“I identified in 1990 the first gene in alcohol addiction. Specifically, we found the A1 allele (the minor form) of the D2 dopamine receptor (DRD2) gene to be associated with addiction. We researched the brain characteristics of the subjects who had the DRD2 A1 allele. To do that, we carried out a pharmacological study on the brains of deceased individuals who had or did not have the A1 allele. What we found was that subjects with the A1 allele, regardless of whether they were that of alcoholics or controls, had fewer D2 dopamine receptors than those who lacked this allele. To compensate for this deficiency state, individuals used their addictive substance to release brain dopamine and activate their few dopamine receptors, which would activate their brain dopamine reward or pleasure system. Some foods significantly increases brain dopamine levels.” — Ernest Noble, MD, PhD.
Consumption of high volumes of natural rewards like foods that are high fat/sugar dense increase Delta FOSB proteins that effects the brain reward system and enhances motivation for more (binge-eating, craving). ΔFosB is a highly stable protein which produce lasting changes in gene expression. Dr. Eric Nestler of the Mt. Sinai School of Medicine on NIMH radio.
Low functioning of the dopamine reward circulatory may cause individuals to overeat to compensate for this low reward deficit, which through conditioning produces greater anticipatory food reward and heightened development of the somatosensory cortex. STICE, SPOOR, BOHON, VELDHUIZEN, AND SMALL. Relation of Reward From Food Intake and Anticipated Food Intake to Obesity: A Functional Magnetic Resonance Imaging Study. Journal of Abnormal Psychology 2008, Vol. 117, No. 4, 924-935.
Ingestion of different nutrients, such as fats vs. sugars, normally prodces different effects on physiology, the brain, and behavior. However, they do share certain neural pathways for reinforcement of behavior including the dopamine system. When these nutrients are consumed in the form of binges, this can release excessive dopamine that causes compensatory changes that are comparable to the effects of drugs of abuse. Nicole M. Avena, Pedro Rada, Bartley G. Hoebel, 2008. Sugar vs. Fat Bingeing: Notable Differences in Addictive-like Behaviors; Department of Psychology, Princeton University.
PET scans reveal that obese subjects show a reduction in dopamine receptor availability that is associated with the body weight of the subject. Wang, G.J., Volkow, N.D., Thanos, P.K., Fowler, J.S., 2004b. Similarity between obesity and drug addiction as assessed by neurofunctional imaging. Journal of Addictive Diseases 23, 39-53.
The decrease in dopamine receptors in obese subjects is similar in magnitude to the reductions reported in drug-dependent subjects. Wang, G.J., Volkow, N.D., Logan, J., Pappas, N.R., Wong, C.T., Zhu, W., Netusil, N., Fowler, J.S., 2001. Brain dopamine and obesity. Lancet, no.9253, 354-357.
The involvement of the dopamine system in reward and reinforcement has led to the hypothesis that alterations on dopamine activity in obese subjects disposes them excessive use of food. Exposure to especially palatable foods, such as cake and ice cream, activates several brain regions including the anterior insula and right orbitofrontal cortex (Wang et al., 2004a), which may underlie the motivation to procure food. Rolls, E.T., 2006. Brain mechanisms underlying flavour and appetite. Philosophical Transactions of the Royal Society of London Series B — Biological Sciences 361, 1123-1136.
Volkow published a study in which her team found that obese people who have fewer dopamine receptors also have less activity in their prefrontal cortex. N. D. Volkow, “Inverse Association Between BMI and Prefrontal Metabolic Activity in Healthy Adults,” Obesity 17, no. 1 (2008), 60–65. doi:10.1038/oby.2008.469.
Drugs of abuse can alter dopamine and opioid receptors in the mesolimbic regions of the brain. N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 28.
The cumulative effect of all this sensory stimuli (about sugar, fat and salt – and combinations of them) amp up the neurons, getting them to fire more. The message to eat becomes stronger, motivating the eater to act more vigorously in pursuit of the stimulus.” Kessler, The End of Overeating: Taking Control of the Insatiable American Appetite, Rodale, New York, 2009
Food and Emotions
Children who ate more junk food (processed, refined, sweets, soda, and snacks) in the first years of life demonstrated more internalizing behaviors, such as worry, sadness, crying, and anxiety. They also exhibited more externalizing behaviors, such as aggression, tantrums, and hyperactivity. Moms who ate more of these foods while pregnant had children with higher levels of externalizing behaviors, independent of the children’s diets. Jacka FN, Ystrom E, Brantsaeter AL, et al. Maternal and early postnatal nutrition and mental health of offspring by age 5 years: a prospective cohort study. J Am Acad Child Adolesc Psychiatry. 2013;52:1038-1047.
A 2012 study of nearly 9000 Spanish adults found that participants who frequently consumed fast food were 40% more likely to develop depression than those who did not. Sánchez-Villegas A, Toledo E, de Irala J, Ruiz-Canela M, Pla-Vidal J, Martínez-González MA. Fast-food and commercial baked goods consumption and the risk of depression. Public Health Nutr. 2012;15:424-432
Dietary patterns characterized by higher intakes of processed or fried foods, refined grains, and sugary were associated with increased depression and anxiety in both Australian and Norwegian adults. Jacka FN, Pasco JA, Mykletun A, et al. Association of Western and traditional diets with depression and anxiety in women. Am J Psychiatry. 2010;167:305-311. Jacka FN, Mykletun A, Berk M, Bjelland I, Tell G. The association between habitual diet quality and the common mental disorders in community-dwelling adults: the Hordaland Health Study. Psychosom Med. 2011;73:483-490.
Unhealthy diets were associated with poorer mental health in more than 3000 adolescents aged 11-18 years. Investigators found that those whose diets were higher in snack and processed foods scored significantly worse on the Pediatric Quality of Life Inventory. Jacka FN, Ystrom E, Brantsaeter AL, et al. Maternal and early postnatal nutrition and mental health of offspring by age 5 years: a prospective cohort study. J Am Acad Child Adolesc Psychiatry. 2013;52:1038-1047.
Binge Eating Disorder
The subset of BED patients classified as having YFAS “food addiction” appear to represent a more disturbed variant characterized by greater eating disorder psychopathology and associated pathology. Classification of “food addiction” was met by 57% of BED patients who had significantly higher levels of depression, negative affect, emotion dysregulation, eating disorder psychopathology, and lower self-esteem. Gearhardt AN, White MA, Masheb RM, Morgan PT, Crosby RD, Grilo CM. An examination of the food addiction construct in obese patients with binge eating disorder. Int J Eat Disord. 2012 Jul;45(5):657-63. doi: 10.1002/eat.20957. Epub 2011 Aug 30.
