Introduction
Neurodegenerative diseases affect over 50 million people worldwide [ 1 ], with prevalence and incidence significantly increasing with age. Globally, these diseases are the leading cause of disability and the second leading cause of mortality [ 2 ]. As the population continues to age, epidemiological studies are predicting a significant rise in the number of people living with these diseases [ 3 ]. A neurodegenerative disease occurs when cells within the central or peripheral nervous system deteriorate and undergo apoptosis [ 4 ]. This occurs in dementia‐type diseases, demyelinating diseases, Parkinson‐type diseases, prion diseases and motor neuron diseases [ 1 ]. The cause of these diseases remains elusive; however, genetics are recognised as a potential influence to some of these diseases, such as multiple sclerosis [ 5 ]. To date, neurodegenerative diseases have no known cure, leading to significant challenges in managing symptoms and maintaining overall well‐being [ 6 ]. Many of these diseases also present with physical and cognitive impairments leading to emotional, social and behavioural disturbances due to brain atrophy. Symptoms are varied including frailty, impaired balance and coordination, tremors, changes in metabolism, mood changes and memory loss [ 7 , 8 , 9 ]. Dietary intake also may be significantly impacted as a result of some symptoms [ 10 ].
Disordered eating is defined as ‘a disturbed and unhealthy eating pattern that can include restrictive dieting, compulsive eating or skipping meals ’ [ 11 ]. Disordered eating behaviours may arise following neurodegenerative disease diagnosis due to changes with a person's metabolism and eating preferences [ 9 , 12 ]. Other contributing factors include memory loss, inadequate eating or, at times, overeating and hyperphagia [ 9 , 12 ]. Studies have shown that both disordered eating behaviours and neurodegenerative diseases individually result in a lower quality of life (QoL) [ 13 , 14 ]. For example, QoL is negatively impacted by inhibited motor function, while disordered eating has been associated with depression and other mental health conditions [ 4 , 11 , 14 ].
The current evidence for neurodegenerative diseases and disordered eating are expanding as separate research areas, and consideration of the potential relationship between these is limited. Few reviews synthesise the evidence between eating behaviours and dementia and Alzheimer's disease; however, to date, no reviews have synthesised the evidence for other neurodegenerative diseases. Understanding this relationship could aid in an awareness of disordered eating behaviours and contribute to health behaviour management for these conditions.
Therefore, the aim of this review was to identify and map the studies related to disordered eating behaviours in individuals who live with a neurodegenerative disease. This review will contribute to our understanding of the relationship between disordered eating behaviours and neurodegenerative disease by providing a synthesis of the connection between the two topics.
Methods
Protocol and Registration
This scoping review followed the Joanna Briggs Institute (JBI) [ 15 ] and the Arksey and O'Malley methodological [ 16 ] frameworks and is reported according to the Reporting Guidelines of the Preferred Reporting Items for Systematic Reviews and Meta‐Analysis extension for Scoping Reviews (PRISMA‐ScR) checklist [ 17 ]. The review protocol was registered with the Open Science Framework (accessed at https://doi.org/10.17605/OSF.IO/T9D34 , 23 October 2024).
Research Questions
Scoping reviews are an ideal method for topics where the established evidence is emerging, limited or inconsistent. They allow for a greater scope of a topic using wider questions and mapping of the evidence to identify knowledge gaps, clarify concepts or investigate areas for further research [ 18 ]. Three broad questions guided the synthesis of this review:
How are disordered eating behaviours identified in neurodegenerative diseases?
What eating behaviours are reported in adults living with neurodegenerative disease?
What are the implications of disordered eating behaviours on overall health outcomes, including QoL, in adults living with a neurodegenerative disease?
Eligibility Criteria
Eligibility criteria were developed based on the population, concept and context (PCC) framework [ 15 ].
Population
The population referred to adults living with a diagnosis of neurodegenerative disease, including dementia‐type diseases, demyelinating diseases (e.g. multiple sclerosis), Parkinson‐type diseases, prion diseases and motor neuron diseases regardless of sex, ethnicity, religion, disease duration and comorbidities. All diseases that aligned with the National Institute of Health and National Cancer Institute definitions of neurodegenerative disease were included [ 4 , 19 ]. The definitions state: ‘ Neurodegenerative diseases are conditions where nerve cells in the brain or peripheral nervous system lose function and die over time, leading to a progressive decline in movement, cognition, or other mental functions. They are a type of disease in which cells of the central nervous system stop working or die. Neurodegenerative disorders usually get worse over time and have no cure .’ Studies that included animal models, paediatric < 18 years old and/or pregnant participants were excluded from the review.
