Food addiction as a proxy for eating disorder and obesity severity, trauma history, PTSD symptoms, and comorbidity

Review
Part of the following topical collections:
  1. Food Addiction

Abstract

Purpose

Food addiction (FA) is a newly defined yet still controversial condition that has important etiological, developmental, treatment, prevention, and social policy implications. In this review, the case is made that FA (or high scores on the Yale Food Addiction Scale) may be used as a proxy measure for a matrix of interrelated clinical features, including greater eating disorder severity, greater obesity severity, more severe trauma histories, greater symptoms of posttraumatic stress disorder (PTSD), greater psychiatric comorbidity, as well as greater medical morbidity and mortality.

Methods

A Medline search was undertaken using the following terms: food addiction cross-referenced with eating disorders (anorexia nervosa, bulimia nervosa, binge eating disorder, and binge eating), obesity, trauma, posttraumatic stress disorder, and comorbidity.

Results

The thesis is that the identification and acknowledgment of the concept of FA, when integrated into an overall, trauma-focused and transdiagnostic treatment approach, are supported and can be useful in understanding clinically the “big picture.”

Conclusions

Food addiction (FA) may be used as a proxy for (1) bulimic eating disorder severity, (2) complex trauma histories, (3) severity of PTSD and PTSD symptoms, (4) intensity of psychiatric comorbidity, (5) severity of obesity, as well as (6) their combination. Implications for developing treatment strategies are discussed. The case for a comprehensive management that requires careful attention to medical and psychiatric assessment and integrated care that incorporates trauma-focused treatment is made.

Keywords

Binge eating disorder Bulimia nervosa Comorbidity Food addiction Posttraumatic stress disorder Severity 

Food addiction as a concept

The term “food addiction” (FA) was originally coined in 1956 by Randolph, who associated it with addictive drinking [59]. However, the phenomenon went relatively unexplored for many years until the last decade when serious scientific interest progressively mushroomed (see Fig. 1). Parallel to this scientific inquiry, FA has increasingly become a useful and defensible clinical entity with marked implications for policy, practice, and research [30, 42, 61]. Highly palatable foods are postulated to act via similar mechanisms as both illicit and licit drugs of abuse in the brain [2, 3, 4, 6, 27, 28, 29, 33, 34, 35, 38, 41, 43, 45]. Much of the work in humans has been facilitated by the development of the Yale Food Addiction Scale (YFAS) by Gearhardt and associates [28, 31, 58]. The YFAS has shown good test–retest reliability and validity, and now, there is a YFAS for children [31], as well as the YFAS-2, which is based on DSM-5 criteria for substance use disorder [52].

Fig. 1

Number of “food addiction” citations in PUBMED by year (1950–2015)

Thesis of this review

The purpose of this theoretical and integrative review is to explore the premise that FA, as evidenced by high scores on the YFAS, may be used as a proxy measure or marker for greater eating disorder severity, greater obesity severity, more severe trauma histories, greater symptoms of posttraumatic stress disorder (PTSD), greater psychiatric comorbidity, as well as greater medical morbidity and mortality. The existing literature through August 2016 was reviewed by the author using a Medline search with the following terms: food addiction cross-referenced with eating disorders (anorexia nervosa, bulimia nervosa, binge eating disorder, and binge eating), obesity, trauma, posttraumatic stress disorder, and comorbidity. The author asserts that the identification and acknowledgment of the concept of FA, when integrated into an overall, trauma-focused treatment approach, can be useful in understanding a more integrated and comprehensive clinical picture. This perspective may also help to bridge the conceptual gaps between eating disorders, weight disorders, addictions, and other related psychiatric and medical comorbidities.

Food addiction as a proxy for eating disorder and obesity severity

Gearhardt and colleagues were the first to demonstrate high rates of FA in individuals with binge eating disorder (BED) [32, 33; Gearhardt, White, et al., 2011]. In one study of 81 obese, treatment-seeking patients with BED, 57% met criteria for FA. This subgroup of BED individuals had significantly higher levels of eating disorder psychopathology, as well as higher measures of depression, negative affect, and emotional dysregulation, and lower measures of self-esteem. Taken together, the BED-FA group was a “more disturbed variant” of BED [33]. In a similar study of a racially diverse group of 96 patients with BED, 41.5% of them met FA criteria. Again, the BED-FA group had significantly higher rates of ED psychopathology, negative affect, emotional dysregulation, and low self-esteem [31]. In addition, higher YFAS scores were significant predictors of binge eating (BE) frequency above and beyond other measures, and were also associated with an earlier age of first being overweight and dieting onset.