There is increasing evidence that disruption of energy homeostasis can affect the reward circuitry and that overconsumption of rewarding food can lead to changes in the reward circuitry that result in compulsive food intake akin to the phenotype seen with addiction. Volkow ND, Wang GJ, Tomasi D, Baler RD. The Addictive Dimensionality of Obesity. Biol Psychiatry. 2013 Jan 29. pii: S0006-3223(13)00011-5. doi: 10.1016/j.biopsych.2012.12.020.
Yale University researchers used functional MRI (fMRI) studies to prove that both lean and obese women who test positive for addictive behavior around food show the exact 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 consuming them. A. Gearhardt et al., “Neural Correlates of Food Addiction,” Archives of General Psychiatry 68, no. 8 (August 2011):808–16. Published electronically April 4, 2011.
Kenney demonstrated that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction. P. Johnson and P. J. Kenny, “Dopamine D2 Receptors in Addiction-Like Reward Dysfunction and Compulsive Eating in Obese Rats,” Nature Neuroscience 13, no. 5 (2010):635–41.
People were 30 to 40 percent more likely to be obese if they had addiction in the family. For women, the chance was 50 percent greater. R. Grucza et al., “The Emerging Link Between Alcoholism Link and Obesity in the US,” Archives of General Psychiatry 67, no. 12 (2010):1301–8.
The overall enhancement of consummatory behaviors (both ethanol and water) suggests that RYGB may facilitate alcohol consumption, which in vulnerable individuals could lead to abuse and addiction. Thanos PK, Subrize M, Delis F, Cooney RN, Culnan D, Sun M, Wang GJ, Volkow ND, Hajnal A. Gastric bypass increases ethanol and water consumption in diet-induced obese rats. Obes Surg. 2012 Dec;22(12):1884-92. doi: 10.1007/s11695-012-0749-2.
Numorous studies have found that sensitization to one drug can lead subsequent increased intake of another drug or substance. Ellgren et al., 2007; Henningfield et al., 1990; Hubbell et al., 1993; Liguori et al., 1997; Nicols et al., 1991; Piazza et al., 1989; Vezina et al., 2002; Volpicelli et al., 1991.
Somatic signs of withdrawal, such as teeth chattering, forepaw tremor, and head shakes are observed in rats that have had sugar eliminated from their diet. Colantuoni, C., Rada, P., McCarthy, J., Patten, C., Avena, N.M., Chadeayne, A., Hoebel, B.G., 2002. Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obesity Research 10, 478-488.
These animals are also anxious, as measured by reduced time spent on the exposed arm of an elevated plus-maze. Colantuoni, C., Rada, P., McCarthy, J., Patten, C., Avena, N.M., Chadeayne, A., Hoebel, B.G., 2002. Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obesity Research 10, 478-488.
Behavioral depression has also been found following naloxone administration in intermittent sugar-fed rats. N.M. Avena, Rada, Hoebel, (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 26.
Screening for food addiction has the potential to identify people with eating difficulties that seriously compromise weight management efforts. Corsica JA, Pelchat ML. Food addiction: true or false? Curr Opin Gastroenterol. 2010 Mar;26(2):165-9. doi: 10.1097/MOG.0b013e328336528d.
Signs of aggressive behavior have been found in response to removing a diet that involves intermittent sugar access. Galic, M.A., Persinger, M.A., 2002. Voluminous sucrose consumption in female rats: increased “nipiness” during periods of sucrose removal and possible oestrus periodicity. Psychological Reports 90, 58-60.
If a drug becomes available again, animals will take more than they did prior to abstinence (i.e., the “deprivation effect”) Sinclair, J.D., Senter, R.J., 1968. Development of an alcohol-deprivation effects in rats. Quarterly Journal of Studies on Alcohol 29, 863-867.
Exposure to especially palatable foods, such as cake and ice cream, activates several brain regions including the anterior insula and right orbitofrontal cortex which may underlie the motivation to procure food. Avena, N.M., Rada, P., Hoebel, B.G., 2008. Evidence for sugar addiction; Behabiorial and neurochemical effects of intermittent, excessive sugar intake. Neuroscience Biobehavioral Review 32(1), 20-39.
Craving-related changes in fMRI signal have been identified in response to palatable foods, similar to drug craving. Pelchat, M.L., Johnson, A., Chan, R., Valdez, J., Ragland, J.D., 2004. Images of desire: food craving activation during fMRI. Neuroimage 23, 1486-1493.
Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in response to food intake. Gearhardt, A.N., Yokum, S., Orr, P.T., Stice, E., Corbin, W.R., & Brownell, K.D. (2011). The neural correlates of food addiction. Archives of General Psychiatry, 68, 808-816. doi:10.1001/archgenpsychiatry.2011.32.
Although there exist important differences between foods and addictive drugs, ignoring analogous neural and behavioral effects of foods and drugs of abuse may result in increased food-related disease and associated social and economic burdens. Public health interventions that have been effective in reducing the impact of addictive drugs may have a role in targeting obesity and related diseases. Gearhardt AN, Grilo CM, DiLeone RJ, Brownell KD, Potenza MN (2011). Can food be addictive? Public health and policy implications. Addiction. 2011 Jul;106(7):1208-12. doi: 10.1111/j.1360-0443.2010.03301.x. Epub 2011 Feb 14.
You can download the Yale Food Addiction Scale at http://www.yaleruddcenter.org/resources/upload/docs/what/addiction/FoodAddictionScale09.pdf
Substance Use Disorder and Eating Disorders
National Center on Addiction and Substance Abuse at Columbia University (CASA), 2003 published the first comprehensive examination of the link between chemical dependency and eating disorders, which indicated that roughly one-half of individuals with eating disorders abuse alcohol or drugs, compared to 9 percent of the general population. Up to 35 percent of substance abusers have eating disorders, compared to 3 percent of the general population. (I believe the numbers are much higher in other research. The report is also outdated.)
- During puberty, a healthy girl will gain anywhere from 20-50 lbs.
- 45% of elementary age children report wanting to be thinner.
- 50% of girls ages 12-14 say they are unhappy because they “feel fat”
- 80% of women in the US report being dissatisfied with their appearance
- 86% of sufferers report onset by age 20 and 33% between ages 11-15
- 40-60% of High School girls in the US are dieting on any given day
- Over 66% of the population of America is overweight. Nearly one-quarter are obese.
- 8-11 million people in the U.S. have eating disorders.
- 35% of “normal dieters” progress to eating disorders
- Anorexia Nervosa has the highest mortality rate of any mental illness
- 60% of women who abuse substances also have an eating disorder.
- 25% of Eating Disorder sufferers are men.
- Thirty percent of post-bariatric patients develop substance addiction.
