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60. Some substances that we think of as drugs may be consumed in a food- like manner, thus confl ating hedonic drug and food mechanisms. See R. J. Sullivan and E. H. Hagen, “Psychotropic Substance- Seeking: Evolutionary Pathology or Adaptation?” Addiction 97 (2002): 389–400.
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61. M. R. Lowe and M. L. Butryn, “Hedonic Hunger: A New Dimension of Appetite?” Physiology and Behavior 91 (2007): 432–439.
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62. Ibid., 438.
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63. American Psychiatric Association, Diagnostic and Statistical Manual.
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64. J. J. Brumberg, Fasting Girls.
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65. J. E. Mitchell and S. Crow, “Medical Complications of Anorexia Nervosa and Bulimia Nervosa,” Current Opinion in Psychiatry 19 (2006): 438–443; S. Nielsen, “Epidemiology and Mortality of Eating Disorders,“Psychiatric Clinics of North America 24 (2001): 201–214.
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66. E. Lambe et al., “Cerebral Gray Matter Volume Defi cits after Weight Recovery from Anorexia Nervosa,” Archives of General Psychiatry 54(1997): 537–542; G. K. Frank, U. F. Bailer, S. Henry, A. Wagner, and W. H. Kaye, “Neuroimaging Studies in Eating Disorders,” CNS Spectrums 9(2004): 539–548.
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67. American Psychiatric Association, Diagnostic and Statistical Manual.
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68. C. M. Bulik et al., “Twin Studies of Eating Disorders: A Review,” International Journal of Eating Disorders 27 (2000): 1–20.
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69. S. Bordo, “Anorexia Nervosa: Psychopathology as the Crystallization of Culture,” in Food and Culture: A Reader, ed. C. Counihan and P. van Esterik, 2nd ed., 162–186 (New York: Routledge, 2008 [1996]), 170.
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70. W. H. Kaye, J. L. Fudge, and M. Paulus, “New Insights into Symptoms and Neurocircuit Function of Anorexia Nervosa,” Nature Reviews Neuroscience 10 (2009): 573–584.
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71. A. J. W. Scheurink et al., “Neurobiology of Hyperactivity and Reward: Agreeable Restlessness in Anorexia Nervosa,” Physiology and Behavior 100 (2010): 490–495.
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72. W. H. Kaye, J. L. Fudge, and M. Paulus, “New Insights.” Quote from page 581.
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73. M. N. Miller and A. J. Pumareiga, “Culture and Eating Disorders: A Historical and Cross- Cultural Review,” Psychiatry 64 (2001): 93–110.
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74. A. E. Becker, “Tele vi sion, Disordered Eating, and Young Women in Fiji: Negotiating Body Image and Identity during Rapid Social Change,“Culture, Medicine, and Psychiatry 28 (2004): 533–559; A. E. Becker et al.,“Facets of Acculturation and Their Diverse Relations to Body Shape Concern in Fiji,” International Journal of Eating Disorders 40 (2007): 42–50.
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75. M. A. Katzman and S. Lee, “Beyond Body Image: The Integration of Feminist and Transcultural Theories in the Understanding of Self Starvation,” International Journal of Eating Disorders 22 (1997): 385–394.
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76. K. M. Pike and A. Borovoy, “The Rise of Eating Disorders in Japan: Issues of Culture and Limitations of the Model of ‘Westernization,’ ” Culture, Medicine, and Psychiatry 28 (2004): 493–531.
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第五章 关于食物的记忆
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1. A. Damasio, Self Comes to Mind (New York: Pantheon, 2010).
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2. L. R. Squire, “Memory and the Hippocampus: A Synthesis from Findings with Rats, Monkeys, and Humans,” Psychological Review 99 (1992): 195–231.
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3. J. R. Manns and H. Eichenbaum, “Evolution of Declarative Memory,” Hippocampus 16 (2006): 795–808, quote from 795.
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4. J. Nolte, The Human Brain: An Introduction to Its Functional Anatomy, 5th ed. (St. Louis: Mosby, 2002).
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5. See J. S. Allen, The Lives of the Brain: Human Evolution and the Organ of Mind (Cambridge, MA: Belknap Press, 2009), 92–99.
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6. R. Carter, Mapping the Mind (Berkeley: University of California Press, 1999); B. Carey, “H. M., an Unforgettable Amnesiac, Dies at 82,” New York Times, December 5, 2008; S. Corkin, “What’s New with the Amnesic Patient H. M. ?” Nature Reviews Neuroscience 3 (2002): 153–160.
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7. In a study I did with my colleagues Dan Tranel, Joel Bruss, and Hanna Damasio, we mea sured the size of the hippocampus in a group of patients who had experienced oxygen deprivation for various lengths of time. These anoxic events can result from carbon dioxide poisoning, a severe asthma attack, cardiac arrest, near drowning, and so on. The hippocampus is particularly vulnerable to oxygen deprivation, and anoxic patients often suffer long- term amnesia. They retain their past memories, but their ability to form new memories is severely compromised. However, some anoxic patients have few or only mild memory problems. In mea sur ing the size of the hippocampus of these patients, we found that there was a strong correlation between the size of the hippocampus and whether or not, and to what extent, a patient suffered from amnesia. Individuals with more severe amnesia had had more of their hippocampus destroyed during the anoxic event, while those who were better at forming new memories tended to have a more intact hippocampus. A bigger hippocampus (in the sense of retaining more of the pre- anoxia hippocampus volume) was better in a functional sense. J. S. Allen et al., “Correlations between Regional Brain Volumes and Memory Per for mance in Anoxia,” Journal of Clinical and Experimental Neuropsychology 28 (2006): 457–476.
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