The FA construct has also been studied in other eating disorders besides BED. In a study of 26 women with current bulimia nervosa (BN), 20 women with remitted BN, and a matched control group of 63 women, 100% of those with active BN met FA criteria, while 30% of the remitted group and none of the controls met FA [53]. The authors concluded that eating behavior within the context of BN can be described as addiction-like and that FA most likely improves when BN symptoms remit, although prospective, long-term studies are needed to clearly demonstrate this.

In a study of 125 patients with a variety of DSM-5 defined EDs versus 82 healthy controls, the Spanish version of the YFAS (YFAS-S) showed good discriminative capacity to distinguish between ED and controls and a good sensitivity to screen for specific ED subtypes [36]. The highest prevalence of FA was found in bingeing ED-subtype patient groups, i.e., AN binge–purge subtype (85.7%), BN (81.5%), and BED (76.9%), while the lowest prevalence was found in the AN restrictive subtype (50%). Again, YFAS-S scores were related to more severe eating pathology, higher levels of negative affect and depression, higher general psychopathology, and greater BMI. In summary, higher YFAS-S scores are associated with bingeing ED-subtype patients and with more eating severity and psychopathology. In addition, the FA construct was able to differentiate between ED and controls, although the authors called for further research on this topic.

Imperatori and colleagues studied 112 patients seeking weight loss treatment and found that 33.9% of these individuals met criteria for FA [39]. Severity of FA was strongly associated with BE. The combination of FA and BE was moderately associated with psychopathology.

Food addiction as a proxy for trauma and posttraumatic stress disorder (PTSD)

It has been well-established previously that bulimic behaviors (BE and purging) and especially eating disorders with bulimic features are highly associated with prior traumatic events and resultant posttraumatic stress disorder (PTSD) and partial PTSD [9, 10, 13, 14, 15, 17, 22, 55, 62]. Similarly, obesity has also been linked to prior victimization and PTSD [16]. It has been hypothesized that overindulgence in hedonic foods and drinks may, therefore, become a legal, inexpensive, and readily available method similar to indulging in other addictive substances or behaviors that traumatized persons use to anaesthetize themselves from unpleasant feelings and memories and to diminish emotional arousal [9, 10, 11, 12, 13, 14, 17].

In substantiation of this model, Hirth and colleagues studied over 3000 adult women who were patients at five public health clinics in respect to (1) their sugary soda and fast-food consumption, (2) their eating disordered behaviors (e.g., dieting, BE, purging), and (3) their PTSD symptoms. The researchers discovered a statistically significant relationship between symptoms of PTSD and (1) their frequency of sugary soda and fast-food intake and (2) their ED symptoms, including severe dieting, purging, and compulsive exercising, but not with BMI [37]. This research paper is distinctive, because it established for the first time a relationship between PTSD symptoms (and thus trauma history) and eating highly palatable foods known to be relatively unhealthy and associated with the concept of FA, i.e., foods with high concentrations of processed sugars and saturated fats, as well as salt and often caffeine.

Studies by Mason and her colleagues have further established the important links between trauma exposure, PTSD and FA. In one study of 57,321 adult participants in the National Nurses’ Health Study II (NNHSII), lifetime histories of childhood physical and sexual abuse in 2001 and current diagnosis of FA in 2009 were obtained [47]. Eighty percent of those with childhood maltreatment histories met criteria for FA. In fact, severe physical and sexual abuse histories were associated with approximately 90% increases in risk of FA. The relative risk (RR) of FA for those with histories of physical abuse was 1.92 (95% CI 1.76–2.09) and for those with histories of sexual abuse it was 1.87 (95% CI 1.69–2.05). The RR for combined severe physical abuse and sexual abuse was 2.40 (95% CI 2.16–2.67). The authors noted the strong relationship between histories of childhood physical and sexual abuse and FA in this population of women registered nurses. It is important to note that other forms of childhood trauma, e.g., emotional abuse, emotional neglect, physical neglect, accidents, disasters, etc., were not reported in this study, nor were symptoms or diagnoses of PTSD reported.

