Food addiction is real; and it is making America FAT.
At 5 foot 9 inches and 300 pounds, Deke Baskins is sadly a perfect representative of 30 percent of the American population, or around 90 million obese people. A staggering 67 percent of Americans are considered overweight (Puhl, 2011). Deke is a self-professed food addict. “[Food is] powerful; it’s like a narcotic, man. It’s gotta be a tasty narcotic to get a man like this (referring to his physical state)” (Leahy, 2004). Deke’s weight-related plights mirror those of many millions of today’s Americans.
Excessive food consumption is a relatively common phenomenon in Western society. Much of it appears to occur seasonally, especially around traditional and festive holidays or family gatherings, but an increasingly larger constituency of individuals are growing up with constant exposure to mammoth quantities of low-quality food: what once constituted a binge is now a regular meal. And with the ease-of-access to highly-processed, highly-palatable foods in the supermarket and on the street corner, excessive caloric intake has become habitual for many Westerners and has seemingly led to what many health professionals refer to as the “Obesity Epidemic.” Some have made the arguments of high fat, sugary, or salty foods as being “addictive” (Cocores & Gold, 2009) or having “addictive qualities,” what Deke refers to as “that tasty taste” (Leahy, 2004). However to make the blanket statement that obesity in general is an addiction would clearly be inappropriate. Obesity is merely a symptom, the result of an addiction. An addiction, as defined by Webster’s New World Medical Dictionary, is “a chronic relapsing condition characterized by compulsive drug-seeking and abuse and by long-lasting chemical changes in thebrain.” The key word we want to focus on for now is compulsive. Until recently, the word “addiction” has been solely used as a descriptor for drug-abuse. In recent decades however, medical professionals and the general public alike have both begun questioning this and proposing theories regarding the addictive properties of food on a widespread level. It is important to note that not every case of obesity involves compulsion.
Some people, like Davis and Carter (2009) hold the view that overeating for many is a passive event, occurring “almost without awareness”. It has become habitual, manifesting itself in the forms of snacking and frequent consumption of large portion sizes. This near-lack –of- awareness is different than a compulsive drive. These individuals eat large amounts out of habit. Lack of proper nutritional education may also play a small role. The food industry spends over $30 billion a year in advertising, while the government allocates a paltry $2-3 million on nutritional education per annum (Leahy, 2004). Overly large serving sizes are served at nearly every fast food restaurant and every diner in America, and subsidized school lunches make it incredibly easy for the nation’s children to get large quantities of low-quality food for next to nothing. The phrase “get more for your money” is hardwired into the consumer mindset, and has become the motivator for a cut-throat food-service industry, to the detriment of consumer health. However, saying that overeating is purely passive is a gross under-recognition of the power behind the chemical reactions taking place in the brain. For many, the consumption of certain foods is driven by compulsion. We must remember that cravings drive choice. Very large populations of Americans are dissatisfied with their bodies and their nutritional choices on a day-to-day basis. They make nutritional choices that they know are not optimal and frequently overeat. The diet industry has exploded over recent decades as obesity numbers continue to climb (Ford, 2010). This correlation is no coincidence. Obese sufferers of food addiction have been shown to exhibit a compulsive drive to excessively overeat: most namely, eating even when uncomfortably full and even when doing so will harm them physically and/or psychologically. For example, in a study done by Cassin and von Ranson (2007), 94% of their adult samples classified themselves as “food addicts” or “compulsive overeaters,” meeting DSM-IV substance-dependence disorder criteria. But why do food addicts consume more food, and poorer quality food, than their body requires to function at an optimal level? Is there some inherent quality to modern food that stimulates pleasure-related cortical pathways in some people more than others? Is food really addictive? And how did we get here with regards to the Obesity Epidemic? What cultural movements and modern historical developments caused such a drastic rise in American obesity in such a short period of time?
This paper will lay out an exhaustive argument for why compulsive overeating is in fact an addiction, caused by a complex interplay of factors including cultural stressors, lack of nutritional quality in modern food, and human neural maladaptational responses to consumption of these foods. My argument will draw upon myriad medical, historical, and cultural literature for support, and will hopefully shed some light onto the dire condition within which a large percentage of the American population now resides: a condition that, I argue, has contributed greatly to the drastic rise in obesity in the United States over the past few decades. Food addiction and compulsive overeating are sister syndromes, intricately linked; I will therefore refer to them interchangeably. They are not the sole cause for obesity, but they are the major player. Food addiction is the under-addressed, over-responsible culprit implicated in the Obesity Epidemic.