- Eating disorder patients can fully recover
- Early intervention and a supportive family or loved ones are factors that seem to improve the chances of recovery
Research has uncovered neurobiological and behavioral similarities between substance dependence and excess consumption of highly processed foods. These findings have led to the theory that food addiction may play a role in obesity and disordered eating. Gearhardt AN, Corbin WR. The role of food addiction in clinical research. Curr Pharm Des. 2011;17(12):1140-2.
There are several biological similarities between dependence of palatable food and drug dependence including cravings and loss of control. Fortuna JL. The obesity epidemic and food addiction: clinical similarities to drug dependence. J Psychoact Drugs. 2012;44 (1):56–63.
In the model of sucrose binging, behavioral components of addiction are demonstrated and related to neurochemical changes that also occur with addictive drugs. Evidence supports the hypothesis that rats can become dependent and “addicted” to sucrose. Avena NM. The study of food addiction using animal models of binge eating. Appetite. 2010 Dec;55(3):734-7. doi: 10.1016/j.appet.2010.09.010. Epub 2010 Sep 16.
This review demonstrates that rats with intermittent access to a sugar solution can show both a constellation of behaviors and parallel brain changes that are characteristic of rats that voluntarily self-administer addictive drugs. This is evidence that under some circumstances sugar can be addictive. N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews p32.
Several studies have correlated the rise in the incidence of obesity with an increase in sugar consumption. Bray et al., 1992; Elliott et al., 2002; Howard and Wylie-Rosett, 2002; Ludwig et al., (2001). N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 31.
Evidence for experimental research on animals has unearthed deep commonalities between overconsumption of sugars and drug addiction. Volkow ND, Wise RA (2005) How can drug addiction help us understand obesity? National Neuroscience 8, 555-60.; Kelley AE (2004) Memory and addiction; shared neural circuitry and molecular mechanisms. Neuron 44: 161-79; Levine AS, Kotz CM, Gosnell BA (2003) Sugars: hedonic aspects, neuroregulation, and energy balance. American Journal of Clinical Nutrition 78, 834S-842S.
Both sweet tastes and drugs of abuse stimulate dopamine signaling in the ventral striatum, a brain signaling pathway critically involved in reward processing and learning. Koob, G.F., Le Moal, M., (2006) The neurobiology of addiction. San Diego: Academic Press. 490 p; Wise RA (2004) Dopamine, learning and motivation. National Review of Neuroscience 5, 483-94.
Our findings clearly demonstrate that intense sweetness can surpass cocaine reward, even in drug-sensitized and addicted individuals. Citation; Lenoir M, Serre F. Cantin L, Ahmed SH (2007) Intense Sweetness Surpasses Cocaine Reward. PLoS ONE 2(8): e698. doi:10.1371/journal.pone.000069.
We speculate that the addictive potential of the intense sweetness results from an inborn hypersensitivity to sweet taste. In most mammals, including rats and humans, sweet receptors evolved in ancestral environments poor in sugars and are thus not adapted to high concentrations of sweet taste. The super normal stimulation of these receptors by sugar-rich diets, such as those now widely available in modern societies, would generate a super normal reward signal in the brain, with the potential to override self-control mechanisms and thus to lead to addiction. Citation; Lenoir M, Serre F, Cantin L, Ahmed SH (2007) Intense Sweetness Surpasses Cocaine Reward. PLoS ONE 2(8): e698. doi:10.1371/journal.pone.0000698
Sugar intake may lead to an increased number of and/or affinity for opioid receptors, which in turn leads to further ingestion of sugar and may contribute to obesity. Fullerton, D.T., Getto, C.J., Swift, W.J., Carlson, I.H., 1985. Sugar, opioids, and binge eating. Brain Research Bulletin 14, 673-680.
Sugar “withdrawal” upsets dopamine/acetylcholine balance in the accumbens. N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 28.
Recent findings using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) in humans have supported the idea that aberrant eating behaviors, including those observed in obesity, may have similarities to drug dependence. Craving-related changes in fMRI signal have been identified in response to palatable foods, similar to drug craving. Pelchat, M.L., Johnson, A., Chan, R., Valdez, J., Ragland, J.D., 2004. Images of desire: food craving activation during fMRI. Neuroimage 23, 1486-1493.
Sugar access repeatedly releases dopamine in response to the taste of sugar, may be important for understanding the bingeing behaviors associated with bulimia. Dopamine has been implicated in bulimia by comparing it to hypothalamic self-stimulation, which also releases dopamine without calories. (Hoebel et al., 1992).
Certain functional markers of genes regulating dopamine signaling in the brain striatal area were associated with binge eating disorder (BED) and eating-related sub-phenotypes of BED. Results support the view that BED may have its causal origins in a hyper- responsiveness to rewarding stimuli such as highly palatable food. Davis C, Levitan RD, Yilmaz Z, et al. Binge eating disorder and the dopamine D2 receptor: Genotypes and sub-phenotypes. Prog Neuropsychopharmacol Bio Psychiatry. 2012;38:328–35.
Some refined ingredients, such as sugars, are progressively more viewed, by laypeople and scientists alike, as addictive substances and their chronic overconsumption as food addiction. Once a controversial concept, food addiction is now considered as serious as other forms of addiction, including cocaine or heroin addiction. In addition, there is growing evidence linking increased sugar availability and consumption, particularly in infants, to the current worldwide obesity epidemic. Despite the focus on sugar addiction, some of the main conclusions drawn can be generalized to other types of food addiction. Serge H. Ahmed Ph.D., Dr. Nicole M. Avena, Dr. Kent C. Berridge, Dr. Ashley N. Gearhardt, Dr. Karine Guillem. (2013). Food Addiction. Neuroscience in the 21st Century, pp 2833-2857.
The overall similarities in behavior and brain adaptation with sugar bingeing and drug intake support the theory that some eating disorders, such as bulimia, may have properties of an “addiction” in certain individuals. Davis and Claridge, (1998); Gillman and Lichtigfeld, (1986); Heubner, (1993); Marrazzi and Luby, (1986, 1990); Mercer and Holder, (1997); Riva et al., (2006). N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 31.
Children in the low-sugar cereal condition consumed, on average, slightly more than 1 serving of cereal whereas children in the high-sugar condition consumed significantly more and almost twice the amount of refined sugar in total. Harris, J.L., Schwartz, M.B., Ustjanauskas, A., Ohri-Vachaspati, P., & Brownell, K.D. (2010). Effects of serving high-sugar cereals on children’s breakfast-eating behavior. Pediatrics, 127, 71- 6. Epub 2010 Dec 13.
