Eating disorders and obesity are difficult to understand and challenging to treat. Anorexia nervosa (AN) patients can starve themselves to death. Most people with obesity regain weight lost by dieting within five years; people with bulimia nervosa and binge eating disorder gorge against their wills (1). Typically, researchers and therapists see these problems as the result of psychological issues, poor choices, thin beauty standards, neurobiological dysfunctions or individual differences in self-control. This website challenges these traditional views of eating disorders and obesity and argues that analyzing anorexia nervosa and obesity outside the context of evolutionary history and behavioral ecology generates incorrect attributions. Many eating and weight problems today have their roots adaptions to survive famine. The dysfunctional behaviors are mediated primarily by complex biological mechanisms rather than choice.
Eating disorders and obesity are responsible for considerable disability and death worldwide (2). Anorexia nervosa (AN) in particular has high morbidity and mortality (3) but, despite a confident literature on theory-driven treatments, none has proven better than any other for adults or even better than a control group’s “supportive clinical management” (4, 5). Merciless fat phobia shames the overweight and obese, yet dieting leads to greater weight gain (6). By the time they are middle-aged, American men have joined women in rating unhappiness about their weight as their greatest source of daily stress (7). From concerns about the economic and societal costs of obesity and eating disorders to the individual emotional costs of a losing battle with eating, researchers, physicians, psychologists, philosophers, patients and their families wonder why it is difficult to nourish ourselves properly. Better understanding and treatment of eating disorders and obesity have enormous potential to increase health and happiness.
Eating problems remind us that the conscious mind takes credit automatically for decisions, actions, hungers and emotions arising from nonconscious brain activity (8). Our subjective experience of the choices we make and actions we take is that they are conscious and volitional, while in fact neuroscience research reveals the opposite to be true much of the time. Non-conscious processes generate decisions to which the conscious mind then assigns rationale and experiences itself as making the choice.
Our subjective experience and our preferred way to think about ourselves as conscious rational choice makers bias us to assign conscious choice. People struggling with their eating, clinicians and researchers are thus vulnerable to believing automatically generated explanations of non-conscious choices. Problematic eating is often seen as psychological, even symbolic; people with obesity, binge eating disorder and bulimia are “feeding a hungry heart;” girls and women with AN crave control or want to be as thin as models.
Alternatively, poor choices are attributed to dysfunctional brain circuits and neurotransmitter levels. Some researchers find a dismal synergy between the two types of explanations. For example, in an article titled, “When nothing tastes as good as skinny feels: the neurobiology of eating disorders,” prominent researchers argued that multiple neurobiological dysfunctions allow perfectionistic women to achieve their goals of becoming model thin (9). Such theories rest on a fundamental misconstrual of the concepts of “choice” and “volition” in the realm of energy homeostasis behaviors.
People with anorexia nervosa (AN) restrict food although they are starving; they hallucinate fat on their emaciated bodies and often exercise energetically (10). The baffling symptoms are remarkably homogeneous and highly heritable (11). Moreover, when people attempt to recover, they find their body and mind fight against eating more and exercising less. Their desire to recover is often undone by fears and compulsions that they do not control or understand.
Many species reduce feeding when it would distract them from migrating (12). In the 1950s, when experimental psychologists deprived lab rats of food to increase motivation to learn, they discovered that when housed with a running wheel, starved rats decreased feeding and increased running from one to 20 kilometers a day. Even normal weight rats limited to feeding only one hour a day will ignore food to run, as though a hypothalamic algorithm read the food limitation as indicating an inadequate foraging environment. They can eventually die of “self-starvation” (13). Lean-bred pigs that lose additional weight can develop “wasting pig syndrome” where they pace incessantly, ignore their feed, but eat straw (14). In rats, mice and humans numerous alterations in appetite and activity regulators could contribute to food restriction and hyperactivity (15). It is hard to imagine how the resultant odd “choices” would be learned or rewarded in pigs, rats or mice.
In a review of habit Anne Graybiel observed that, “habits invoke a dichotomy between the conscious, voluntary control over behavior, considered the essence of higher-order deliberative behavioral control, and lower-order behavioral control that is scarcely available to consciousness” (14). There is another way that “habits” can be coded in dorsolateral striatum circuits: through natural selection of genetic changes that control hormones and neurotransmitters. Graybiel noted that behaviors that animals do automatically upon birth, hatching, or when hormones beckon for mating and rearing are encoded the same way as learned habits in neural architecture (16).