However, in another study by Mason and co-investigators using the NNHSII, 49,408 participants completed a modified version of the YFAS as well as measures of lifetime trauma exposure and PTSD symptoms [48]. Approximately 80% of the study sample reported some type of trauma exposure, and 66% of those who were trauma-exposed reported at least one lifetime PTSD symptom. Eight percent of the entire cohort met FA criteria, and the prevalence of FA increased with the number of lifetime PTSD symptoms endorsed. The women with the greatest number of PTSD symptoms (6–7 symptoms) had more than twice the prevalence of FA as women with neither trauma histories nor PTSD symptoms. Symptoms of PTSD were more strongly related to FA when symptom onset occurred at a younger age. The PTSD–FA link did not differ significantly by type of trauma. The authors noted that approaches to reduce obesity associated with PTSD may require psychological and behavioral interventions that address dependence on food and/or use of food to cope with distress.

Food addiction as a proxy for trauma and obesity

The links between obesity and childhood maltreatment and/or PTSD are well-recognized [1, 24, 25, 46, 49]. In a recent study using results from the National Women’s Study, Brewerton and coworkers showed strong associations between extreme obesity (BMI ≥ 40) and histories of rape, childhood sexual abuse, any childhood maltreatment, as well as current and lifetime PTSD [15]. In addition, those with extreme obesity were more likely to engage in BE and purging behaviors and to meet criteria for BN, any bulimic disorder (BN or BED), and major depressive disorder.

Other recent studies report important links between trauma histories, FA, and obesity. In the study noted above by Mason and colleagues using the NNHSII, FA was not only strongly associated with childhood abuse but with significantly higher weights as well, i.e., six units of BMI higher than women without FA [47].

In a report involving 301 overweight and obese women seeking weight loss treatment, self-report measures of childhood trauma histories, BE, and FA were obtained [40]. The authors found that the severity of childhood trauma was moderately and independently associated with severity of both FA and BE, even after controlling for potential confounders. However, the co-occurrence of FA and BE was associated with higher BMI and more severe anxiety and depressive symptoms. In another study by Imperatori and colleagues in 112 men and women seeking weight loss interventions, the authors found that 33.9% of these individuals met criteria for FA [39]. The severity of FA was strongly associated with BE, and the combination of FA and BE was moderately associated with psychopathology.

Food addiction as a proxy for psychiatric comorbidity

As noted above, the links between FA, trauma exposure, and obesity extend to PTSD and its symptoms. The presence of PTSD is highly predictive of increased psychiatric comorbidity [8, 9, 10, 13].

In a group of trauma-exposed female (n = 55) and male (n = 642) veterans, the links between FA and PTSD were examined [56]. PTSD was found to be significantly and positively associated with ED symptoms, FA, expressive suppression of emotions, and cognitive reappraisal in the full sample and with all constructs except cognitive reappraisal in the male subsample. Expressive suppression of emotions was significantly associated with ED symptoms and mediated the PTSD—ED link. These results highlight the importance of investigating PTSD as a risk factor for FA and ED symptoms and the potential mediating role of emotion regulation in the development of PTSD, EDs, and all related disorders to identify targets for treatments.

As noted above in the studies by Imperatori and coworkers, the combination of FA and BE was associated with general psychopathology, particularly greater levels of anxiety and depression [39, 40].

Food addiction as a proxy for medical morbidity and mortality

Obesity has long been identified as a risk factor for many medical conditions and causes of death. However, it is only since the advent of the adverse childhood experiences (ACE) research studies that childhood adversity has been identified as a risk factor for all the major causes of death [1, 18, 24, 26]. Since the advent of these initial studies, other researchers have replicated these findings and have searched for potential mechanisms. These studies have incorporated findings from studies of stress in animals and PTSD in humans, which have identified major changes in various biological systems, including the central and autonomic nervous systems, the cardiovascular system, as well as endocrine and immunological systems [5, 7, 19, 20, 21, 51, 54, 57, 60]. Other investigators have found evidence of telomere shortening as a result of severe stress, which may be a marker for increased aging and early death [23, 50]. An extensive discussion of this topic is beyond the scope of this article. However, suffice it to say that obesity, severe bulimic disorders, childhood trauma, PTSD, and major depression have all been linked to significant morbidity and increased mortality. This places even more responsibility on the clinician to implement comprehensive psychiatric and medical evaluations, to identify any and all treatable medical conditions and to institute prophylactic measures against further health decline.

Implications for treatment

Gearhardt and colleagues have outlined some of the inherent conflicts between traditional conceptualizations of eating disorders treatment and substance use treatment, including food addiction [34]. One of the cornerstones within the eating disorders treatment community is that there are “no bad foods.” Unless there is a medically documented food allergy or intolerance, e.g., gluten, peanuts, etc., then all foods should be eating in moderation and in balance with each other. This has been an especially important concept when treating anorexia nervosa, an illness characterized by irrational fears about gaining weight and hence eating certain foods that are perceived to be “fattening” or “bad.”