Because the obese condition can be reached several ways, and because not all instances of excessive food intake can be regarded as dysfunctional, it would not be suitable to group these two entities into a subclass of addiction. Addiction requires compulsive action and lasting changes on the neural level. Therefore, as a distinct phenotype of obese individuals, compulsive overeaters may very well be classified as “addicts.”
The dysfunctional behavior and neural maladaptations of compulsive overeaters adhere to DSM-IV criteria and parallel drug-addicted patients sufficiently enough to implicate substance addiction as playing the key role in their non-homeostatic physical and mental states. Food can be addictive. Just as some individuals can recreationally use drugs, many people can casually/passively eat to meet their caloric requirements. However, similar to the compulsive drug-taking and seeking behavior seen in addicts, food inspires compulsive behaviors in a distinct class of individuals, consciously and unconsciously driving their thoughts and actions to the point where homeostasis is no longer an issue: compulsive overeating is an addiction.
The DSM-IV defines substance-dependence (addiction) as exhibiting three or more of the following in regards to a substance of abuse, which in this case, is food: tolerance, withdrawal, consuming large amounts over a long period of time, having unsuccessful efforts to stop use or to cut down, time spent in obtaining, thinking about, and consuming the substance replaces social, occupational, and recreational activities, and lastly, exhibiting continued use despite adverse consequences. With this in mind, we can relatively easily classify compulsive overeating as a substance-dependence disorder, or addiction.
In empirical research, compulsive overeaters display characteristics of developing tolerance; they’ve been found to progressively require more and more food to achieve the desired “drugged” effect (e.g. “the sugar high”) as time goes on (Davis & Carter, 2009). Much of the human evidence of this comes from clinical anecdotes given by the patients themselves. Picot and Linfield (2003) also found that higher body weight correlated with the frequency and severity of bingeing episodes. This may indicate that as level of obesity increases, the disorder worsens. More indirect evidence of tolerance can be found in animal studies. Avena et al. (2008) found that rodents on a high sugar chow diet exhibit addictive-like behaviors, increasing daily sugar intake over a period of 28 days. The rats also exhibit opioid-like withdrawal symptoms when given the opioid antagonist naloxone (3 mg/kg). Symptoms include anxiety, teeth chattering, tremor, head shakes, and a drop in body temperature (Avena et al, 2008) suggesting that natural rewards such as sugar act on similar neural substrates as illicit drugs. In Deke’s words, “I’d go crazy if I didn’t get some of my food” (Leahy, 2004). And with all of the warnings from medical practitioners as well as nutritional education in the public school systems from a young age, it would be absolutely inappropriate to assume that compulsive overeaters were not aware of their behaviors’ adverse affects on their health. They continue compulsive overeating despite awareness of how detrimental it is. Guilt is just one of the many cultural and personal fuels for the fire that is the compulsive overeating cycle.
In the mid-1980’s, a resonating societal movement was made to impose a “fat-tax” or “Twinkie tax.” The movement and idea were pioneered by Kelly Brownell, a psychologist at Yale University (Gilman, p10). Brownell proposed that a tax be placed on junk foods and snacks in order to discourage individuals from purchasing the items, with hopes that the negative feedback would slow the growth of the obesity epidemic. On a more personal level, guilt about one’s poor eating habits can counter-intuitively become a major reason for eating more and more in attempts to self-medicate a sense of depression or low level of bodily satisfaction. This process can become a difficult cycle to break because of the addictive effect that low-quality (high sugar, high fat) foods can have on the brain.