Sugar’s potential for abuse, coupled with its toxicity and pervasiveness in the Western diet make it a primary culprit of this worldwide health crisis. University of California, San Francisco (UCSF) (2012, February 1). Societal control of sugar essential to ease public health burden, experts urge. ScienceDaily. Retrieved October 15, 2012, from http://www.sciencedaily.com /releases/2012/02/120201135312.htm
Dr. Yvonne Sanders-Butler started the first “Sugar Free Zone” elementary school in the United States. She eliminated all the high fat/high sugar foods from the cafeteria menus, refused to allow soft drinks in the school’s vending machines and instead allowed only water and healthy fruit juices to be sold. She also added a fitness program that incorporates nutrition and exercise into class lesson plans.
The result: a 28% drop in disciplinary referrals, a 23% drop in counseling referrals and higher test scores. The kids say they have more energy and feel much better. There are also less illness related absences.
SEE the Keys Semi-Starvation Experiment, 1950 showing the long-term effects of restricting food and the creation of eating disorder behaviors. You can also read the blog about this study at http://www.rebeccacooper.com/the-keys-semi-starvation-study/.
Cyclic binging and food deprivation may produce alterations in opioid receptors, which help perpetuate bingeing behavior. In support, appetite dysfunctions in the form of binge eating and self-starvation can stimulate endogenous opioid activity. Aravich, P.F., Rieg, T.S., Lauterio, T.J., Doerries, L.E., 1993. Betaendorphin and dynorphin abnormalities in rats subjected to exercise and restricted feeding; relationship to anorexia nervosa? Brain Research 622, 1-8.
Bulimia and Binge Eating
Bulimics often restrict intake early in the day and then binge later in the evening, usually on sweet food. Gendall, K.A., Sullivan, P.E., Joyce, P.R., Carter, F.A., Bulik, C.M., 1997. The nutrient intake of women with bulimia nervosa. International Journal of Eating Disorders 21, 115-127.
Bulimic patients have increased opioid receptor binding in the insula compared with controls, which correlates with recent bingeing behavior. Bencherif, B., Guarda, A.S., Colantuoni. C., Ravert, H.T., Dannals, R.F., Frost, J.J., 2005. Regional mu-opioid receptor binding in insular cortex is decreased in bulimia nervosa and correlates inversely with fasting behavior. Journal of Nuclear Medicine 46, 1349-1351.
Acetylcholine is normally important for the satiation process. Hoebel, B.G., Rada, P., Mark, G.P., Pothos, E., 1999. Neural systems for reinforcement and inhibition of behavior: Relevance to eating, addiction, and depression. In: Kahneman, D., et al. (Eds.), Wellbeing: the Foundations of Hedonic Psychology. Russell Sage Foundation, New York, 558-572.
By purging, one eliminates the acetylcholine response that opposes dopamine. Thus when “bingeing” on sugar is accompanied by purging, the behavior is reinforced by dopamine without acetylcholine, which is more like taking a drug and less like normal eating. N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 29.
The behavioral signs of drug withdrawal are usually accompanied by alterations in dopamine/ acetylcholine balance. During withdrawal, dopamine decreases while acetylcholine is increased. This imbalance has been shown during chemically induced withdrawal with several drugs of abuse, including morphine, nicotine and alcohol. Rada, P., Avena, N.M., Hoebel, B.G., 2005b. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience 134, 737-744.
Bulimic patients have low central dopamine activity as reflected in the analysis of dopamine metabolites in the spinal fluid, which also indicates a role for dopamine in their abnormal responses to food. Jimerson, D.C., Lesem, M.D., Kaye, W.H., Brewerton, T.D., (1992) Low serotonin and dopamine metabolite concentrations in cerebrospinal fluid from bulimic patients with frequent binge episodes. Archives of General Psychiatry 49, 132-138.
We have shown that purging leaves dopamine unopposed by satiety-associated acetylcholine in the accumbens. This neurochemical state may be conducive to exaggerated binge eating. Moreover, the findings that intermittent sugar intake cross sensitizes with amphetamine and fosters alcohol intake may be related to the co-morbidity between bulimia and substance abuse. Holderness, C.C., Brooks-Gunn, J., Warren, M.P., 1994. Co-morbidity of eating disorders and substance abuse review of the literature. International Journal of Eating Disorder 16, 1-34.
The overall similarities in behavior and brain adaptation with sugar bingeing and drug intake support the theory that some eating disorders, such as bulimia, may have properties of an “addiction” in certain individuals. Davis and Claridge, (1998); Gillman and Lichtigfeld, (1986); Heubner, (1993); Marrazzi and Luby, (1986, 1990); Mercer and Holder, (1997); Riva et al., (2006). N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 31.
High Corn Fructose
High Corn Fructose now represents more than 40% of caloric sweeteners added to foods and beverages. It is the sole caloric sweetener in soft drinks in the United States. The increased use of high-fructose corn syrup in the United States mirrors the rapid increase in obesity. Bray, Nielsen, Popkin (April 2004) Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. American Journal of Clinical Nutrition, Vol. 791, No. 4, 537-543.
Fructose is a unique sweetener that has different metabolic effects on the body than glucose or sucrose. Fructose is absorbed further down the intestine, and whereas circulating glucose releases insulin from the pancreas, fructose stimulates insulin syntheses but does not release it. Insulin modifies food intake by inhibiting eating and by increasing leptin release, which also can inhibit food intake. Meals of high-fructose corn syrup can reduce circulating insulin and leptin levels, contributing to increased body weight. Fructose intake might not result in the degree of satiety that would normally ensue with an equally caloric meal of glucose or sucrose. Based on our results showing that sweet taste is sufficient to elicit the repeated release of dopamine, we hypothesize that any sweet taste consumed in a binge-like manner is a candidate for producing signs of dependence. N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 28.
Meals of high-fructose corn syrup can reduce circulating insulin and leptin levels, contributing to increased body weight. Elliot, S.S., Keim, N.L., Stern, J.S., Teff, K., Havel, P.J., 2002. Fructose, weight gain, and the insulin resistance syndrome. American Journal of Clinical Nutrition 76, 911-922.
Bingeing on sugar can cause dopamine sensitization and opioid dependency, with withdrawal symptoms and long lasting aftereffects. Bingeing on sucrose does not cause obesity; the rats compensate for the added calories by eating less lab chow. But, if the sugar is high-fructose corn syrup, then the animals do gain excess weight. N.M. Avena, Rada, Hoebel (2008) Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 31.
Greater anticipated reward form food intake increases risk for overeating. Pelchat, M. L., Johnson. A., Chan, R., Valdez, J., & Ragland, J. D. (2004). Images of desire: food-craving activation during fMRI. NeuroImage, 23, 1486-1493: Roefs, A., Herman, C.P., MacLeod, C. M., Smulders, F. T., & Jansen, A. (2005). At first sight: How do restrained eaters evaluate high-fat palatable foods? Appetite, 44, 103-114.