In contrast, the addiction treatment community is comfortable with the concept of elimination of and abstinence from particular substances, including specific foods that are addicting. A classic example of this philosophy in Overeaters Anonymous (OA), which was founded in 1960 in Los Angeles under the premise that individuals struggling with compulsive overeating, BE, overweight, and/or obesity, are addicted to processed foods, including white sugar and white flour. More recently, the substance abuse treatment community has embraced a middle ground, i.e., the concept of harm avoidance, as opposed to an all-or-nothing stance, where there is no room for error [44].

Although evidence-based, integrated treatment approaches for FA remain to be determined in randomized, controlled trials, there is some clarity about what the concept of FA does not imply for treatment. It does not mean that a 12-step program is the only treatment or is the treatment of choice for FA. Some professionals mistakenly think that the only effective treatment for any type of addiction is a 12-step approach. It does not mean that the Overeaters Anonymous (OA) doctrine of eliminating white flour and sugar is valid. This has never been studied scientifically; there are only anecdotes for and against this strategy. It also does not mean that total abstinence from the addictive substance or behavior is necessary for improvement.

On the contrary, FA may mean that treatments used for substance-related disorders may be indicated. Although this requires further investigation, using already established, evidence-based approaches for addictions in the treatment of FA may be a good place to start. Such approaches include cognitive behavioral therapy (CBT), dialectical behavior therapy (DBT), motivational interviewing (MI) and motivational enhancement therapy (MET), mindfulness-based therapies (MBT), family therapies, and pharmacotherapies. Twelve-step facilitation, which has been effective for alcohol and cocaine dependence, may be effective for certain individuals with FA. Abstinence from or reduction of addictive substances (e.g., highly palatable foods) and behaviors (e.g., BE) may be necessary, although a harm reduction (HR) strategy, similar to what has evolved for alcohol and drugs (both illicit and licit), may be especially useful given how ubiquitous processed foods have become. The HR approach was developed in response to the excesses of a “zero tolerance approach” and to more effectively meet the needs of patients struggling with chronic conditions. HR emphasizes practical rather than idealized goals and is grounded in the ever evolving public health and advocacy movements. HR has been proven to be effective and has gained increasing official acceptance [44]. For example, it is now the basis of Canada’s Drug Strategy. A principle feature of HR is acceptance of the fact that some drug users for multiple reasons cannot be expected to cease their drug use at the present time.

Summary

In this overview of the emerging literature on FA and its relationship to eating and related disorders, the case has been made that FA may be used as a proxy for (1) bulimic eating disorder severity, (2) complex trauma histories, (3) severity of PTSD and PTSD symptoms, (4) intensity of psychiatric comorbidity, (5) severity of obesity, as well as (6) their combination. In addition, the implications for treatment have been discussed, and the case for a comprehensive management that requires careful attention to medical and psychiatric assessment and integrated care that incorporates trauma-focused treatment is made.

Notes

Compliance with ethical standards

Conflict of interest

On behalf of all authors, the corresponding author states that there is no conflict of interest.

Research involving human participants and/or animals

This article does not contain any studies with human participants or animals performed by any of the authors.

Informed consent

No new results are being reported in this paper, so informed consent is not applicable.