Donald Hebb describes eating as being a learned behavior that is reinforcing because it reverses unpleasant bodily signals and comes to be associated with environmental cues which can trigger craving (Hebb, 1949). Just like walking into drug-taking-associated room can elicit physiological responses from an addict, including craving, TV commercials and advertisements, even encountering a stressful environment, can trigger craving for certain foods. Deke (Leahy, 2004) once again sheds some light on the issue at hand, “The world’s hard, you know, man? Stressful. And then somebody says, ‘This food is gonna make you feel good, and it tastes so good, and everybody’s tryin’ it. Why aren’t you tryin’ it?’ Gotta try it!” Food is considered a natural reward. Food, as a substance of abuse, becomes a rather complicated matter because, unlike illicit drugs, food is intrinsically necessary for survival. However, in excess, it can have such adverse effects as to lead to diabetes, heart disease, and consequently, premature death. When viewed through the scope of evolution, food cravings can be seen as a necessary biological mechanism for survival in unpredictable environments. Early hunter-gatherer societies never knew how long it would be before they found their next meal. It was not uncommon to go for days without food, or with very little food. In these cases, the human body has developed in such a way that it will store fat for energy, especially after large meals. When food enters the body and blood glucose levels rise, insulin is released and fat is no longer used as an energy source. The body preserves it for later use. It instead utilizes the energy from the incoming calories, carbohydrate being the most readily consumed. This “fat-preservation” mechanism is what allowed our ancestors to survive for long periods of time between meals. However, in our current nutritional condition, food is readily available. “You can get all the Church’s Chicken you want,” says Deke (Leahy, 2004). Not only that, modern food is also calorically dense, with most processed varieties being high in sugar as well. The steady influx of sugar into the human body keeps blood glucose levels high, never giving it the chance to use fat stores as fuel. Instead, excess fat is stored and over time accumulates until the individual is in the obese state. Many individuals also become insulin resistant, resulting in Type II Diabetes. At some point, a line is crossed. The individual goes from liking food, and guiltlessly enjoying the eating experience, to wanting it and feeling guilty about the experience.
So what is the difference between liking and wanting food? And why can making such a distinction help develop a better understanding of compulsive overeating as an addiction disorder? First, to differentiate between the two, liking of food refers to the pleasure one gets from eating the food. Wanting food refers to appetite. Excessive wanting leads to compulsion. There is no doubt that food addicts experience compulsive food-seeking/consuming behavior. But why do they do so, when others don’t? To answer this question, we look to Robinson and Berridge (2000) and their incentive-sensitization theory. According to sensitization theory, the drug/food will have an increased effect on the reward system following repeated doses/eating. Individuals with easily sensitized brains will therefore be more likely to develop an addiction. The critical prediction made by incentive-sensitization is that the brains of addicted individuals will no doubt contain a region or pathway that has been sensitized by drugs, or in our case food. To add to it, sensitization is dose dependent, meaning the higher the dose, the more pronounced the sensitization. Unhealthy meals, such as a Super-Sized Value Meal, and binge episodes may constitute consuming thousands of calories, definitely a large amount of food. Therefore, according to this theory, sensitization would be greatly increased in over eaters. The main point here is that when sensitized, the food/drug ‘wanting’ produces compulsive patterns of seeking-behavior. Herein lies the critical connection. Certain individuals are more easily sensitized than others; as the doses increase, sensitization increases, creating a heightened wanting for food; this wanting thus manifests in compulsive food-seeking behavior: addiction. They outline two different types of wanting: implicit and explicit wanting (Finlayson et al, 2003). These involve separate processes but they complement each other to contribute to food preference. Implicit wanting is how hard an individual is willing to work for food. This is the independent risk factor for overconsumption. The harder someone is willing to work to get the food, the more likely they are to eat too much of it. Food has a heightened value to them. Explicit wanting refers to an individual’s desire to eat a specific kind of food. Preference for high fat, high sugar foods would reflect explicit wanting.
Incentive-sensitization is one of several popular theories for why people compulsively overeat. It is important to realize that the processes leading to food consumption are not all explicit. Implicit processes play just as much of a role, if not more, in food seeking behavior. With this in mind, is eating necessarily under voluntary control? We usually see it as such because of utilization of musculature to obtain and consume food. We can perceive our outstretched arm as our hand reaches for the food. But knowing what we do about wanting, the importance of implicit wanting cannot be overlooked, because without it, explicit wanting would not matter. If the individual is not willing to work to get food, say get off the couch, then of course they will not care about the type of food they eat. So what drives implicit wanting? On the surface, we might say hunger, because it does. However, this doesn’t account for why someone will continue to eat past feeling ‘full.’ There must be a relationship between the hedonics of food and bodily homeostasis, with hedonics having the ability to override the innate desire for a homeostatic internal environment. Our knowledge of liking and wanting in food-related behaviors is relatively limited. So, in order to strengthen our understanding, it helps to draw upon separate theoretical models for guidance.