Humans have dealt with famine and migrated extensively in the evolutionary past. For most of our time on earth people lived in sparsely distributed bands of hunter-gatherers that shared food; thus, starvation reliably indicated that food resources were depleted. A starving hunter-gatherer band faced a life and death gamble: either conserve energy and wait out the famine or mobilize their last reserves to search for better lands. If some individuals felt energetic and optimistic about their health and were better at ignoring hunger and fatigue, they could be sent to look for new territory.
The adapted-to-flee-famine hypothesis (AFFH) (17) proposes that AN is caused by ancient adaptations selected when migration was indeed the best solution to local famine; then individuals high in self-control, energy, optimism and perseverance had a selective advantage, as would their bands. All of the features of anorexia would have facilitated successful migration. Fear of eating kept migrators from being distracted by the occasional berry or bird; restless energy facilitated travel; hallucinating fat stores helped emaciated migrators convince themselves that they could keep moving.
Many scouts surely died, but those individuals and bands that did expand into new rich new land would have passed down their genes when the population expanded, leading to a higher frequencies of the genetic potentials for AN in the face of starvation. The pattern of genetic data as humans dispersed around the world is consistent with a long series of genetic bottlenecks and founder events (18). Apparently only about 70 individuals who crossed the land bridge from Asia during the last Ice Age founded the entire indigenous population of the Americas (19). Significantly, Native Americans, who migrated furthest from Africa, report the highest levels of AN of any American ethnic group (20). Africans appear not to have a genetic liability to develop AN; perhaps migration was most adaptive when travelers were moving out of Africa into unsettled lands.
Although frequency of genes involved in AN symptoms have most likely decreased over the course of time, still today weight loss can still trigger urges to migrate in the descendants of early anorexic explorers (21).
Problems with current explanations for anorexia nervosa
The first Diagnostic and Statistical Manual of Mental Disorders was published in 1952 when psychosocial explanations were predominantly accepted for serious mental disorders. Although considerable and diverse evidence reviewed here supports an evolutionary explanation for AN, the latest Diagnostic and Statistical Manual of Mental Disorders-5th Edition (DSM-5) maintains traditional psychosocial explanations for the disorder; this stance perpetuates a mistaken view of AN. Criteria include “persistent restriction of energy intake leading to significantly low body weight,” “intense fear of gaining weight or of becoming fat” and “undue influence of body shape and weight on self-evaluation” (10). The DSM-5’s assumption that the illness is proximally caused by patients’ restrictive food choices rather than by weight loss itself is outdated. Researchers in Germany have shown that a critical fall in leptin, the hormone that represents fat stores to the brain, triggers a cascade of neurobiological changes in rats, mice and AN patients that lead to food restriction and hyperactivity (11, 22-25).
Weight loss, not restrictive eating choices, is the trigger for anorexia in the genetically susceptible. It seems to patients and observers that AN is due to “persistent restriction of energy intake” because today the triggering weight loss is often the result of weight loss dieting. However, clinicians have long observed that anorexia nervosa symptoms can also be initiated by inadvertent weight loss (17, 26). This is especially common in 12- to 14-year-old girls when height increases faster than weight; girls that lose additional weight from illness or over-training can suddenly find themselves terrified of gaining weight although not previously trying to lose weight (17, 27). Multiple pathways can lead to weight loss, including growth spurts, illness, surgery, trauma, and dieting.
Fear of fat is a recent explanation
Listing fear of fat as a core and causally explanatory symptom is another inaccuracy of the DSM. Before the mid 1960s patients rarely mentioned a fear of being fat to explain food restriction and hyperactivity (28). Historically, reports of an AN-like syndrome have surfaced whenever Europeans, Asians or Indigenous Americans have starved for any reason (29). In each era victims provided historically- and culturally-bound explanations. In the early Middle Ages the Catholic Church canonized over 100 very thin people in Italy alone, in part for their ability to live with little food and tireless activity on behalf of others (30); these “holy anorexics” believed God allowed them to renounce bodily needs. Perhaps Paleolithic scouts understood the syndrome as divinely given powers to find better lands for their band.