References

  1. 1.
    Anda RF, Dong M, Brown DW, Felitti VJ, Giles WH, Perry GS, Dube SR (2009) The relationship of adverse childhood experiences to a history of premature death of family members. BMC Public Health 9:106. doi:10.1186/1471-2458-9-106 CrossRefPubMedPubMedCentralGoogle Scholar
  2. 2.
    Avena NM, Gold JA, Kroll C, Gold MS (2012) Further developments in the neurobiology of food and addiction: update on the state of the science. Nutrition 28(4):341–343. doi:10.1016/j.nut.2011.11.002 CrossRefPubMedPubMedCentralGoogle Scholar
  3. 3.
    Avena NM, Rada P, Hoebel BG (2009) Sugar and fat bingeing have notable differences in addictive-like behavior. J Nutr 139(3):623–628. doi:10.3945/jn.108.097584 CrossRefPubMedPubMedCentralGoogle Scholar
  4. 4.
    Avena NM, Wang M, Gold MS (2011) Implications of food addiction and drug use in obesity. Psychiatr Ann 41(10):478–482. doi:10.3928/00485713-20110921-06 CrossRefGoogle Scholar
  5. 5.
    Baker DG, Nievergelt CM, O’Connor DT (2012) Biomarkers of PTSD: neuropeptides and immune signaling. Neuropharmacology 62(2):663–673. doi:10.1016/j.neuropharm.2011.02.027 CrossRefPubMedGoogle Scholar
  6. 6.
    Benton D (2010) The plausibility of sugar addiction and its role in obesity and eating disorders. Clin Nutr 29(3):288–303. doi:10.1016/j.clnu.2009.12.001 CrossRefPubMedGoogle Scholar
  7. 7.
    Bick J, Nguyen V, Leng L, Piecychna M, Crowley MJ, Bucala R, Grigorenko EL (2015) Preliminary associations between childhood neglect, MIF, and cortisol: potential pathways to long-term disease risk. Dev Psychobiol 57(1):131–139. doi:10.1002/dev.21265 CrossRefPubMedGoogle Scholar
  8. 8.
    Brady KT, Killeen TK, Brewerton T, Lucerini S (2000) Comorbidity of psychiatric disorders and posttraumatic stress disorder. J Clin Psychiatry 61(suppl 7):22–32PubMedGoogle Scholar
  9. 9.
    Brewerton TD (2004) Eating disorders, victimization, and comorbidity: principles of treatment. In Brewerton TD (ed), Clinical handbook of eating disorders: an integrated approach. Marcel Decker, New York, pp 509–545Google Scholar
  10. 10.
    Brewerton TD (2007) Eating disorders, trauma, and comorbidity: focus on PTSD. Eat Disord 15(4):285–304. doi:10.1080/10640260701454311 CrossRefPubMedGoogle Scholar
  11. 11.
    Brewerton TD (2011) Posttraumatic stress disorder and disordered eating: food addiction as self-medication. J Womens Health (Larchmt) 20(8):1133–1134. doi:10.1089/jwh.2011.3050 CrossRefGoogle Scholar
  12. 12.
    Brewerton TD (2015) Stress, trauma, and adversity as risk factors in the development of eating disorders. In: Smolak L, Levine M (eds) Wiley handbook of eating disorders. Guilford, New York, pp 445–460CrossRefGoogle Scholar
  13. 13.
    Brewerton TD, Brady K (2014) The role of stress, trauma, and PTSD in the etiology and treatment of eating disorders, addictions, and substance use disorders. In: Brewerton TD, Dennis AB (eds) Eating disorders, addictions, and substance use disorders: research, clinical and treatment perspectives. Springer, Berlin, pp 379–404CrossRefGoogle Scholar
  14. 14.
    Brewerton TD, Dansky BS, Kilpatrick DG, O’Neil PM (1999) Bulimia nervosa, PTSD, and forgetting results from the National Women’s Study. In: Williams LM, Banyard VL (eds) Trauma and memory. Sage, Durham, pp 127–138Google Scholar
  15. 15.
    Brewerton TD, Dansky BS, O’Neil PM, Kilpatrick DG (2015) The number of divergent purging behaviors is associated with histories of trauma, PTSD, and comorbidity in a national sample of women. Eat Disord 1-8 doi:10.1080/10640266.2015.1013394
  16. 16.
    Brewerton TD, O’Neil PM, Dansky BS, Kilpatrick DG (2015) Extreme obesity and its associations with victimization, PTSD, major depression and eating disorders in a national sample of women. J Obes Eat Disord 1(2):1–9Google Scholar
  17. 17.
