela Peeke, MD, MPH, FACP, is a Pew Foundation Scholar in nutrition and metabolism and an assistant professor of medicine at the University of Maryland. She serves as WebMD’s lifestyle expert and is the national spokesperson for the Exercise is Medicine global initiative. Her latest book is The Hunger Fix: The Three-Stage Detox and Recovery Plan for Overeating and Food Addiction (Rodale 2012).
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What have scientists discovered about food addiction?
Dr. Nora Volkow, director of the National Institute of Drug Abuse at the National Institutes of Health has been a leading scientist exploring the relationship between food and addiction, along with her colleague Dr. Gene Jack-Wang, of the Brookhaven Labs. Their teams found that it was primarily the continuous exposure to the “hyperpalatables”—sugary/fatty/salty foods, often refined and processed—that caused profound changes in the brain’s reward center, resulting in a decreased number of receptors for the reward/pleasure neurotransmitter dopamine. This then leads to a vicious cycle of overeating and bingeing.
Dr. Volkow used tools such as PET scans and functional MRIs of the brain to determine that cues in the environment (such as ads on TV and radio, as well as smells and visuals) trigger an unstoppable yearning for a food. Scientists have added to these findings by showing that the prefrontal cortex, the center for executive function, was impaired during active addiction. As a consequence, the ability to use willpower and make the right decision was grossly hampered. Thus, two essential parts of the brain undergo significant organic changes leading to the perpetuation of food addiction. Food addiction, then, involves a serious psychobiological challenge.
How many people have food addiction?
A recent study of 652 men and women in which researchers used the Yale Food Addiction Scale to assess the prevalence of the addiction, found that:
This is one of the first studies to provide a glimpse into the magnitude of this problem in the general population. It’s important to note that people who struggle with food addiction span the range of body sizes, from skinny to obese. The difference is in controlling the total daily number of calories ingested and expended.
Am I a food addict?
There’s a validated and peer-reviewed assessment you can take to find out if you have or are on the verge of food addiction. Known as the Yale Food Addiction Scale, this quiz is used by scientists for clinical and research work. You can take the full 27-item assessment, which is provided in The Hunger Fix, or complete the shorter version. Food addiction is indicated when there are three or more symptoms present within the past 12 months and the individual experiences serious functional impairment or distress in his or her daily life.
What’s the relationship between food addiction and binge eating?
Researchers have found a significant crossover between these two conditions. Yale researcher Ashley Gearhardt published data noting that those who experience binge eating and meet the criteria for food addiction are more likely to experience a higher level of mental and physical distress than binge eaters who do not meet the criteria. What exactly is binge eating? It’s the most common form of disordered eating and involves at least 30 percent of the population. Standard criteria for the diagnosis of binge eating include the presence of recurring episodes (at least once per week) of eating much more food than normal in a short period of time, often when not hungry, followed by feelings of being out of control, as well as shame, blame, and guilt. You can clearly see the overlap with food and addiction.
An exciting recent development is the inclusion of binge eating disorder in the fifth edition of Diagnostic and Statistical Manual of Mental Disorders (the DSM-V). This means that those seeking help for weight management who have issues with binge eating and its often-associated food addiction will soon have insurance coverage for inpatient and outpatient treatment programs.
How do you treat food addiction?
The Hunger Fix is the first consumer book to provide readers with both the science and the solution for overeating and food addiction. There is a range of options—from 12-step to cognitive behavioral therapy—to tackle the problem of food addiction. I have found that most people cherry-pick from many of these resources to customize a plan that works best for them. The book will help guide you through this process.
The over-arching goal is to create a new strategy for lifelong recovery. Food addiction presents a unique challenge. It’s unlike an addiction to drugs or alcohol in that you need food to live. You’re surrounded by cues to eat 24/7, as well as the daily stresses that drive overeating. The recovery strategy has to include a healthy lifestyle to provide the mental, nutritional, and physical activity elements that will support lifelong recovery. The Hunger Fix lays down a framework for healing and strengthening the brain’s reward and executive function centers. In three stages—Detox and then Beginner and Master Recovery—you’ll learn how to substitute False Fixes (the hyperpalatables, people, places, and things that enable your overeating) with Healthy Fixes (whole foods, stress resilience, and mental and physical fitness).