Most renaissance victims complained that food disagreed with them or thought they could live on air. By the Victorian era the illness was attributed to a fear of sex. Explanations blaming a patients’ ambivalence about maturation dominated medicine until the mid-twentieth century when Hilde Bruch convinced the western world that teenage girls with AN were trapped in a desperate struggle for psychological autonomy from controlling mothers (31). When culturally ideal weights for women in the industrialized world dropped to 85% of normal in the late 1960s, AN patients began to blame their food restriction and excessive exercising on fear of getting fat. Today many patients attribute their AN behaviors and cognitions to needs for control or desire to eat only certain foods.
In an important review article published in 2003, Patricia Keel and Kelly Klump cautioned against naively believing patients’ explanations for their food restriction:
Although motivations for food refusal may have differed across periods (in many cases this information is simply lacking), purported motivations may not represent the true causes of self-starvation. Instead, they may represent culturally meaningful attempts to understand an affliction that leaves women feeling unable and unwilling to eat. The extent to which fear of fat is viewed as causing AN may be, in part, an illusion. (27)
Such errors come from viewing eating behavior as always arising from conscious choice and observers’ credulous acceptance of individuals’ post hoc explanations. Psychogenic theories for AN persist despite considerable evidence from careful neuroendocrine research that weight loss leads to the distinctive syndrome in both rats and humans (11, 22-25).
Hyperactivity is a primary symptom
The English and French physicians who independently described the syndrome in 1873 included hyperactivity as a primary symptom. Frances Gull wrote, “[t]he patient complained of no pain, but was restless and active. …it seemed hardly possible that a body so wasted could undergo the exercise which seemed agreeable.” His French counterpart, Charles Lasègue wrote, “…far from muscular power being diminished, this abstinence tends to increase the aptitude for movement. The patient feels more light and active…. …is never tired. ”
Although the DSM-5 authors assumed hyperactivity is secondary to desire to lose weight, prominent anorexia researchers maintain it is a core symptom (26). Casper pointed out that a level of energy greater than normal is measurably present in all patients at some time during the illness (32). This is important because relegating hyperactivity to secondary status has obscured the similarity between AN in humans and anorexia in animals.
Researchers searching for genes associated with longevity in yeast and mice have found a gene, Sirt-1, which turns on hyperactivity in starving mice and rats (33). Sirt-1 is a regulator involved in fatty acid oxidation and respiration; during famine it increases mitochondrial biogenesis and remodeling to become more efficient by increasing the proportion of respiration coupled to ATP production, reducing overall oxygen consumption and detoxifying the byproducts of increased metabolism(34). These changes transform ordinary mice into super mice, able to run over twice as long on a treadmill before collapsing in exhaustion (35)
Calorie restriction can lead to increased mitochondria in humans as well (36). Perhaps this explains the expression in some sports that “the thinner is the winner.” In sports such as endurance cycling where performance weight is lower than training weight, athletes’ memoirs have described how coaches and players, perhaps unwittingly, elicit AN symptoms (37). The ability to develop AN in response to calorie restriction may have become a de facto requirement for elite competition. Ignorance about the actual cause of AN allows these practices to continue without debate.
The homogeneous phenomenology of AN points towards the biological mechanisms and structures involved in restricting food, hyperactivity and hallucinating body fat. It has been difficult for even the most articulate sufferers to explain the anguish of being asked to eat. People with AN often think obsessively about food and cook elaborate meals for others that they cannot bring themselves to eat. One patient said, “I know if I continue like this I will die, but eating is even more terrifying.”
Endocrinologists were first in noting that some appetite signals in AN are the opposite of normal starvation (38). In 2001 Akio Inui noted that while people with anorexia nervosa have high levels of hunger hormones they also have increased satiety and anorexigenic signaling (39). For example, a potent satiety signal, cholecystokinin, increases rapidly when underweight people with AN begin to eat, leading to queasy satiety along with gnawing hunger. Inui wrote, “This may explain why many anorexics cannot easily reverse their illness in contrast to simple starvation. It is possible that the mixed signals about satiety and desire to feed could contribute to the ambivalence about food, i.e., the dissociation that anorexics often display between reduced caloric intake and obsessive thoughts about food” (39, p. 623). Inui’s conclusions had no discernable impact on psychogenic theories for AN.