    Brewerton TD, Rance SJ, Dansky BS, O’Neil PM, Kilpatrick DG (2014) A comparison of women with child-adolescent versus adult onset binge eating: results from the National Women’s Study. Int J Eat Disord 47(7):836–843. doi:10.1002/eat.22309 CrossRefPubMedGoogle Scholar
  18. 18.
    Brown DW, Anda RF, Tiemeier H, Felitti VJ, Edwards VJ, Croft JB, Giles WH (2009) Adverse childhood experiences and the risk of premature mortality. Am J Prev Med 37(5):389–396. doi:10.1016/j.amepre.2009.06.021 CrossRefPubMedGoogle Scholar
  19. 19.
    Cohen S, Janicki-Deverts D, Doyle WJ, Miller GE, Frank E, Rabin BS, Turner RB (2012) Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proc Natl Acad Sci USA 109(16):5995–5999. doi:10.1073/pnas.1118355109 CrossRefPubMedPubMedCentralGoogle Scholar
  20. 20.
    Danese A, Moffitt TE, Harrington H, Milne BJ, Polanczyk G, Pariante CM, Caspi A (2009) Adverse childhood experiences and adult risk factors for age-related disease: depression, inflammation, and clustering of metabolic risk markers. Arch Pediatr Adolesc Med 163(12):1135–1143. doi:10.1001/archpediatrics.2009.214 CrossRefPubMedPubMedCentralGoogle Scholar
  21. 21.
    Danese A, Moffitt TE, Pariante CM, Ambler A, Poulton R, Caspi A (2008) Elevated inflammation levels in depressed adults with a history of childhood maltreatment. Arch Gen Psychiatry 65(4):409–415. doi:10.1001/archpsyc.65.4.409 CrossRefPubMedPubMedCentralGoogle Scholar
  22. 22.
    Dansky BS, Brewerton TD, O’Neil PM, Kilpatrick DG (1997) The National Womens Study: relationship of victimization and posttraumatic stress disorder to bulimia nervosa. Int J Eat Disord 21:213–228CrossRefPubMedGoogle Scholar
  23. 23.
    Epel ES, Blackburn EH, Lin J, Dhabhar FS, Adler NE, Morrow JD, Cawthon RM (2004) Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci USA 101(49):17312–17315. doi:10.1073/pnas.0407162101 CrossRefPubMedPubMedCentralGoogle Scholar
  24. 24.
    Felitti VJ (1991) Long-term medical consequences of incest, rape, and molestation. South Med J 84:328–331CrossRefPubMedGoogle Scholar
  25. 25.
    Felitti VJ (1993) Chldhood sexual abuse, depression and family dysfunction in adult obese patients: a case control study. South Med J 86:732–736CrossRefPubMedGoogle Scholar
  26. 26.
    Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, Marks JS (1998) Relationshiop of childhood abuse and household dysfunction to many of the leading causes of death in adults. Am J Prev Med 14:245–258CrossRefPubMedGoogle Scholar
  27. 27.
    Fortuna JL (2012) The obesity epidemic and food addiction: clinical similarities to drug dependence. J Psychoactive Drugs 44(1):56–63. doi:10.1080/02791072.2012.662092 CrossRefPubMedGoogle Scholar
  28. 28.
    Gearhardt AN, Corbin WR, Brownell KD (2009) Preliminary validation of the yale food addiction scale. Appetite 52(2):430–436. doi:10.1016/j.appet.2008.12.003 CrossRefPubMedGoogle Scholar
  29. 29.
    Gearhardt AN, Davis C, Kuschner R, Brownell KD (2011) The addiction potential of hyperpalatable foods. Curr Drug Abuse Rev 4(3):140–145CrossRefPubMedGoogle Scholar
  30. 30.
    Gearhardt AN, Grilo CM, DiLeone RJ, Brownell KD, Potenza MN (2011) Can food be addictive? Public health and policy implications. Addiction 106(7):1208–1212. doi:10.1111/j.1360-0443.2010.03301.x CrossRefPubMedPubMedCentralGoogle Scholar
  31. 31.
    Gearhardt AN, Roberto CA, Seamans MJ, Corbin WR, Brownell KD (2013) Preliminary validation of the yale food addiction scale for children. Eat Behav 14(4):508–512. doi:10.1016/j.eatbeh.2013.07.002 CrossRefPubMedGoogle Scholar
  32. 32.
    Gearhardt AN, White MA, Masheb RM, Grilo CM (2013) An examination of food addiction in a racially diverse sample of obese patients with binge eating disorder in primary care settings. Compr Psychiatry 54(5):500–505. doi:10.1016/j.comppsych.2012.12.009 CrossRefPubMedPubMedCentralGoogle Scholar