Anticipated reward from food is a stronger determinant of caloric intake than the reward experienced when the food is actually consumed. STICE, SPOOR, BOHON, VELDHUIZEN, AND SMALL. Relation of Reward From Food Intake and Anticipated Food Intake to Obesity: A Functional Magnetic Resonance Imaging Study. Journal of Abnormal Psychology 2008, Vol. 117, No. 4, 924-935.
With functional MRI’s obese patients showed greater activation in the primary gustatory cortex and in the somatosensory cortex and anterior cingulate in response to our measure of anticipatory food reward compared with lean participants. STICE, SPOOR, BOHON, VELDHUIZEN, AND SMALL. Relation of Reward From Food Intake and Anticipated Food Intake to Obesity; A Functional Magnetic Resonance Imaging Study. Journal of Abnormal Psychology 2008, Vol. 117, No. 4, 924-935.
A mantra of the food and beverage industry is that “there is no bad food.” Brownell, K.D., & Koplan, J.P. (2011). Front-of-package nutrition labeling – an abuse of trust by the food industry? New England Journal of Medicine, 364, 2373-2375.
Sugar Awareness Scale
Download at www.SugarAwareness.com
Note from Rebecca:
Thank you for attending my workshop. I hope you enjoy researching some of the information I presented. I am always interested in new research on this topic. I would very much appreciate you sharing your research, findings, comments, questions and opinions with me personally by commenting at www.RebeccaCooper.com/contact.
I have many more forms, charts and questionnaires that can be downloaded free from www.DietsDontWork.org. You can also buy my books, workbooks, CDs, DVD’s, and obtain the PDF download of the Diets Don’t Work® book at www.DietsDontWork.org.
The Diets Don’t Work® book is available as an eBook and Kindle on
Please visit www.SugarAwareness.com to record your experiences and beliefs about sugar consumption and/or see what others are saying about their experiences with sugar.
If you want a free eating disorder assessment call 800-711-2062. To get information about eating disorders and treatment options go to www.RebeccasHouse.org.
Many Blessings, Rebecca
P.S. I would also like to give you my free e-Pub, “Living Diet-Free” by clicking the red box on www.RebeccaCooper.com/links.
Ancel Keys wanted to find out the physical and psychological effects of what happens to the human body when it starves and how it recovers from starvation. He thought his information would be useful if the soldiers were captured in the war and they reached the point of starvation.
Keys conducted a study to determine the effects of food restriction. His results were amazing. We know that restriction causes weight loss but look at all the other symptoms of the experiment. They are classic eating disorder symptoms. The study shows that restricting food affects us not only physically, but psychologically and behaviorally as well. Note that even after the subjects started eating normally the psychological and behavioral effects remained.
The experiment involved carefully studying 36 young, healthy, psychologically normal men while restricting their caloric intake for 6 months. More than 100 men volunteered for the study as an alternative to military service; the 36 selected had the highest levels of physical and psychological health, as well as the most commitment to the objectives of the experiment. What makes the “starvation study” (as it is commonly known) so important is that many of the experiences observed in the volunteers are the same as those experienced by patients with eating disorders. This section of this chapter is a summary of the changes observed in the Minnesota study.
During the first 3 months of the semi-starvation experiment, the volunteers ate normally while their behavior, personality, and eating patterns were studied in detail. During the next 6 months, the men were restricted to approximately half of their former food intake and lost, on average, approximately 25% of their former weight. Although this was described as a study of “semi-starvation,” it is important to keep in mind that cutting the men’s rations to half of their former intake is precisely the level of caloric deficit used to define “conservative” treatments for obesity (Stunkard, 1993). The 6 months of weight loss were followed by 3 months of rehabilitation, during which the men were gradually refed. A subgroup was followed for almost 9 months after the re-feeding began. Most of the results were reported for only 32 men, since 4 men were withdrawn either during or at the end of the semi-starvation phase. Although the individual responses to weight loss varied considerably, the men experienced dramatic physical, psychological, and social changes. In most cases, these changes persisted during the rehabilitation or re-nourishment phase.
Attitudes and Behavior Related to Food and Eating
One of the most of the striking changes that occurred in the volunteers was a dramatic increase in food preoccupations. The men found concentration on their usual activities increasingly difficult, because they became plagued by incessant thoughts of food and eating. During the semi-starvation phase of the experiement, food became a principal topic of conversation, reading, and daydreams. Rating scales revealed that the men experienced an increase in thinking about food, as well as corresponding declines in interest in sex and activity during semi-starvation. The actual words used in the original report are particularly revealing and the following quotations followed by page numbers in parentheses are from Keys et al. (1950) with permission of the University of Minnesota Press.
As starvation progressed, the number of men who toyed with their food increased. They made what under normal conditions would be weird and distasteful concoctions, (p. 832). . . Those who ate in the common dining room smuggled out bits of food and consumed them on their bunks in a long-drawn-out ritual, (p. 833). . . Toward the end of starvation some of the men would dawdle for almost two hours after a meal which previously they would have consumed in a matter of minutes, (p. 833). . . Cookbooks, menus, and information bulletins on food production became intensely interesting to many of the men who previously h ad little or no interest in dietetics or agriculture, (p. 833). The volunteers often reported that they got a vivid vicarious pleasure from watching other persons eat or from just smelling food. (p. 834)
In addition to cookbooks and collecting recipes, some of the men even began collecting coffeepots, hot plates, and other kitchen utensils. According to the original report, hoarding even extended to non-food-related items such as “old books, unnecessary second-hand clothes, knick knacks, and other ‘junk. Often after making such purchases, which could be afforded only with sacrifice, the men would be puzzled as to why they had bought such more or less useless articles” (p. 837). One man even began rummaging through garbage cans. This general tendency to hoard has been observed in starved anorexic patients (Crisp, Hsu, & Harding, 1980) and even in rats deprived of food (Fantino & Cabanac, 1980). Despite little interest in culinary matters prior to the experiment, almost 40% of the men mentioned cooking as part of their postexperiment plans. For some, the fascination was so great that they actually changed occupations after the experiment; three became chefs, and one went into agriculture!
The Minnesota subjects were often caught between conflicting desires to gulp their food down ravenously and consume it slowly so that the taste and odor of each morsel would be fully appreciated. Toward the end of starvation some of the men would dawdle for almost two hours over a meal which previously they would have consumed in a matter of minutes. . .they did much planning as to how they would handle their day’s allotment of food. (p. 833) The men demanded that their food be served hot, and they made unusual concoctions by mixing foods together, as noted above. There was also a marked increase in the use of salt and spices. The consumption of coffee and tea increased so dramatically that the men had to be limited to 9 cups per day; similarly, gum chewing became excessive and had to be limited after it was discovered that one man was chewing as many as 40 packages of gum a day and “developed a sore mouth from such continuous exercise” (p. 835).