In the last decade functional magnetic resonance imaging (fMRI) from independent laboratories reported the same pattern of abnormal activation when subjects were asked to eat or imagine eating. Thinking about food stimulates excessive prefrontal cortical activity (40-43). The prefrontal cortex provides executive control over motivational drives; it is responsible for identifying and carrying out the individual’s goals. All mammals have an executive cortical area sending “top-down” instructions to more primitive deep-brain centers. For example, during breeding it directs the devoted behavior required for successful reproduction, including ignoring hunger and fatigue when necessary. People with AN behave as though it is necessary to ignore hunger and fatigue although starving. Brooks and colleagues found that enhanced working memory (WM) interacted with limbic processes to foster impulse control in AN (44).Normally when hungry people imagine drinking chocolate milk neural activity increases in reward and taste centers. The insula connects and interprets sensory information from the body into self-awareness of the condition of the body, including hunger and pain, thus is important in homeostasis. When hungry people with AN imagine food, activity is inhibited in parts of the insula that evaluate the meaning of hunger signals and anticipate taste (45-47). They pay little attention to food when hungry(48). Reduced activation of somatosensory appetite-related regions is combined with greater activity in the amygdala and the cingulate cortex, emotional centers that evaluate and respond to dangers (45, 49). In other words, thinking about eating silences neural regions that complain of hunger and activates of anxiety and fear centers. One of the most startling symptoms of AN is that victims see fat on their emaciated bodies (1); this body image distortion increases as more weight is lost. Now, brain-imaging researchers have discovered part of the reason. When underweight women with AN look at their own bodies, fMRI images show inhibition of the primary visual and visual association cortex (50). Meanwhile the part of the parietal cortex responsible for body image is hyperactive, filling in a fattened likeness (51). We think that the visual illusion of extra fat stores would have given starving migrators the confidence to make a difficult journey.
Thus, for underweight people with AN, self-control is strengthened while awareness (imagination) of food and its taste is dampened and fear centers are excessively active. Behaviors that everyone–including the victims– attributed to conscious choices could be seen to activate furious activity in deep brain structures involved in decision making, controlling behavior, evaluating primal danger, and evaluating food. These findings help explain what people with AN must overcome in order to recover.
Gene x environment interactions
The specific environmental triggers that activate AN genes point to its function for hunter gather bands (52). High levels of estrogen are often required in addition to weight loss for the genetic program to manifest (52, 53). AN genes are more rarely activated in males or in prepubertal girls. This indicates that it was a better bet for teen-aged girls than for small children and males to travel in times of famine. Why would that be? According to ethnographic records, when travelers encountered an enemy band, a reproductive female was more likely to survive and be adopted into the new group; molecular genetic evidence also supports the idea that females migrated farther in the Paleolithic (54). The preponderance of females developing anorexia nervosa has often been explained by female weaknesses. These gene and environment interactions suggest a very different conclusion; during Paleolithic famine, brave, self-controlled young women searched for better lands for their bands.
Over-controlled or self-controlled?
Before AN derailed them, patients were typically high-achievers on track to a successful life. Their premorbid personalities were typically ascetic; in one study 23% had autism spectrum traits (55). However, in their brothers the same scholarly and anxious childhood temperament often leads to success in technically demanding fields, while the same traits in their anorectic sisters is retroactively deemed pathological.
In general self-control is a positive trait. Mischel and his colleagues’ longitudinal research found, “Resisting temptation in favor of long-term goals is an essential component of social and cognitive development and of societal and economic gain”(56). Yet, these very traits are seen as causative factors for AN. When patients first present for treatment they usually exhibit high levels of anxiety, depression and compulsivity, and clinicians and researchers commonly attribute the disorder to their over-controlled, anxious and perfectionist traits (9, 57). However, Ansel Keys’ landmark starvation study found that healthy subjects develop pathological anxiety, depression, obsessions and compulsions when starved that remitted with re-feeding (58). We believe that observers have mistaken the pathological psychological sequelae of starvation for a predisposing and psychogenic pathological trait.