  33. 33.
    Gearhardt AN, White MA, Masheb RM, Morgan PT, Crosby RD, Grilo CM (2012) An examination of the food addiction construct in obese patients with binge eating disorder. Int J Eat Disord 45(5):657–663. doi:10.1002/eat.20957 CrossRefPubMedGoogle Scholar
  34. 34.
    Gearhardt AN, White MA, Potenza MN (2011) Binge eating disorder and food addiction. Curr Drug Abuse Rev 4:201–207CrossRefPubMedPubMedCentralGoogle Scholar
  35. 35.
    Gold MS, Graham NA, Cocores JA, Nixon SJ (2009) Food addiction? J Addict Med 3(1):42–45. doi:10.1097/ADM.0b013e318199cd20 CrossRefPubMedGoogle Scholar
  36. 36.
    Granero R, Hilker I, Aguera Z, Jimenez-Murcia S, Sauchelli S, Islam MA, Fernandez-Aranda F (2014) Food addiction in a Spanish sample of eating disorders: DSM-5 diagnostic subtype differentiation and validation data. Eur Eat Disord Rev 22(6):389–396. doi:10.1002/erv.2311 CrossRefPubMedGoogle Scholar
  37. 37.
    Hirth JM, Rahman M, Berenson AB (2011) The association of posttraumatic stress disorder with fast food and soda consumption and unhealthy weight loss behaviors among young women. J Womens Health (Larchmt) 20(8):1141–1149. doi:10.1089/jwh.2010.2675 CrossRefGoogle Scholar
  38. 38.
    Hoebel BG, Avena NM, Bocarsly ME, Rada P (2009) Natural addiction: a behavioral and circuit model based on sugar addiction in rats. J Addict Med 3(1):33–41. doi:10.1097/ADM.0b013e31819aa621 CrossRefPubMedPubMedCentralGoogle Scholar
  39. 39.
    Imperatori C, Innamorati M, Contardi A, Continisio M, Tamburello S, Lamis DA, Fabbricatore M (2014) The association among food addiction, binge eating severity and psychopathology in obese and overweight patients attending low-energy-diet therapy. Compr Psychiatry 55(6):1358–1362. doi:10.1016/j.comppsych.2014.04.023 CrossRefPubMedGoogle Scholar
  40. 40.
    Imperatori C, Innamorati M, Lamis DA, Farina B, Pompili M, Contardi A, Fabbricatore M (2016) Childhood trauma in obese and overweight women with food addiction and clinical-level of binge eating. Child Abuse Negl 58:180–190. doi:10.1016/j.chiabu.2016.06.023 CrossRefPubMedGoogle Scholar
  41. 41.
    Joranby, L, Pineda, KF, Gold, MS (2005). Addiction to Food and Brain Reward Systems. Sexual Addict Compulsivity 12(2–3), 201–217. doi:10.1080/10720160500203765 CrossRefGoogle Scholar
  42. 42.
    Lee NM, Lucke J, Hall WD, Meurk C, Boyle FM, Carter A (2013) Public views on food addiction and obesity: implications for policy and treatment. PLoS One 8(9):e74836. doi:10.1371/journal.pone.0074836 CrossRefPubMedPubMedCentralGoogle Scholar
  43. 43.
    Liu Y, von Deneen KM, Kobeissy FH, Gold MS (2010) Food addiction and obesity: evidence from bench to bedside. J Psychoactive Drugs 42(2):133–145. doi:10.1080/02791072.2010.10400686 CrossRefPubMedGoogle Scholar
  44. 44.
    Logan DE, Marlatt GA (2010) Harm reduction therapy: a practice-friendly review of research. J Clin Psychol 66(2):201–214. doi:10.1002/jclp.20669 PubMedPubMedCentralGoogle Scholar
  45. 45.
    Lustig RH (2010) Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc 110(9):1307–1321. doi:10.1016/j.jada.2010.06.008 CrossRefPubMedGoogle Scholar
  46. 46.
    Mason SM, Bryn Austin S, Bakalar JL, Boynton-Jarrett R, Field AE, Gooding HC, Rich-Edwards JW (2016) Child Maltreatment’s Heavy Toll: The Need for Trauma-Informed Obesity Prevention. Am J Prev Med 50(5):646–649. doi:10.1016/j.amepre.2015.11.004 CrossRefPubMedGoogle Scholar
  47. 47.
    Mason SM, Flint AJ, Field AE, Austin SB, Rich-Edwards JW (2013) Abuse victimization in childhood or adolescence and risk of food addiction in adult women. Obesity (Silver Spring) 21(12):E775–E781. doi:10.1002/oby.20500 CrossRefGoogle Scholar
  48. 48.