The ultimate reward, once you reclaim your brain as well as your life, is the joy and happiness you’ll feel pursuing cherished dreams. That’s a hunger you can spend a lifetime satisfying.
How to Bust Your Binge
Pizza and ice cream are calling. Here’s how to avoid their tempting siren songs.
Before eating a plate of donuts, ask yourself two important questions. There’s a scene in “Sex and the City” where Miranda comes home from a particularly rotten day, takes a distressing phone call and then whips up a batch of brownies, gobbling one after the other. Disgusted with herself, she tosses the rest into the garbage. Hearing more bad news from another call, she stumbles back into the kitchen, grabs the trash can and does a full-on dumpster dive, stuffing her mouth with whatever brownies she can retrieve. Now, consumed with shame, she calls her best friend Carrie and solemnly declares her need to be admitted to the Betty Crocker rehab center. Sound familiar?
The Oxford dictionary defines a binge as “a short period devoted to indulging in an activity to excess, especially eating.” Miranda qualifies. It’s funny how tuna on a bed of greens doesn’t quite do it when you’re anxious and want to soothe yourself. Instead, it’s a bingeable food/beverage product which, in my book “Fight Fat after Forty,” I have defined as any food that:
In “The Hunger Fix: The Three Stage Detox and Recovery Plan for Overeating and Food Addiction,” I noted that science has demonstrated that bingeing is highly associated with addictive eating behavior. It’s no surprise that research has also shown that the top 10 addictive bingeables include pizza, chocolate, chips, cookies, ice cream, French fries, cheeseburgers, sugared sodas, cake and cheese. The problem is that we’re surrounded with 24/7 temptation and often feel helpless, hopeless and defeated as we try to navigate the ubiquitous, multimedia bingeable land mines without overeating.
Here’s a simple guide to help you avoid the bingeables’ tempting siren songs, and stay on track to optimize your health and wellness.
1. Always ask these two questions before you consider eating.
Since bingeing is so highly tied to addictive eating, these two simple yet powerful questions help ground you as you contemplate whether to eat at all.
If the answer to each question is “yes,” then you’re sitting in front of a bingeable. Say to yourself, “this doesn’t work for me,” and leave it. Out of sight, out of mind.
2. HALT before you cave to the crave.
Make the connection between mood and food by using the acronym HALT and asking yourself if, when you feel like overeating, you’re really:
3. Here’s your license to chill.
Sleep deprivation will impair the ability of your hunger and appetite hormones (ghrelin and leptin) to function properly making controlling your eating mission impossible. Start prioritizing high-quality sleep, and you’ll be rewarded with a greatly improved ability to say “no” to temptation.
4. Stressed spelled backwards is desserts.
Toxic stress is associated with feelings of helplessness, hopelessness and defeat. When that happens, people want to feel soothed and comforted, and kale’s not going to do it. Learning how to become more stress resilient is key. Staying centered with mindful living and meditation and mind-body modalities like yoga is essential to avoiding self-destructive behaviors like bingeing.
5. Ditch the m’nage a trois.
There you are in bed, late at night watching another “Law and Order” marathon with your two best friends, Ben and Jerry. Ditch these guys and get some real people in your life. Bag the loneliness, and reach out to help others by volunteering, connecting with others and getting out of yourself and into someone else’s needs.
6. Stay mindful, and beware of cues and triggers to binge.
Science shows that it’s actually the cues to overeat, not the act of eating, that cause the highest levels of the pleasure brain chemical (dopamine) to be secreted. The anticipation of bingeing is really what’s driving you to binge. Protect yourself by being very aware of, and trying to avoid if possible, the persons, places and things that are likely to trigger you to cave and overeat.
7. Eat crave killers.
Combine healthy protein with fiber to feel full and satisfied, thus decreasing the need to binge. For snacks, try nut butter on apple or banana slices, yogurt with walnuts and berries or carrots and hummus.
8. Try a smarter soothing strategy.
Create a repertoire of ways to soothe yourself without bingeing. If you really want something sweet, throw together a fruit smoothie or yogurt parfait with fresh blueberries. Non-food strategies can include getting up and walking outside to breathe some fresh air and move away from a stressor. Calling a friend to unload a problem helps. Prayer and meditation can keep you grounded. And don’t forget the power of a truly soothing bath.
Throw these tips and techniques into your mental tool box and grab ’em as needed. Consider yourself locked and loaded, prepared to bust an oncoming binge anytime.
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