Preponderance of evidence
“The weight of evidence for an extraordinary claim must be proportional to its strangeness.” Pierre-Simon Laplace (59)
The adapted-to-flee famine hypothesis is a radical departure from today’s paradigm guiding eating disorders research and treatment. Anorexia researchers refer to the genetically-controlled biological changes they find as dysfunctions, deficits, dysregulation, impairment and defects, in other words, “bugs” in energy homeostasis, reward, fear, executive control or other regulatory systems. Many speculate about finding the biological change that explains AN, ignoring dozens described by others (9, 60).
A number of facts indicate that the biological changes are not mistakes but rather “features” arising from natural selection. First, loss of function is the usual result of dysfunctions, but these particular alleles give ordinary people, even children, extraordinary self-control over hunger, increased pain tolerance, athletic ability and endurance (61). Super abilities come from accidents only in comic books.
Second, when starving, the drive to eat is normally too fierce to be denied; a hunger strike is a powerful moral protest because it is agonizing. Many women would like to weigh at least 15% less than they do to meet today’s ultra thin beauty standards, but most find this impossible. While AN is the only psychiatric disorder that healthy people joke about wanting to “catch,” people with AN are not enviable; a suicide risk forty times normal speaks to their misery (62). Yet, observers’ envy acknowledges that the symptoms of AN cannot be voluntarily enacted.
Third, the genetic ability to develop AN is more common than would be expected if alleles had not been selected. European and Australian population studies indicate that over 4% of women of European descent develop anorexia nervosa in their lifetimes, although most did not seek medical care and recovered spontaneously (63). Given that AN is initiated by starvation and famine is rare in the industrialized world, it follows that even more than 4% of non-African populations carry behaviorally un-expressed susceptibility genes.
Finally, the AN syndrome has marks of evolved mechanisms: The behaviors and attitudes are opposite normal yet stereotyped. The syndrome requires dozens of biological processes to change together every time a person develops AN. If the underlying biological changes were indeed random accidents and truly independent (that is, not selected as part of an adaptation), the probability that they would occur together to produce AN would be the product of their individual probabilities and vanishingly small.
Evidence supporting the adapted-to-flee-famine hypothesis is drawn from diverse research in endocrinology, neuroscience, genetics, epidemiology, psychology and behavioral ecology, providing an extraordinarily broad cross-disciplinary network of evidence (64). The widespread acceptance of traditional explanations attributing AN to patients’ psychologically-motivated or learned choices rests on neither broad empirical support nor on the absence of a plausible and more comprehensive explanation.
The adapted-to-flee-famine hypothesis explains what initiates AN (considerable weight loss in genetically susceptible individuals) and the mechanisms by which the cause operates (via a critical fall in leptin that is exacerbated by the presence of estrogen); it explains quantitative features (sex ratio and epidemiology); it accounts for more AN phenomena than other AN theories (why starving people eat little, move restlessly and hallucinate fat stores); it reveals the unity that underlies the apparent diversity of AN (the core symptoms have remained the same while explanations differed); and, it points toward more fruitful research questions in the psychology, genetics and neuroscience of AN, and toward more effective interventions. Thus, the AFFH meets the criteria for a sound scientific explanation, providing precision, scope, simplicity, prediction, and usefulness (65).
In the Paleolithic some behavioral mechanism probably helped anorectic tribal members to eat when food was once again plentiful. If the traditions of extant nomadic tribes are an indication, this mechanism involved social support. When more food becomes available after a shortage, traditional societies celebrate with a feast (66). Refusing such food would be a profound breech of social norms and insult the giver. Humans are deeply social (67) and AN is probably most easily “switched off” with social support. For a starving tribe an anorectic’s energy, optimism, and grandiosity could inspire them to undertake an arduous journey, much as the anorectic Joan of Arc inspired soldiers to march with her (68). When they reached better lands, bands would in turn have helped their heroic scouts recover through eating and weight restoration.
People with AN must eat although eating fills them with shame, regret and dread; they get full quickly, and they cannot see how thin they are. They must reduce exercising while the anorexic voice castigates them as lazy and weak. Today the two most popular therapies for AN — Cognitive Behavior Therapy for eating disorders, which focuses on changing patients’ “fears of getting fat,” and Interpersonal Psycho-Therapy, which focuses on relationship problems (5) — did less well in a randomized clinical trial than a control group. At a 6-year follow-up the theory-based therapies were still no better (69).