During the 12-week re-feeding phase of the experiment, most of the abnormal attitudes and behaviors in regard to food persisted. A small number of men found that their difficulties in this area were quite severe during the first 6 weeks of re-feeding:
During the restrictive dieting phase of the experiment, all of the volunteers reported increased hunger. Some appeared able to tolerate the experience fairly well, but for others it created intense concern and led to a complete breakdown in control. Several men were unable to adhere to their diets and reported episodes of binge eating followed by self-reproach. During the eighth week of starvation, one volunteer flagrantly broke the dietary rules, eating several sundaes and malted milks; he even stole some penny candies. He promptly confessed the whole episode, and became self-deprecatory” (p. 884). While working in a grocery store, another man suffered a complete loss of will power and ate several cookies, a sack of popcorn, and two overripe bananas before he could “regain control” of himself. He immediately suffered a severe emotional upset, with nausea, and upon returning to the laboratory he vomited . . .He was self-deprecatory, expressing disgust and self-criticism (p. 887).
One man was released from the experiment at the end of the semi-starvation period because of suspicions that he was unable to adhere to the diet. He experienced serious difficulties when confronted with unlimited access to food “He repeatedly went through the cycle of eating tremendous quantities of food, becoming sick, and then starting all over again” (p. 890). During the re-feeding phase of the experiment, many of the men lost control of their appetites and “ate more or less continuously” (p. 843).
Even after 12 weeks of re-feeding, the men frequently complained of increased hunger immediately following a large meal.
One of the volunteers ate immense meals (a daily estimate of 5,000-6,000 cal.) and yet started “snacking” an hour after he finished a meal. Another ate as much as he could hold during the three regular meals and ate snacks in the morning, afternoon and evening. (p. 846). Several men had spells of nausea and vomiting. One man required aspiration and hospitalization for several days. (p. 843)
During the weekends in particular, some of the men found it difficult to stop eating. Their daily intake commonly ranged between 8,000 and 10,000 calories, and their eating patterns were described as follows:
Subject No. 20 stuffs himself until he is bursting at the seams, to the point of being nearly sick and still feels hungry; No. 120 reported that he had to discipline himself to keep from eating so much as to become ill; No. 1 ate until he was uncomfortably full; and subject No. 30 had so little control over the mechanics of “piling it in” that he simply had to stay away from food because he could not find a point of satiation even when he was “full to the gills.”. . .”I ate practically all weekend,” reported subject No. 26. . .Subject No. 26 would just as soon have eaten six meals instead of three. (p. 847)
After about 5 months of re-feeding, the majority of the men reported some normalization of their eating patterns, but for some the extreme overconsumption persisted “No. 108 would eat and eat until he could hardly swallow any more and then he felt like eating half an hour later” (p. 847). More than 8 months after renourishment began, most men had returned to normal eating patterns; however, a few were still eating abnormal amounts “No. 9 ate about 25 percent more than his pre-starvation amount; once he started to reduce but got so hungry he could not stand it” (p. 847).
Factors distinguishing men who rapidly normalized their eating from those who continued to eat prodigious amounts were not identified. Nevertheless, the main findings here are as follows: Serious binge eating developed in a subgroup of men, and this tendency persisted in come cases for months after free access to food was reintroduced; however, the majority of men reported gradually returning to eating normal amounts of food after about 5 months of re-feeding. Thus, the fact that binge eating was experimentally produced in some of these normal young men should temper speculations about primary psychological disturbances as the cause of binge eating in patients with eating disorders. These findings are supported by research indicating that habitual dieters display marked overcompensation in eating behaviors that are similar to the binge eating observed in eating disorders (Polivy & Herman, 1985, 1987; Wardle & Beinart, 1981). Polivy et al., (1994) compared a group of former World War II prisoners of war and non-interned veterans and found that the former prisoners lost an average of 10.5 Kg. They also reported a significantly higher frequency of binge eating than non-interned veterans according to a self-report questionnaire sent by mail.
Emotional and Personality Changes
The experimental procedures involved selecting volunteers who were the most physically and psychologically robust. “The psychobiological ‘stamina’ of the subjects was unquestionably superior to that likely to be found in any random or more generally representative sample of the population” (pp. 915-916).
Although the subjects were psychologically healthy prior to the experiment, most experienced significant emotional deterioration as a result of semi-starvation. Most of the subjects experienced periods during which their emotional distress was quite severe; almost 20% experienced extreme emotional deterioration that markedly interfered with their functioning. Depression became more severe during the course of the experiment. Elation was observed occasionally, but this was inevitably followed by “low periods.” Mood swings were extreme for some of the volunteers:
One subject experienced a number of periods in which his spirits were definitely high. . . These elated periods alternated with times in which he suffered “a deep dark depression.” (p. 903)
Irritability and frequent outbursts of anger were common, although the men had quite tolerant dispositions prior to starvation. For most subjects, anxiety became more evident. As the experiment progressed, many of the formerly even-tempered men began biting their nails or smoking because they felt nervous. Apathy also became common, and some men who had been quite fastidious neglected various aspects of personal hygiene. During semi-starvation, two subjects developed disturbances of “psychotic” proportions. During the re-feeding period, emotional disturbance did not vanish immediately but persisted for several weeks, with some men actually becoming more depressed, irritable, argumentative, and negativistic than they had been during semi-starvation. After two weeks of re-feeding, one man reported his extreme reaction in his diary:
I have been more depressed than ever in my life. . .I thought that there was only one thing that would pull me out of the doldrums, that is release from C.P.S. the experiment I decided to get rid of some fingers. Ten days ago, I jacked up my car and let the car fall on these fingers. . .It was premeditated. (pp. 894-895)
Several days later, this man actually did chop off three fingers of one hand in response to the stress.
Standardized personality testing with the Minnesota Multiphasic Personality Inventory (MMPI) revealed that semi-starvation resulted in significant increases on the Depression, Hysteria, and Hpochondriasis scales. The MMPI profiles for a small minority of subjects confirmed the clinical impression of incredible deterioration as a result of semi-starvation. One man who scored well within normal limits at initial testing, but after 10 weeks of semi-starvation and a weight loss of only about 4.5 kg (10 pounds, or approximately 7% of his original body weight), gross personality disturbances were evident on the MMPI. Depression and general disorganization were particularly striking consequences of starvation for several of the men who became the most emotionally disturbed.
