DISMANTLING FAULTY BELIEFS ABOUT EATING DISORDERS 

Jillian Rigert, D.M.D, M.D. 

Oral Medicine Specialist & Patient with Lived Experience 

The University of Texas M.D. Anderson Cancer Center 

To provide high quality care to patients with potentially life-threatening eating disorders, it is imperative to dismantle the faulty beliefs that the conditions are mostly about food, exercise, weight, and body image. From my perspective as a healthcare professional and a patient who has lived with anorexia nervosa, portrayals of people with eating disorders described in medicine, media, and Hollywood are superficial, misguided, and contribute to harm. 

Due to the complex nature of eating disorders, the education provided in medical schools and residencies remains suboptimal.1 From my experience, teachings continue to portray an individual with anorexia in a reductionist manner (i.e., as a young, Caucasian cisgendered woman fixated on calorie control and exercise with intense fear of gaining weight). The reality is that restrictive eating disorders may impact patients of all gender identities, ethnicities, and body sizes. While the clinical manifestations of eating disorders appear to revolve around food, exercise, weight, and body size, these signs warrant a comprehensive evaluation of the patient’s psychosocial-spiritual and physical wellbeing. 

Demystifying eating disorders through improved education will hopefully increase the quality of care provided. Change is urgently needed to reduce patient harm and address unmet needs which include the following: 

  1. Delays in diagnosis: Weight biases in medical practice often contribute to delays or missed diagnoses of eating disorders in normal to higher weight patients. Further, weight loss is often celebrated without identifying if the change was accomplished using harmful methods. It is important to accept that people with restrictive eating behaviors may present overweight or at normal weight, and thus patients of all body sizes must be screened to detect disordered eating. Delays in diagnosis may worsen a patient’s prognosis and invalidate the harm an eating disorder has on their mental and physical health.2,3
  •  Siloed care: Eating disorder education, research, and treatments are often inappropriately separated from other psychiatric conditions and considered a specialty of psychiatry. About 95% of patients with eating disorders have a co-occurring affective illness, thus improved training in medical and psychiatry residencies is needed.4 Up-to-date, research-based knowledge needs to be published in mainstream medical journals rather than specialty-specific journals, and patients need to be provided concurrent treatment for co-occurring conditions.4
  1. Therapeutic gaps: The majority of people with eating disorders never receive any intervention,4 and for those who do receive treatment, many approaches hyperfocus on improving the patient’s energy-balance as the outcome measure for recovery. While an essential part of treatment, a properly fueled body is often able to feel what the eating disorder has numbed. Energy-balance should not be the end point, but rather marks the beginning – a time when further therapeutic healing modalities should be explored. Disordered eating has multifactorial etiologies and thus warrants a multidisciplinary approach. Each patient must be evaluated as an individual and provided personalized care that addresses needs across psychosocial, spiritual, and physical dimensions.

Takeaways

  1. Increase the education about eating disorders in medical training; aim to reduce and/or eliminate biases.
  2. Evaluate personal biases (especially of weight-related issues) which may contribute to harmful delays in access to compassionate, comprehensive eating disorder care.
  3. When screening and treating patients, focus on providing a safe space and listen with compassionate curiosity. 
  4. Consider the role(s) that disordered eating behaviors may have in a person’s life that go deeper than some overt signs imply. Provide holistic, multidisciplinary care according to each patient’s individual needs, fostering psychosocial-spiritual and physical wellbeing. 

References 

  1. Mahr F, Farahmand P, Bixler EO, et al. A national survey of eating disorder training. Int J Eat Disord. 2015;48(4):443-445. doi:10.1002/eat.22335
  1. Lebow J, Sim LA, Kransdorf LN. Prevalence of a history of overweight and obesity in adolescents with restrictive eating disorders. J Adolesc Health. 2015;56(1):19-24. doi:10.1016/j.jadohealth.2014.06.005
  1. Neumark-Sztainer D. Higher weight status and restrictive eating disorders: an overlooked concern. J Adolesc Health. 2015;56(1):1-2. doi:10.1016/j.jadohealth.2014.10.261
  1. Haynos AF, Egbert AH, Fitzsimmons-Craft EE, et al. Not niche: eating disorders as an example in the dangers of overspecialisation. Brit J Psych. 2023:1-4.  doi:10.1192/bjp.2023.160.