Preliminary data indicate that our evolutionary neurobiological explanation improves recovery. Explaining that compulsions to move and fear of feeding were evolutionary adaptations that once saved their ancestors helps patients resist them (70). This also improves patients’ motivation and confidence that they can recover and helps clinicians and loved ones empathize and support them in recovering their weight.
- A. P. Association, Diagnostic and statistical manual of mental disorders, (DSM-5®). (American Psychiatric Pub, 2013).
- M. Chavez, T. R. Insel, Special issue on diagnosis and classification. Int J Eat Disord 40, S2-S2 (2007).
- H. W. Hoek, Incidence, prevalence and mortality of anorexia nervosa and other eating disorders. Current opinion in psychiatry 19, 389-394 (2006).
- H. Watson, C. M. Bulik, Update on the treatment of anorexia nervosa: review of clinical trials, practice guidelines and emerging interventions. Psychological medicine 43, 2477-2500 (2013).
- V. V. McIntosh et al., Three psychotherapies for anorexia nervosa: a randomized, controlled trial. Am J Psychiatry 162, 741-747 (2005).
- T. Mann et al., Medicare’s search for effective obesity treatments: diets are not the answer. American Psychologist; American Psychologist 62, 220 (2007).
- A. D. Kanner, J. C. Coyne, C. Schaefer, R. S. Lazarus, Comparison of two modes of stress measurement: Daily hassles and uplifts versus major life events. Journal of behavioral medicine 4, 1-39 (1981).
- J. A. Bargh, T. L. Chartrand, The unbearable automaticity of being. Am Psychol 54, 462-479 (1999).
- W. H. Kaye, C. E. Wierenga, U. F. Bailer, A. N. Simmons, A. Bischoff-Grethe, Nothing tastes as good as skinny feels: the neurobiology of anorexia nervosa. Trends in neurosciences 36, 110-120 (2013).
- American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders (DSM-5). (American Psychiatric Pub, 2013).
- C. M. Bulik et al., Genetic epidemiology, endophenotypes, and eating disorder classification. Int J Eat Disord 40 Suppl, S52-60 (2007).
- N. Mrosovsky, D. F. Sherry, Animal anorexias. Science 207, 837-842 (1980).
- W. F. Epling, W. B. Pierce, Activity based anorexia: A biobehavioral perspective. Int J Eat Disord 5, 475-485 (1988).
- J. L. Treasure, J. B. Owen, Intriguing links between animal behavior and anorexia nervosa. Int J Eat Disord 21, 307-311 (1997).
- K. M. Pirke, A. Broocks, T. Wilckens, R. Marquard, U. Schweiger, Starvation-induced hyperactivity in the rat: the role of endocrine and neurotransmitter changes. Neuroscience and biobehavioral reviews 17, 287-294 (1993).
- A. M. Graybiel, Habits, rituals, and the evaluative brain. Annu. Rev. Neurosci. 31, 359-387 (2008).
- S. Guisinger, Adapted to flee famine: adding an evolutionary perspective on anorexia nervosa. Psychological review 110, 745-761 (2003).
- S. Ramachandran et al., Support from the relationship of genetic and geographic distance in human populations for a serial founder effect originating in Africa. Proceedings of the National Academy of Sciences of the United States of America 102, 15942-15947 (2005).
- J. Hey, On the number of New World founders: a population genetic portrait of the peopling of the Americas. PLoS biology 3, e193 (2005).
- M. Crago, C. M. Shisslak, L. S. Estes, Eating disturbances among American minority groups: a review. Int J Eat Disord 19, 239-248 (1996).
- J. Hebebrand, T. Muller, K. Holtkamp, B. Herpertz-Dahlmann, The role of leptin in anorexia nervosa: clinical implications. Molecular psychiatry 12, 23-35 (2007).
- K. Holtkamp et al., Physical activity and restlessness correlate with leptin levels in patients with adolescent anorexia nervosa. Biological psychiatry 60, 311-313 (2006).
- C. Exner et al., Leptin suppresses semi-starvation induced hyperactivity in rats: implications for anorexia nervosa. Molecular psychiatry 5, 476-481 (2000).
