Eating Disorders and Parkinson's Disease—1: Comorbidities, Neurobiology, and Family History

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Main Authors: Angeline Krueger, Andrew W. Bergen, Irene Litvan, Vincent Filoteo, Carolina Makowski, Susan Murray, Karlee McGlone, Michael Garvin, Andi Drouin, Alyssa Kauffman, Caroline Steele, Heather Hower, Walter H. Kaye
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Published: Wiley 2026
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author Angeline Krueger
Andrew W. Bergen
Irene Litvan
Vincent Filoteo
Carolina Makowski
Susan Murray
Karlee McGlone
Michael Garvin
Andi Drouin
Alyssa Kauffman
Caroline Steele
Heather Hower
Walter H. Kaye
author_facet Angeline Krueger
Andrew W. Bergen
Irene Litvan
Vincent Filoteo
Carolina Makowski
Susan Murray
Karlee McGlone
Michael Garvin
Andi Drouin
Alyssa Kauffman
Caroline Steele
Heather Hower
Walter H. Kaye
Angeline Krueger
Andrew W. Bergen
Irene Litvan
Vincent Filoteo
Carolina Makowski
Susan Murray
Karlee McGlone
Michael Garvin
Andi Drouin
Alyssa Kauffman
Caroline Steele
Heather Hower
Walter H. Kaye
collection Wiley Open Access
contents Eating Disorders and Parkinson's Disease—1: Comorbidities, Neurobiology, and Family History Angeline Krueger Andrew W. Bergen Irene Litvan Vincent Filoteo Carolina Makowski Susan Murray Karlee McGlone Michael Garvin Andi Drouin Alyssa Kauffman Caroline Steele Heather Hower Walter H. Kaye European Eating Disorders Review ABSTRACT Objective Eating disorders (ED), particularly anorexia nervosa (AN), share neurobiological characteristics with Parkinson's Disease (PD) (e.g., premorbid anxiety, dopaminergic dysfunction, harm avoidance, weight loss), suggesting common vulnerability. The present study built upon these observations, an AN patient's reported family history of Parkinson's Disease (RFHoPD), and AN:PD genetic correlation estimates, by ascertaining RFHoPD in families of individuals with PD. Method We ascertained RFHoPD among ED patients and community participants, and estimated relative risks (RRs) for AN, Bulimia Nervosa (BN), and Binge Eating Disorder (BED). Results In the total sample ( N  = 1135), we observed increased RFHoPD among patients and community participants meeting criteria for ED diagnoses ( n  = 727) versus community participants without an ED diagnosis ( n  = 408). For AN, RFHoPD prevalence was 6.6%, versus 3.4% ( χ 2  = 4.638, p  = 0.031, RR = 1.935, 95% Confidence Interval [CI] = 1.012–3.768). For BN, RFHoPD prevalence was 7.4%, versus 3.4% ( χ 2  = 4.941, p  = 0.026, RR = 2.169, 95% CI = 1.023–4.620). For BED, RFHoPD prevalence was 13.3%, versus 3.4% ( χ 2  = 6.953, p  = 0.008, RR = 3.886, 95% CI = 1.108–11.524). Conclusions ED are associated with elevated RFHoPD. Analyses leveraging disorder‐specific research may improve understanding of shared risk factors. 10.1002/erv.70121 http://onlinelibrary.wiley.com/termsAndConditions#vor
doi_str_mv 10.1002/erv.70121
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institution Wiley Open Access
license_str_mv http://onlinelibrary.wiley.com/termsAndConditions#vor
publishDate 2026
publisher Wiley
record_format wiley_oa
spellingShingle Eating Disorders and Parkinson's Disease—1: Comorbidities, Neurobiology, and Family History
Angeline Krueger
Andrew W. Bergen
Irene Litvan
Vincent Filoteo
Carolina Makowski
Susan Murray
Karlee McGlone
Michael Garvin
Andi Drouin
Alyssa Kauffman
Caroline Steele
Heather Hower
Walter H. Kaye
European Eating Disorders Review
Eating Disorders and Parkinson's Disease—1: Comorbidities, Neurobiology, and Family History Angeline Krueger Andrew W. Bergen Irene Litvan Vincent Filoteo Carolina Makowski Susan Murray Karlee McGlone Michael Garvin Andi Drouin Alyssa Kauffman Caroline Steele Heather Hower Walter H. Kaye European Eating Disorders Review ABSTRACT Objective Eating disorders (ED), particularly anorexia nervosa (AN), share neurobiological characteristics with Parkinson's Disease (PD) (e.g., premorbid anxiety, dopaminergic dysfunction, harm avoidance, weight loss), suggesting common vulnerability. The present study built upon these observations, an AN patient's reported family history of Parkinson's Disease (RFHoPD), and AN:PD genetic correlation estimates, by ascertaining RFHoPD in families of individuals with PD. Method We ascertained RFHoPD among ED patients and community participants, and estimated relative risks (RRs) for AN, Bulimia Nervosa (BN), and Binge Eating Disorder (BED). Results In the total sample ( N  = 1135), we observed increased RFHoPD among patients and community participants meeting criteria for ED diagnoses ( n  = 727) versus community participants without an ED diagnosis ( n  = 408). For AN, RFHoPD prevalence was 6.6%, versus 3.4% ( χ 2  = 4.638, p  = 0.031, RR = 1.935, 95% Confidence Interval [CI] = 1.012–3.768). For BN, RFHoPD prevalence was 7.4%, versus 3.4% ( χ 2  = 4.941, p  = 0.026, RR = 2.169, 95% CI = 1.023–4.620). For BED, RFHoPD prevalence was 13.3%, versus 3.4% ( χ 2  = 6.953, p  = 0.008, RR = 3.886, 95% CI = 1.108–11.524). Conclusions ED are associated with elevated RFHoPD. Analyses leveraging disorder‐specific research may improve understanding of shared risk factors. 10.1002/erv.70121 http://onlinelibrary.wiley.com/termsAndConditions#vor
title Eating Disorders and Parkinson's Disease—1: Comorbidities, Neurobiology, and Family History
topic European Eating Disorders Review
url https://onlinelibrary.wiley.com/doi/10.1002/erv.70121