Homeostatic and hedonic hungers, while fundamentally different in motivation, are both evolutionary important. Both motivations would’ve helped drive an individual to eat plenty of calories in order to satisfy the body’s energy needs in times of food scarcity or uncertainty. Thus, humans either learned, or innately possessed, the ability to eat past satiety. Hypothetically, if a hunter-gatherer were to stop eating at the first sign of satiety then experience a prolonged period of time between their next meal, say the hunting was slow or they were traveling through an area with little vegetation, they would put their body at risk for usurping its energy stores. To protect against this, they would use hedonic hunger to override homeostatic hunger. We still possess this ability today, though because we live in a time of food abundance, developing the habit of continually eating past our homeostatic set-points has proven to be severely detrimental to health and the main cause of obesity. The theory of ‘motivating operations’ (Tapper, 2005) focuses on explaining the motivations for food seeking. However, they completely ignore any aspect of overeating. They claim that food seeking will increase and hedonic enjoyment of food will be enhanced with deprivation. The reverse implies that with satiety, seeking behaviors and enjoyment of food will decrease. This does not account for the phenomenon that is binge eating. However, ‘motivating operations’ remains somewhat in line with the incentive sensitization model in that they both involve a decrease in food liking during overeating. When wanting increases due to sensitization, liking decreases.
The µ-opioid system plays a key role in hedonics. In a study using highly-palatable foods (high sugar and fat), opioid administration to sated rats resulted in a stronger desire for food than seen in rats who had been deprived of food (Hayward & Low, 2005). Opioids are thought to increase the hedonic properties of food. More evidence comes from a study where administration of opioids in the nucleus accumbens of rats induced episodes of binge eating on fat (Hayward & Low, 2005). Taken alone, a pure fat foodstuff, such as Crisco, has very little rewarding taste properties unless it is mixed with another highly-palatable food such as sugar. Therefore this study serves as a good indicator of the role of opioids in increasing a food’s hedonic qualities, suggesting that individuals with food addiction may be hypersensitive to opioids in the brain or have an overactive reward system. Sugar is thought to act in the brain similarly to an opioid. Referring back to the aforementioned Avena et al. (2008) study, recall that they found that rodents on a high sugar chow diet exhibit addictive-like behaviors as the researchers increased daily sugar intake over a period of 28 days. The rats also exhibit opioid-like withdrawal symptoms when given the opioid antagonist naloxone (3 mg/kg). Their symptoms included anxiety, teeth chattering, tremor, head shakes, and a drop in body temperature (Avena et al, 2008) suggesting that natural rewards such as sugar act on similar neural substrates as illicit drugs. Hopefully now the correlation between compulsive overeating and other addiction disorders is becoming apparent.
Individuals with food addiction undoubtedly exhibit certain behaviors and personality traits that are strikingly similar to those of drug addicts. The main difference lies in the fact that food addiction is more accurately referred to as a ‘behavioral addiction:” one involving abuse of natural rewards (Davis et al, 2009). Drugs of addiction also act directly on the brain. Food acts indirectly, through the gut. However, gut peptides have strong connections to the dopaminergic (DA) system (Dagher, 2009), a system closely-linked to liking and wanting of illicit drugs. Eating, unlike drug-taking, is intrinsically required for human survival. And just as higher doses of drugs result in higher potential for addiction, we can see that larger ‘meals,’ or more accurately, binges, can also result in high potential for addiction. Grigson (2002) asserts that foods, like drugs, have the ability to alter brain mechanisms in ways that contribute to their increasingly compulsive use. In their paper on the neurobiology of eating and drug abuse, Corwin & Hajnal (2005) outline four things that must be considered when operationally defining non-homeostatic appetitive behavior: quantity consumed, quality or type consumed, context in which the behavior occurs, and the specific kind of behavior that is directed toward obtaining and consuming the commodity of interest. These aspects are to be used in for defining all types of non-homeostatic behavior, including compulsive overeating, not just drug addiction behavior. It is normal to overeat on occasion. Such overeating can be effectively regulated by the body’s systems because they are prepared to work harder at certain times than others. This type of overeating is referred to as compensatory. However, when it becomes compulsive, it renders itself dysfunctional because the human body is maladapted to deal with chronic stress to the degree that excessive sugar and fat intake will induce. Long-term health issues follow. Parallels can be made to drug taking in this regard as well. Recreational use, with adequate detoxification periods between use episodes, does not result in chronic negative effects on physical and mental health. However, when use escalates to abuse, extremely negative effects follow.