    Mason SM, Flint AJ, Roberts AL, Agnew-Blais J, Koenen KC, Rich-Edwards JW (2014) Posttraumatic stress disorder symptoms and food addiction in women by timing and type of trauma exposure. JAMA Psychiatry 71(11):1271–1278. doi:10.1001/jamapsychiatry.2014.1208 CrossRefPubMedPubMedCentralGoogle Scholar
  49. 49.
    Mason, SM, MacLehose, RF, Katz-Wise, SL, Austin, SB, Neumark-Sztainer, D, Harlow, BL, Rich-Edwards, JW (2015). Childhood abuse victimization, stress-related eating, and weight status in young women. Ann Epidemiol, 25(10), 760–766 e762. doi:10.1016/j.annepidem.2015.06.081 Google Scholar
  50. 50.
    Mason SM, Prescott J, Tworoger SS, DeVivo I, Rich-Edwards JW (2015) Childhood physical and sexual abuse history and leukocyte telomere length among women in middle adulthood. PLoS One 10(6):e0124493. doi:10.1371/journal.pone.0124493 CrossRefPubMedPubMedCentralGoogle Scholar
  51. 51.
    Menard, C, Pfau, ML, Hodes, GE, Russo, SJ (2016) Immune and neuroendocrine mechanisms of stress vulnerability and resilience. Neuropsychopharmacology 1–19. doi:10.1038/npp.2016.90
  52. 52.
    Meule A, Gearhardt AN (2014) Food addiction in the light of DSM-5. Nutrients 6(9):3653–3671. doi:10.3390/nu6093653 CrossRefPubMedPubMedCentralGoogle Scholar
  53. 53.
    Meule A, von Rezori V, Blechert J (2014) Food addiction and bulimia nervosa. Eur Eat Disord Rev 22(5):331–337. doi:10.1002/erv.2306 CrossRefPubMedGoogle Scholar
  54. 54.
    Michopoulos V, Norrholm SD, Jovanovic T (2015) Diagnostic biomarkers for posttraumatic stress disorder: promising horizons from translational neuroscience research. Biol Psychiatry 78(5):344–353. doi:10.1016/j.biopsych.2015.01.005 CrossRefPubMedPubMedCentralGoogle Scholar
  55. 55.
    Mitchell KS, Mazzeo SE, Schlesinger MR, Brewerton TD, Smith BN (2012) Comorbidity of partial and subthreshold ptsd among men and women with eating disorders in the national comorbidity survey-replication study. Int J Eat Disord 45(3):307–315. doi:10.1002/eat.20965 CrossRefPubMedGoogle Scholar
  56. 56.
    Mitchell KS, Wolf EJ (2016) PTSD, food addiction, and disordered eating in a sample of primarily older veterans: the mediating role of emotion regulation. Psychiatry Res 243:23–29. doi:10.1016/j.psychres.2016.06.013 CrossRefPubMedPubMedCentralGoogle Scholar
  57. 57.
    Pace TW, Heim CM (2011) A short review on the psychoneuroimmunology of posttraumatic stress disorder: from risk factors to medical comorbidities. Brain Behav Immun 25(1):6–13. doi:10.1016/j.bbi.2010.10.003 CrossRefPubMedGoogle Scholar
  58. 58.
    Pursey KM, Stanwell P, Gearhardt AN, Collins CE, Burrows TL (2014) The prevalence of food addiction as assessed by the yale food addiction scale: a systematic review. Nutrients 6(10):4552–4590. doi:10.3390/nu6104552 CrossRefPubMedPubMedCentralGoogle Scholar
  59. 59.
    Randolph TG (1956) The descriptive features of food addiction; addictive eating and drinking. Q J Stud Alcohol 17(2):198–224PubMedGoogle Scholar
  60. 60.
    Rooks C, Veledar E, Goldberg J, Bremner JD, Vaccarino V (2012) Early trauma and inflammation: role of familial factors in a study of twins. Psychosom Med 74(2):146–152. doi:10.1097/PSY.0b013e318240a7d8 CrossRefPubMedPubMedCentralGoogle Scholar
  61. 61.
    The National Center on Addiction and Substance Abuse (2016). Understanding and addressing food addiction. A science-based approach to policy, practice and researchGoogle Scholar
  62. 62.
    Wonderlich SA, Brewerton TD, Jocic Z, Dansky BS, Abbott DW (1997) Relationship of childhood sexual abuse and eating disorders. J Am Acad Child Adolesc Psychiatry 36(8):1107–1115CrossRefPubMedGoogle Scholar

Copyright information

© Springer International Publishing Switzerland 2017

Authors and Affiliations

  1. 1.Department of Psychiatry and Behavioral SciencesMedical University of South CarolinaCharlestonUSA
  2. 2.Mount PleasantUSA

Personalised recommendations