- J. J. Hillebrand, M. P. Koeners, C. E. de Rijke, M. J. Kas, R. A. Adan, Leptin treatment in activity-based anorexia. Biol Psychiatry 58, 165-171 (2005).
- C. E. de Rijke, J. J. Hillebrand, L. A. Verhagen, T. A. Roeling, R. A. Adan, Hypothalamic neuropeptide expression following chronic food restriction in sedentary and wheel-running rats. Journal of molecular endocrinology 35, 381-390 (2005).
- J. Hebebrand, R. Casper, J. Treasure, U. Schweiger, The need to revise the diagnostic criteria for anorexia nervosa. Journal of Neural Transmission 111, 827-840 (2004).
- P. K. Keel, K. L. Klump, Are eating disorders culture-bound syndromes? Implications for conceptualizing their etiology. Psychological bulletin 129, 747-769 (2003).
- R. C. Casper, On the emergence of bulimia nervosa as a syndrome: A historical view. Int J Eat Disord 2, 3-16 (1983).
- W. Vandereycken, R. van Deth, From fasting saints to anorexic girls. (New York University Press, New York, 1994).
- R. Bell, Holy Anorexia. (University of Chicago Press, Chicago, 1985).
- H. Bruch, Anorexia Nervosa: therapy and theory. Am J Psychiatry 139, 1531-1538 (1982).
- R. C. Casper, The ‘drive for activity’ and “restlessness” in anorexia nervosa: potential pathways. Journal of affective disorders 92, 99-107 (2006).
- D. Chen, A. D. Steele, S. Lindquist, L. Guarente, Increase in activity during calorie restriction requires Sirt1. Science 310, 1641 (2005).
- L. Guarente, Calorie restriction and SIR2 genes–towards a mechanism. Mechanisms of ageing and development 126, 923-928 (2005).
- N. L. Price et al., SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. Cell metabolism 15, 675-690 (2012).
- A. E. Civitarese et al., Calorie restriction increases muscle mitochondrial biogenesis in healthy humans. PLoS med 4, e76 (2007).
- T. a. C. Hamilton, Daniel, The secret race: Inside the hidden world of the Tour de France. (Bantum, 2012), pp. 304.
- R. K. Stoving, J. Hangaard, C. Hagen, Update on endocrine disturbances in anorexia nervosa. J Pediatr Endocrinol Metab 14, 459-480 (2001).
- A. Inui, Eating behavior in anorexia nervosa–an excess of both orexigenic and anorexigenic signalling? Molecular psychiatry 6, 620-624 (2001).
- U. F. Bailer et al., Altered 5-HT(2A) receptor binding after recovery from bulimia-type anorexia nervosa: relationships to harm avoidance and drive for thinness. Neuropsychopharmacology 29, 1143-1155 (2004).
- A. Zastrow et al., Neural correlates of impaired cognitive-behavioral flexibility in anorexia nervosa. Am J Psychiatry 166, 608-616 (2009).
- S. J. Brooks et al., Differential neural responses to food images in women with bulimia versus anorexia nervosa. PLoS One 6, e22259 (2011).
- F. A. Cowdrey, R. J. Park, C. J. Harmer, C. McCabe, Increased neural processing of rewarding and aversive food stimuli in recovered anorexia nervosa. Biological psychiatry 70, 736-743 (2011).
- S. J. Brooks, S. G. Funk, S. Y. Young, H. B. Schiöth, The Role of Working Memory for Cognitive Control in Anorexia Nervosa versus Substance Use Disorder. Frontiers in psychology 8, 1651 (2017).
- S. Vocks, S. Herpertz, C. Rosenberger, W. Senf, E. R. Gizewski, Effects of gustatory stimulation on brain activity during hunger and satiety in females with restricting-type anorexia nervosa: an fMRI study. Journal of psychiatric research 45, 395-403 (2011).
- R. Uher et al., Medial prefrontal cortex activity associated with symptom provocation in eating disorders. Am J Psychiatry 161, 1238-1246 (2004).
- K. Nunn, I. Frampton, T. S. Fuglset, M. Törzsök-Sonnevend, B. Lask, Anorexia nervosa and the insula. Medical hypotheses 76, 353-357 (2011).