Financial Disclosure

J. Rigert receives support from the National Institute of Dental and Craniofacial Research Diversity Supplement 3R01DE028290-02S1 for the project “Utilizing novel advanced imaging techniques with clinical biomarkers to predict and prevent radiation-attributable oro-dental sequelae.” This manuscript was written during time unrelated to my funding support hours. 

Member Highlight

Dr. Zubi Suleman, appointed by Governor Beshear, has been a key figure in the advocation for the well-being of Kentuckians through her membership on the Eating Disorder Advisory Council. 

Through this council, Dr. Suleman has taken on a leadership role as one of the committee chairs dedicated to Health Service Providers education. The core objective of this council is to address existing gaps and barriers in the care of individuals grappling with eating disorders within the state of Kentucky.

Committed to raising awareness about the grave implications of eating disorders and the imposing weight stigma within both the general population and healthcare professionals, Dr. Zubi Suleman undertook the initiative of presenting a resolution on eating disorders and weight stigma in Kentucky to the KMA Reference Committee.

It is with great pleasure to announce that this resolution was recently voted on and passed by KMA House of delegates on August 28, 2023, and is now formally integrated into the KMA’s policy framework. 

We extend our heartfelt congratulations to Dr. Zubi Suleman and her dedicated team for their unwavering efforts and for laying the foundation for advocacy endeavors in this critical area.

The Hybrid Model: New Normal or Unstable Transition Phase?

ROBERT CAUDILL, M.D., & PETER YELLOWLEES, M.D., M.B.B.S

Before the world ground to a halt in an effort to contain the COVID-19 virus, the hybrid model of telepsychiatry was envisioned as a means of encouraging greater adoption of telehealth. With hybrid care, psychiatrists could connect in person with patients in the clinic as well as virtually with those at home or in community settings. Most of those practicing telepsychiatry divided their time between seeing patients in person and online, but they did not move their practice out of their clinics. Instead, a portion of the established caseload was strategically offered a virtual care option after some degree of screening and orientation of the patients. While slow at first, the adoption of a hybrid model of telepsychiatry was making gradual inroads among psychiatrists, where it was seen as having little threat to the overturning of more traditional workflows. Read more!

Neuregulin I: A Gene Linking Mental Illness and Creativity?

Caleb He1

Steven Lippmann, M.D.2

  1. University Student, University of Louisville, School of Arts and Sciences, Louisville, KY
  2. Emeritus Professor, University of Louisville, School of Medicine, Louisville, KY

Corresponding Author

Steven Lippmann, M.D.

University of Louisville School of Medicine

401 East Chestnut Street, #610

Louisville, KY 40202

502-681-6788

steven.lippmann@louisville.edu

The neuregulin 1 (NRG1) gene has associations with psychotic symptoms in individuals with schizophrenia.1High levels of creativity and intelligence are other possible polymorphisms associated with this gene. This may partially explain the persistence of schizophrenia in the gene pool despite adverse health effects affecting patients with this condition.

Among 200 subjects with high intellectual achievement (mean IQ = 124.7, SD = 9.5), those with the promoter gene for the NRG1 genotype had higher creativity scores as compared to controls.2 This may be the only known experiment demonstrating a correlation between positive psychological function and polymorphisms associated with severe mental illness.2

Low latent inhibition (LI), which refers to the inability to distinguish the relevance between novel and familiar stimuli, is associated with NRG1. People with schizophrenia demonstrated a low or absent LI.3 There is also a link between high IQ and low LI with greater creativity; high-IQ university students with excellent creative achievement were seven times more likely to have low LI.4 Creative achievement and psychotic tendencies might be positively correlated.