The neuro-anatomical substrates associated with compulsive overeating are the same as those implicated in all appetitive behaviors, including drug taking. The main regions involved in appetitive behavior are the amygdala, hippocampus, orbitofrontal cortex, insula, and striatum (Dagher, 2009). When considered as a pathway, one entity, these substrates are all implicated in the following: learning about (food) rewards, setting the incentive value of stimuli in the environment, budgeting attention and efforts toward (food) rewards, and integrating homeostatic information about energy stores and gut contents with information about the outside world (availability of food)(Dagher, 2009). These substrates have been found to respond equally to food cues and drugs cues (Dagher, 2009) as well as contain prominent DA projections. When a blockade was applied to this DA pathway, all rodent responding for drugs and food was abolished (Wise et al, 1978). And lesions to these areas impair feeding behavior (Wise et al, 1978). In order to fully understand eating behavior, one must understand the interaction between the gut (enteric nervous system) and the central nervous system. The key players in these interactions are hormones, which project to the hypothalamus.
So what leads people to eat past homeostatic levels? And are these factors seen in drug addicts as well? We’ve looked at some cultural factors such as environmental cues and guilt thus far. Now let’s take a look at stress. Unarguably, stress is the main external influence that will drive an individual to develop addiction. Whether the stress comes from a family environment, social peer pressure, body dissatisfaction, work-related issues, school-related issues, etcetera, it all activates the same glucocorticoid response in the body. In a study comparing compulsive-overeating and non-compulsive-overeating obese women, researchers found that body dissatisfaction strongly correlated with binge eating (Wardle et al., 2001). This was partly a direct effect, but also found to be partly mediated by depression. The obese women who compulsively overate were found to overall be more depressed and had lower self-esteem than non-compulsive-overeating obese women. These factors undoubtedly lead to socially-stressful situations, in which the women, if functioning at baseline and able to work and hold their job, would have to encounter on a day to day basis. Stressful situations such as these have been attributed to drug relapsing and dieting failures (Wansink & Van Ittersum, 2007). But why? Hebb proposed a theory to address this: stress can become a conditioned incentive for food. Just as the smoker reaches for a cigarette, the musician heads to the piano, or the addict shoots up in times of stress, food addicts reach for food. Eating is their response to stress. It has been found (Rosmond et al, 1998) that obese individuals have a greater cortisol response than lean individuals. Cortisol is the body’s hormonal response to stress. High cortisol responders (those who are particularly susceptible to react severely to stress) have been found to increase food intake during stressful situations (Takeda, 2004), particularly sweets. An interesting theory as to why people are driven to eat sugary foods when stressed is because they are high in carbohydrates. This is important when you consider the fact that carbohydrate consumption enhances tryptophan uptake and serotonin release: the carbohydrate-rich diet leads to increased insulin secretion, decreasing large neutral amino acids, increasing tryptophan uptake and consequently serotonin release (Takeda, 2004). During stressful situations, there is an increase in 5-HT breakdown. Is carbohydrate craving simply part of a compensatory mechanism to increase levels of circulating serotonin? Stress, especially body image concerns or peer pressure threatens the ego. In a study to investigate stress-eating relationships (Wallis & Hetherington, 2009) propose that overeating is caused by an attempt to shift attention away from an ego-threatening stimulus that may cause aversive self-awareness. This is known as ‘Escape Theory.’ Applying this would lead us to believe that food addicts eat as a retreat from an emotionally stressful situation (either acute or chronic situations). So is ‘comfort food’ really a means of retreating? No, of course eating will not solve any problems. However, the compulsive overeater, comfort food reduces activity in the HPA axis (Dallman et al, 2003) making them ‘feel better,’ if only for the moment. “You get it, you’re done. And it’s tasty; it’s got that tasty taste. You have stress in your life, and food is the one thing they can’t take from you” (Leahy, 2004).
Substantial evidence has been evaluated in order to classify compulsive overeating as an addiction disorder, and to implicate food addiction as the under-addressed, over-responsible culprit in the Obesity Epidemic. Food has strikingly similar effects on the dopamine pathway as drugs of addiction. Food intake also activates the µ-opioid system, the same system activated by illicit opioid drugs. Excessive food intake has been proven to create lasting changes on the brain, sensitizing the reward pathway, increasing wanting to the point of the development of compulsion. Food addiction and drug addiction are also caused, and perpetuated by, very similar stressful situations. While, on the surface, obesity seems to be the result of a potent amalgamation of cultural, personal, and other environmental stressors that dominate the American lifestyle and society, the Obesity Epidemic, at the most fundamental level of human biology and psychology, is caused by food addiction.
Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral andneurochemical effects of intermittent, excessive sugar intake. Neurosci BiobehavRev. 2008;32(1):20-39. Epub 2007 May 18. Review. PubMed PMID: 17617461; PubMedCentral PMCID: PMC2235907.
Blundell JE, Finlayson G. Is susceptibility to weight gain characterized byhomeostatic or hedonic risk factors for overconsumption? Physiol Behav. 2004Aug;82(1):21-5. Review. PubMed PMID: 15234585.
Cocores JA, Gold MS. The Salted Food Addiction Hypothesis may explainovereating and the obesity epidemic. Med Hypotheses. 2009 Dec;73(6):892-9. Epub2009 Jul 29. PubMed PMID: 19643550.
Corwin RL, Hajnal A. Too much of a good thing: neurobiology of non-homeostaticeating and drug abuse. Physiol Behav. 2005 Sep 15;86(1-2):5-8. Review. PubMedPMID: 16081112; PubMed Central PMCID: PMC1769469.
Dagher A. The neurobiology of appetite: hunger as addiction. Int J Obes(Lond). 2009 Jun;33 Suppl 2:S30-3. PubMed PMID: 19528977.
Davis C, Carter JC. Compulsive overeating as an addiction disorder. A reviewof theory and evidence. Appetite. 2009 Aug;53(1):1-8. Epub 2009 Jun 12. Review.PubMed PMID: 19500625.
Davis C. Psychobiological traits in the risk profile for overeating and weightgain. Int J Obes (Lond). 2009 Jun;33 Suppl 2:S49-53. PubMed PMID: 19528980.
Ford ES, Li C, Zhao G, Tsai J.Trends in obesity and abdominal obesity amongadults in the United States from 1999-2008.Int J Obes (Lond). 2010 Sep 7. [Epubahead of print]PubMed [citation] PMID: 20820173
Finlayson G, Bryant E, Blundell JE, King NA. Acute compensatory eatingfollowing exercise is associated with implicit hedonic wanting for food. PhysiolBehav. 2009 Apr 20;97(1):62-7. Epub 2009 Feb 7. PubMed PMID: 19419671.
Finlayson G, King N, Blundell J. The role of implicit wanting in relation toexplicit liking and wanting for food: implications for appetite control.Appetite. 2008 Jan;50(1):120-7. Epub 2007 Jun 28. PubMed PMID: 17655972.
Finlayson G, King N, Blundell JE. Liking vs. wanting food: importance forhuman appetite control and weight regulation. Neurosci Biobehav Rev.2007;31(7):987-1002. Epub 2007 Mar 27. Review. PubMed PMID: 17559933.
Gallagher JP, Orozco-Cabal LF, Liu J, Shinnick-Gallagher P. Synapticphysiology of central CRH system. Eur J Pharmacol. 2008 Apr 7;583(2-3):215-25.Epub 2008 Feb 1. Review. PubMed PMID: 18342852; PubMed Central PMCID: PMC2424315.
Gilman, Sander L. Fat: A Cultural History of Obesity. Polity Press: 2008.
Gosnell BA, Levine AS. Reward systems and food intake: role of opioids. Int JObes (Lond). 2009 Jun;33 Suppl 2:S54-8. PubMed PMID: 19528981.
Green SM, Blundell JE. Effect of fat- and sucrose-containing foods on thesize of eating episodes and energy intake in lean dietary restrained andunrestrained females: potential for causing overconsumption. Eur J Clin Nutr.1996 Sep;50(9):625-35. PubMed PMID: 8880042.
Green SM, Burley VJ, Blundell JE. Effect of fat- and sucrose-containing foodson the size of eating episodes and energy intake in lean males: potential forcausing overconsumption. Eur J Clin Nutr. 1994 Aug;48(8):547-55. PubMed PMID:7956999.
Hebb DO. The Organization of Behavior: A NeuropsychologicalTheory. Wiley: New York, 1949.
Henry BA, Clarke IJ. Adipose tissue hormones and the regulation of foodintake. J Neuroendocrinol. 2008 Jun;20(6):842-9. Review. PubMed PMID: 18601708.