- S. Santel, L. Baving, K. Krauel, T. F. Münte, M. Rotte, Hunger and satiety in anorexia nervosa: fMRI during cognitive processing of food pictures. Brain research 1114, 138-148 (2006).
- A. A. Joos et al., Amygdala hyperreactivity in restrictive anorexia nervosa. Psychiatry Research: Neuroimaging 191, 189-195 (2011).
- P. Sachdev, N. Mondraty, W. Wen, K. Gulliford, Brains of anorexia nervosa patients process self-images differently from non-self-images: an fMRI study. Neuropsychologia 46, 2161-2168 (2008).
- A. Wagner, M. Ruf, D. F. Braus, M. H. Schmidt, Neuronal activity changes and body image distortion in anorexia nervosa. Neuroreport 14, 2193-2197 (2003).
- K. L. Klump, M. McGue, W. G. Iacono, Differential heritability of eating attitudes and behaviors in prepubertal versus pubertal twins. Int J Eat Disord 33, 287-292 (2003).
- M. F. A. Fernandes et al., Leptin suppresses the rewarding effects of running via STAT3 signaling in dopamine neurons. Cell metabolism 22, 741-749 (2015).
- M. T. Seielstad, E. Minch, L. L. Cavalli-Sforza, Genetic evidence for a higher female migration rate in humans. Nature genetics 20, 278-280 (1998).
- E. Wentz et al., Childhood onset neuropsychiatric disorders in adult eating disorder patients. European child & adolescent psychiatry 14, 431-437 (2005).
- W. Mischel et al., Willpower” over the life span: Decomposing impulse control. Social Cognitive Affective Neuroscience 6, 252-256 (2011).
- K. A. Halmi et al., Perfectionism in anorexia nervosa: variation by clinical subtype, obsessionality, and pathological eating behavior. Am J Psychiatry 157, 1799-1805 (2000).
- A. Keys, J. Brožek, A. Henschel, O. Mickelsen, H. L. Taylor, The biology of human starvation.(2 vols). (1950).
- P. S. LaPlace, Essai philosophique sur les probabilités. (Chez H. Remy, Brussels, 1814/1829).
- K. Nunn, I. Frampton, I. Gordon, B. Lask, The fault is not in her parents but in her insula—a neurobiological hypothesis of anorexia nervosa. European Eating Disorders Review 16, 355-360 (2008).
- H. Papežová, A. Yamamotova, R. Uher, Elevated pain threshold in eating disorders: Physiological and psychological factors. Journal of psychiatric research 39, 431-438 (2005).
- P. K. Keel et al., Predictors of mortality in eating disorders. Archives of general psychiatry 60, 179-183 (2003).
- A. Keski-Rahkonen et al., Epidemiology and course of anorexia nervosa in the community. Am J Psychiatry 164, 1259-1265 (2007).
- D. P. Schmitt, J. J. Pilcher, Evaluating evidence of psychological adaptation: How do we know one when we see one? Psychological Science 15, 643-649 (2004).
- P. Lipton, Inference to the best explanation. (Routledge, London, ed. 2nd, 2004).
- G. Isaac, The food-sharing behavior of protohuman hominids. Scientific American, (1978).
- S. Guisinger, S. Blatt, Individuality and relatedness: Evolution of a fundamental dialectic. Am Psychol 49 104-111 (1994).
- M. Warner, Joan of Arc. (University of California Press, Berkeley, 1981).
- F. A. Carter et al., The long‐term efficacy of three psychotherapies for anorexia nervosa: A randomized, controlled trial. Int J Eat Disord 44, 647-654 (2011).
- S. Guisinger, D. Schuldberg, paper presented at the International Conference on Eating Disorders, Baltimore, MD, May 2-5, 2007 2007.
On this site you will find essays, journal articles, patient guides, podcasts, and more. Most things in psychology make more sense in the light of evolution. Consider,
- Patient Guide
- Adapted to Famine: An Evolutionary Explanation for Anorexia (journal article)
- Client-Therapist Script and Instructional Tool for Utilizing the Adapted to Famine Theory In-Session
Explore the site to read additional papers and publications by Dr. Guisinger and colleagues on topics of eating disorders, neurology, clinical psychology, and biological evolution.