Persons with schizophrenia and also high intelligence often have less disorganization and better-preserved functioning. Patients with schizophrenia and superior premorbid and current IQ (mean = 120) performed just as well on neurocognitive tests as healthy controls with similar scores.5

 Individuals affected by schizophrenia have elevated levels of NRG1 and receptor ERBB4 activity in the prefrontal cortex.6 NRG1 and ERBB4 receptors play a significant role in regulating neurotransmission within the prefrontal cortex.7,8 The prefrontal cortex has a critical role in creativity;9,10 individuals with decreased prefrontal cortex function due to focal brain injury can have evidence of creative activity. This may be explained by the prefrontal cortex’s association with LI capabilities.11

Schizophrenia affects approximately 1% of all populations, but an elevated risk of schizotypal symptoms exists in first-degree relatives of individuals with schizophrenia.12 Genes coding for serious illnesses in homogeneous carriers may confer beneficial, adaptive traits to relatives who are heterozygous carriers.13 Perhaps increased creativity and intelligence is one of these traits. Parallels include that sickle-cell anemia can confer tolerance to malarial infection,14 Ashkenazi Jewish carriers of Tay-Sachs genes have elevated resistance against tuberculosis,15 and heterozygote carriers of cystic fibrosis have decreased susceptibility to cholera.16,17

These observations indicate the need for further research into the role of beneficial traits for survival of people with schizophrenia as a condition counter to evolutionary selection. Any correlation between increased creativity and heterozygous carriers of schizophrenia remains yet unclarified.

References

  1. Yang JZ, Si TM, Ruan Y, et al: Association study of neuregulin 1 gene with schizophrenia. Molecular Psychiatry 2003; 8:706–709.
  2. Kéri S: Genes for psychosis and creativity: a promoter polymorphism of the neuregulin 1 gene is related to creativity in people with high intellectual achievement. Psychological Science 2009; 20(9):1070-1073.
  3. Rascle C, Mazas O, Vaiva G, et al: Clinical features of latent inhibition in schizophrenia. Schizophrenia Research 2001; 51:149-161.
  4. Carson SH, Peterson JB, Higgins DM: Decreased latent inhibition is associated with increased creative achievement in high-functioning individuals. Journal of Personality and Social Psychology 2003; 85(3):499-506.
  5. Černis E, Vassos E, Brébion G, et al: Schizophrenia patients with high intelligence: A clinically distinct sub-type of schizophrenia? European Psychiatry 2015; 30(5):628-632.
  6. MacCabe J, Brébion G, Reichenberg A: Superior intellectual ability in schizophrenia: neuropsychological characteristics. Neuropsychology 2012; 26(2):181-190.
  7. Chong VZ, Thompson M, Beltaifa S, et al: Elevated neuregulin-1 and ErbB4 protein in the prefrontal cortex of schizophrenic patients. Schizophrenia Research 2008; 100(1-3):270-280.
  8. Woo RS, Li XM, Tao YM, et al: Neuregulin-1 Enhances Depolarization-Induced GABA Release. Neuron 2007; 54(4):599-610.
  9. Stefansson H, Petursson H, Sigurdsson E, et al: Neuregulin 1 and Susceptibility to Schizophrenia. American Journal of Human Genetics 2002; 71(4):877-892.
  10. Dietrich A: The cognitive neuroscience of creativity. Psychonomic Bulletin & Review 2004; 11:1011-1026.
  11. Wei DT, Yang JY, Li WF, et al: Increased resting functional connectivity of the medial prefrontal cortex in creativity by means of cognitive stimulation. Cortex 2014; 51:92-102.
  12. Walter EE, Fernandez F, Snelling M, et al: Genetic Consideration of Schizotypal Traits: A Review. Frontiers in Psychology 2016; 7:1769.
  13. Withrock IC, Anderson SJ, Jefferson MA, et al: Genetic diseases conferring resistance to infectious diseases. Genes & Diseases 2015; 2(3):247-254.
  14. Ferreira A, Marguti I, Bechmann I, et al: Sickle Hemoglobin Confers Tolerance to Plasmodium Infection. Cell 2011; 145(3):398-309.
  15. Spyropoulos B, Moens PB, Davidson J, et al: Heterozygote advantage in Tay-Sachs carriers? American Journal of Human Genetics 1981; 33(3):375-380.
  16. Gabriel SE, Brigamn KN, Koller BH, et al: Cystic fibrosis heterozygote resistance to cholera toxin in the cystic fibrosis mouse model. Science 1994; 266(5182):107-109.
  17. Asimi A: “Cystic fibrotics could survive cholera, choleraics could survive cystic fibrosis”; hypothesis that explores new horizons in treatment of cystic fibrosis. Medical Hypotheses 2015; 85(6):715-717.