Social and Sexual Changes
The extraordinary impact of semi-starvation was reflected in the social changes experienced by most of the volunteers. Although originally quite gregarious, the men became progressively more withdrawn and isolated. Humor and the sense of comradeship diminished amidst growing feelings of social inadequacy. The volunteers’ social contacts with women also declined sharply during semi-starvation. Those who continued to see women socially found that the relationships became strained. These changes are illustrated in the account from one man’s diary:
I am one of about three or four who still go out with girls. I fell in love with a girl during the control period but I see her only occasionally now. It’s almost too much trouble to see her even when she visits me in the lab. It requires effort to hold her hand. Entertainment must be tame. If we see a show, the most interesting part of it is contained in scenes where people are eating. (p. 853)
Sexual interests were likewise drastically reduced. Masturbation, sexual fantasies, and sexual impulses either ceased or became much less common. One subject graphically stated that he had “no more sexual feeling than a sick oyster.” (Even this peculiar metaphor made reference to food.) Keys et al. observed that “many of the men welcomed the freedom from sexual tensions and frustrations normally present in young adult men” (p. 840). The fact that starvation perceptibly altered sexual urges and associated conflicts is of particular interest, since it has been hypothesized that this process is the driving force behind the dieting of many anorexia nervosa patients. According to Crisp (1980), anorexia nervosa is a adaptive disorder in the sense that it curtails sexual concerns for which the adolescent feels unprepared. During rehabilitation, sexual interest was slow to return. Even after 3 months, the men judged themselves to be far from normal in this area. However, after 8 months of renourishment, virtually all of the men had recovered their interest in sex.
Cognitive and Physical Changes
The volunteers reported impaired concentration, alertness, comprehension, and judgment during semi-starvation; however, formal intellectual testing revealed no signs of diminished intellectual abilities. As the 6 months of semi-starvation progressed, the volunteers exhibited many physical changes, including gastrointestinal discomfort; decreased need for sleep; dizziness; headaches; hypersensitivity to noise and light; reduced strength; poor motor control; edema (an excess of fluid causing swelling); hair loss; decreased tolerance for cold temperatures (cold hands and feet); visual disturbances (i.e., inability to focus, eye aches, “spots” in the visual fields); auditory disturbances (i.e., ringing noise in the ears); and paresthesias (i.e., abnormal tingling or prickling sensations, especially in the hands or feet).
Various changes reflected an overall slowing of the body’s physiological processes. There were decreases in body temperature, heart rate, and respiration, as well as in basal metabolic rate (BMR). BMR is the amount of energy (in calories) that the body requires at rest (i.e., no physical activity) in order to carry out normal physiological processes. It accounts for about two-thirds of the body’s total energy needs, with the remainder being used during physical activity. At the end of semi-starvation, the men’s BMRs had dropped by about 40% from normal levels. This drop, as well as other physical changes, reflects the body’s extraordinary ability to adapt to low caloric intake by reducing its need for energy. More recent research has shown that metabolic rate is markedly reduced even among dieters who do not have a history of dramatic weight loss (Platte, Wurmser, Wade, Mecheril & Pirke, 1996). During re-feeding, Keys et al. found that metabolism speeded up, with those consuming the greatest number of calories experiencing the largest rise in BMR. The group of volunteers who received a relatively small increment in calories during re-feeding (400 calories more than during semi-starvation) had no rise in BMR for the first 3 weeks. Consuming larger amounts of food caused a sharp increase in the energy burned through metabolic processes.
Significance of the “Starvation Study”
As is readily apparent from the preceding description of the Minnesota experiment, many of the symptoms that might have been thought to be specific to anorexia nervosa and bulimia nervosa are actually the results of starvation (Pirke & Ploog, 1987). These are not limited to food and weight, but extend to virtually all areas of psychological and social functioning. Since many of the symptoms that have been postulated to cause these disorders may actually result from undernutrition, it is absolutely essential that weight be returned to “normal” levels so that psychological functioning can be accurately assessed.
The profound effects of starvation also illustrate the tremendous adaptive capacity of the human body and the intense biological pressure on the organism to maintain a relatively consistent body weight. This makes complete evolutionary sense. Over hundreds of thousands of years of human evolution, a major threat to the survival of the organism was starvation. If weight had not been carefully modulated and controlled internally, early humans most certainly would simply have died when food was scarce or when their interest was captured by countless other aspects of living. The Keys et al. “starvation study” illustrates how the human being becomes more oriented toward food when starved and how other pursuits important to the survival of the species (e.g., social and sexual functioning) become subordinate to the primary drive toward food.
One of the most notable implications of the Minnesota experiment is that it challenges the popular notion that body weight is easily altered if one simply exercises a bit of “willpower.” It also demonstrates that the body is not simply “reprogrammed” at a lower set point once weight loss has been achieved. The volunteers’ experimental diet was unsuccessful in overriding their bodies’ strong propensity to defend a particular weight level. Again, it is important to emphasize that following the months of re-feeding, the Minnesota volunteers did not skyrocket into obesity. On the average, they gained back their original weight plus about 10%; then, over the next 6 months, their weight gradually declined. By the end of the follow-up period, they were approaching their pre-experiment weight levels.
Providing patients with eating disorders with the above account of the semi-starvation study can be very useful in giving them an “explanation” for many of the emotional, cognitive and behavioral symptoms that they experience. This as well as other educational materials (Garner, 1997) is based on the assumption that eating disorder patients often suffer from misconceptions about the factors that cause and then maintain symptoms. It is further assumed that patients may be less likely to persist in self-defeating symptoms if they are made truly aware of the scientific evidence regarding factors that perpetuate eating disorders. The educational approach conveys the message that the responsibility for change rests with the patient; this is aimed at increasing motivation and reducing defensiveness. The operating assumption is that the patient is a responsible and rational partner in a collaborative relationship.
Excerpts from the Handbook for the Treatment of Eating Disorders, D.M. Gardner and P.E. Garfinkel (editors), Gilford Press, New York, N.Y., 1997.
Crisp, A. J. (1980)). Anorexia Nervosa: Let me be. London: Academic Press.
Crisp, A. H., Hsu, L. K. G., & Harding, B. (1980). The starving hoarder and voracious spender: Stealing in anorexia nervosa. Journal of Psychosomatic Research, 24, 225-231.
Garner, D.M. (1997). Psychoeducational principles in the treatment of eating disorders. In: Handbook for Treatment of Eating Disorders. (145-177). D.M. Garner & P.E. Garfinkel (Eds). New York, NY: Guilford Press.
Fantino, M., & Cabanac, M. (1980). Body weight regulation with a proportional hoarding response in the rat. Physiology and Behavior, 24, 939-942.
Keys, A., Brozek, J., Henschel, A., Mickelsen, O., & Taylor, H. L. (1950). The biology of human starvation (2 vols.). Minneapolis: University of Minnesota Press.