Heyne A, Kiesselbach C, Sahún I, McDonald J, Gaiffi M, Dierssen M, WolffgrammJ. An animal model of compulsive food-taking behaviour. Addict Biol. 2009Sep;14(4):373-83. PubMed PMID: 19740365.
Ifland JR, Preuss HG, Marcus MT, Rourke KM, Taylor WC, Burau K, Jacobs WS,Kadish W, Manso G. Refined food addiction: a classic substance use disorder. MedHypotheses. 2009 May;72(5):518-26. Epub 2009 Feb 14. PubMed PMID: 19223127.
Leahy, Michael. The Weight. The Washington Post Magazine July 18, 2004; 14-33.
Mason P, Foo H. Food consumption inhibits pain-related behaviors. Ann N YAcad Sci. 2009 Jul;1170:399-402. PubMed PMID: 19686166.
McFarlane SI, Chaiken RL, Hirsch S, Harrington P, Lebovitz HE, Banerji MA.Near-normoglycaemic remission in African-Americans with Type 2 diabetes mellitusis associated with recovery of beta cell function. Diabet Med. 2001Jan;18(1):10-6. PubMed PMID: 11168335.
Nathan PJ, Bullmore ET. From taste hedonics to motivational drive: centralmu-opioid receptors and binge-eating behaviour. Int J Neuropsychopharmacol. 2009May 12:1-14. [Epub ahead of print] PubMed PMID: 19433009.
Oliver G, Wardle J, Gibson EL. Stress and food choice: a laboratory study.Psychosom Med. 2000 Nov-Dec;62(6):853-65. PubMed PMID: 11139006.
Rosmond R, Dallman MF, Björntorp P. Stress-related cortisol secretion in men:relationships with abdominal obesity and endocrine, metabolic and hemodynamicabnormalities. J Clin Endocrinol Metab. 1998 Jun;83(6):1853-9. PubMed PMID:9626108.
Schlosser, Eric. Fast Food Nation. Harper Perennial: 2004.
Schwartz GJ. Biology of eating behavior in obesity. Obes Res. 2004 Nov;12Suppl 2:102S-6S. Review. PubMed PMID: 15601957.
Swithers SE, Davidson TL. A role for sweet taste: calorie predictiverelations in energy regulation by rats. Behav Neurosci. 2008 Feb;122(1):161-73.PubMed PMID: 18298259.
Takeda E, Terao J, Nakaya Y, Miyamoto K, Baba Y, Chuman H, Kaji R, Ohmori T,Rokutan K. Stress control and human nutrition. J Med Invest. 2004Aug;51(3-4):139-45. Review. PubMed PMID: 15460899.
Wallis DJ, Hetherington MM. Emotions and eating. Self-reported andexperimentally induced changes in food intake under stress. Appetite. 2009Apr;52(2):355-62. Epub 2008 Nov 24. PubMed PMID: 19071171.
Wansink B, van Ittersum K. Portion size me: downsizing our consumption norms.J Am Diet Assoc. 2007 Jul;107(7):1103-6. PubMed PMID: 17604738.
Wardle J, Haase AM, Steptoe A, Nillapun M, Jonwutiwes K, Bellisle F. Genderdifferences in food choice: the contribution of health beliefs and dieting. AnnBehav Med. 2004 Apr;27(2):107-16. PubMed PMID: 15053018.
Wardle J, Waller J, Rapoport L. Body dissatisfaction and binge eating inobese women: the role of restraint and depression. Obes Res. 2001Dec;9(12):778-87. PubMed PMID: 11743062.
Westenhoefer J. Age and gender dependent profile of food choice. Forum Nutr.2005;(57):44-51. Review. PubMed PMID: 15702587.
Wise RA, Spindler J, deWit H, Gerberg GJ. Neuroleptic-induced “anhedonia” inrats: pimozide blocks reward quality of food. Science. 1978 Jul21;201(4352):262-4. PubMed PMID: 566469.
Zanutto BS, Staddon JE. Bang-bang control of feeding: role of hypothalamicand satiety signals. PLoS Comput Biol. 2007 May;3(5):e97. Erratum in: PLoS ComputBiol. 2007 Jun;3(6):e127. PubMed PMID: 17530919; PubMed Central PMCID:PMC1876490.
Food addiction is real; and it is making America FAT.