Pirke, K. M., & Ploog, D. (1987). Biology of human starvation. In P. J. V. Beumont, G. D. Burrows, & R. C. Casper (Eds.), Handbook of eating disorders: Part 1 Anorexia and bulimia nervosa (pp. 79-102). New York: Elsevier.
Platte, P., Wurmser, H., Wade, S. E., Mecheril, A., & Pirke, K. M. (1996). Resting metabolic rate and diet-induced thermogenesis in restrained and unrestrained eaters. International Journal of Eating Disorders, 20, 33-41.
Polivy, J., Zeitlin, S.B., Herman, C.P. & Beal, A.L. (1994). Food restriction and binge eating: A study of former prisioners of war. Journal of Abnormal Psychology, 103, 409-411.
Polivy, J., & Herman, C.P. (1985). Dieting and bingeing: A causal analysis. American Psychologist, 40, 193-201.
Polivy, J., & Herman, C. P. (1987). Diagnosis and treatment of normal eating. Journal of Consulting and Clinical Psychology, 55, 635-644.
Over the years I have been asked if there is such a thing as food addiction. First, let’s look at what is an addiction? Here is one definition: An addiction causes people to engage in a recurring activity that causes harm to the person. It is often described as a compulsion to engage in some specific activity to produce mood-altering experiences, and this experience has life-damaging consequences.
Addictions often have both physical and psychological components. There is discomfort upon quitting the addiction. Most people would not overindulge in anything that hurts them physically, emotionally, mentally or spiritually. With addiction, one or more of these areas are negatively affected.
Now look at how addiction can relate to food. Ask yourself these questions:
- Does your eating behavior create a problem in your life, but you continue to do the same thing over and over?
- Do you eat to change how you feel?
- Do thoughts of food, weight and body size enter your mind at unrelated times? Do you feel out of control with your eating?
- Are you afraid to start eating something because you are afraid you cannot stop?
- Do you obsess about eating certain foods?
- Do you find yourself eating when you had resolved not to eat?
- Do you eat more than you want to?
- Do you use other activities or substances to stop your eating behaviors?
Not long ago, there was a potato chip ad that challenged, “Betcha can’t eat just one!” Many took on the challenge and lost. Food manufacturers have done an exquisite job of recognizing and tapping into our cravings. Why does this challenge some of us and not others?
It is a widely accepted fact that some people are more susceptible to becoming addicted than others. Some have a hereditary disposition to becoming dependent on mood-altering substances. Sometimes people are self-medicating, stuffing their feelings or are deficient in emotional regulating skills.
Any behavior engaged in repeatedly can become a habit. A habit is simply an activity that you do so often that it becomes a part of your routine. Most people observe that any activity repeated for about a month becomes a habit. It is important to be aware of the habits that we are forming. This can be used as a positive, life-enhancing activity or the building blocks of an addiction.
Even our thinking becomes habitual. Our negative self-talk can become so well established that we don’t even realize that we are beating ourself up or that it is having an effect on our life. It takes work to create a good habit, but it makes life easier. Bad habits are easily formed but make life harder.
Common Food Addictions
I have never met a client who was addicted to broccoli. Why? Although broccoli is good for your body, it does not produce mind-altering effects like some other non-foods. Isn’t it interesting that the most common food addictions are comprised of manufactured fats, chemicals, salt and/or sugar?
Many of us have our favorite food, but what makes food an addiction? If we apply our previous addiction definition of craving, obsessive thinking, and compulsion even in the face of harmful effects, we may come up with a list. See if any of these foods cause a problem for you:
|potato chips||ice cream||processed snacks|
It is important to note that broccoli and other whole foods usually are not addictive, but this list can be expanded. Looking at these items, we can see some similar ingredients – sugar, carbohydrates or white flour.
Carbohydrates are our major energy-producing food. We need carbohydrates like vegetables, fruit, whole grains, nuts and beans. Note that different types of carbohydrates turn into sugar at different rates in your body. For addiction purposes, let’s look at refined carbohydrates. These are the ones that spike your insulin level, and then drop you onto the blood-sugar rollercoaster. Even the blood sugar drop causes cravings, bingeing, depression, lethargy, irritability and drowsiness.
But there is more going on than just blood sugar fluctuations. During functional MRIs, scientists have observed that refined carbohydrates light up the reward system of the brain for some people – just like an addicted person using their drug of choice.
It is a good idea to think it through when you are tempted to consume one of these products. Do I really want to feel that way afterwards? Do I want to battle the incessant cravings again? This is one rollercoaster I choose not to ride. There are too many other factors that occur that triggers overeating. There is one sure way to eliminate this physiological response. Don’t put these blood sugar spiking foods in your mouth.
Food and Other Types of Addictions
Food addictions can progress to other addictions, starting with appetite suppressants and diet pills. Many patients at Rebecca’s House Eating Disorder Treatment Programs have progressed to methamphetamines, cocaine, speed and heroin to curb their appetite and stay skinny.
There are many forms of addictions, but let’s look at how we may be addicted to a few commonly ingested legal substances. Alcohol is probably a good place to start. Many people do not have a problem with alcohol, and they can drink normally without any consequences. They don’t obsess about it or try to control their intake. It has no power over them.
Then there are others who become alcoholics. They will tell you of the constant thinking about drinking, not drinking, getting their next drink or recovering from the effects of their last bout of drinking. This is the hell an active alcoholic lives with. The person may quit drinking only to find the obsessive thinking and surfacing feelings are too much to bear.
Is this anything like our compulsion to eat? Have you experienced that numbed out feeling during eating? Do you eat to make the feelings or thoughts go away? When something upsets you, do you look for comfort in food? I have had people tell me that they are thinking about food, weight, diets, body image, exercise, and so on about 95% of their waking hours. Does this make sense? Not for someone who has no problem with food. However, if you are trapped in the obsession of a food addiction, you know what I am talking about. Does eating really fix the situation or feeling, or does it often compound the problem?
Over the years, I have seen a great number of people recover from alcoholism only to switch to a food addiction. They use food in a similar way to how they used alcohol. I don’t need to go into the debate of which is better; I just want to point out the similarities.
I especially see people who are recovering from alcoholism also being addicted to sugar. That makes so much sense. Alcohol is metabolized in the body as sugar. Although it may not have the same devastating effects short-term, sugar can and does kill. Refined sugar is in almost everything now, even in some brands of potato chips!
You can get scientific articles about sugar addiction and download a Sugar Awareness assessment at www.SugarAwareness.com.
If you can relate to any items discussed in this article, you can get a free eating disorder assessment by calling 800-711-2062 or visit www.RebeccasHouse.org.