Concept
The concept explored was disordered eating behaviours. Disordered eating, as defined by the Butterfly Foundation, was used to select the studies included [ 11 ]. In this review, eating disorders refers to clinically diagnosed conditions (e.g., anorexia nervosa or bulimia nervosa), while disordered eating behaviours refers to broader maladaptive eating patterns. Studies that explored eating disorders and abnormal eating behaviours in neurodegenerative diseases aligned with the definition were eligible for inclusion. Studies focusing on feeding difficulties were excluded as they primarily addressed the physical limitations related to process of eating rather than the behaviour of eating.
Context
Studies published in peer‐reviewed scientific journals were considered in the context of this review, irrespective of the study setting. Observational or experimental study designs were included, with no limitations placed on the year of publication. No limitations were placed on the publication language; however, if studies were unable to be translated to the English language using Google Translate ( https://translate.google.com ), they were excluded. Grey literature, review studies (narrative, scoping and systematic), letters to the editor and conference reports were excluded.
Search Strategy
The search strategy was initiated with pilot searches in April 2024, using various search term combinations. These combinations were compared to guide the viability of the search. Free text keywords, medical subject headings (MESH) terms and keywords from sentinel studies ( n = 4) were used to guide the final search strategy (see Supporting Information S1: Table S1 ). The PubMed, Medline, Scopus and the Web of Science scientific databases were searched, using the following search string, ‘(“neurodegenerat* dis*” OR “dementia” OR “multiple sclerosis” OR “motor neurone disease” OR “Alzheimer's” OR “creutzfeldt‐jakob disease” OR “Parkinson's disease” OR “Huntington's disease” OR “amyotrophic lateral sclerosis”) AND (“disordered eating” OR “eating disorder*” OR “eating behavio*” OR “body image”)’. Bramer's recommendations for optimal database combinations [ 20 ] were used to ensure the most efficient and adequate coverage of literature. A final search was conducted on 17 May 2024, by two independent researchers. Forward and backward citation chasing was performed by one researcher (E.B.) to maximise the included studies.
Study Selection
The selection of studies was conducted using a systematic approach, utilising data management software, Covidence (Veritas Health Innovation, Melbourne, Australia; available at https://www.covidence.org ). Studies were screened at multiple stages. Initially, the title and abstracts were screened in duplicate independently by three reviewers (E.B., S.A. and Y.P.). Studies then underwent duplicate full‐text screening in duplicate by three reviewers (E.B., S.A. and Y.P.) to determine final inclusion for data extraction. When the full text of potentially relevant sources was not accessible through open access, copies were obtained from other university library sources. Conflicts at each stage were discussed amongst reviewers, with involvement of a senior reviewer (Y.P.) when consensus could not be reached. The selection process is documented in Figure 1 .
Data Extraction
The data extraction process followed JBI recommendations, to compile a master data extraction table [ 15 ]. One researcher (E.B.) completed the data extraction, while two researchers (S.A. and Y.P.) source data verified the table to ensure the quality of the data extracted [ 21 ]. Study design, age, sex, tools used, outcomes and results of the studies (e.g., number of participants with a disordered eating behaviour) were extracted to determine and interpret key findings (Supporting Information S1: Table 2 ).
Result Synthesis
The synthesis of evidence sources occurred as studies were categorised by the type of disordered eating behaviours present among the neurodegenerative disease types. A narrative descriptive analysis was used to map existing evidence and identify key patterns and concepts from the included studies that were categorised by the type of eating behaviour that they explored. This was conducted across the neurodegenerative disease types identified (dementia and Alzheimer's disease, amyotrophic lateral sclerosis, multiple sclerosis [MS] and Parkinson's disease [PD]). The research questions were also used to guide the synthesis of the results.
Results
Study Selection
The final scientific database search yielded 4336 records with 1898 records removed as duplicates. Of this, 93 full texts were screened, and 36 studies were eligible for inclusion (see Figure 1 ).
Characteristics of Included Studies
The general characteristics of evidence sources have been identified, studies were sourced from various countries, with most ( n = 8, 22%) from the United Kingdom [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 ], followed by the United States ( n = 7, 19%) [ 30 , 31 , 32 , 33 , 34 , 35 , 36 ] and Australia ( n = 5, 14%) [ 37 , 38 , 39 , 40 , 41 ]. Females were more apparent within the sample populations ( n = 16, 44%) [ 24 , 25 , 26 , 30 , 31 , 38 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 ], though five studies did not report sex [ 22 , 28 , 33 , 35 , 51 ]. The average age of participants ranged from 24.0 to 84.1 years. Case‐control studies were the most common study design ( n = 8, 22%) [ 24 , 28 , 37 , 38 , 40 , 50 , 52 , 53 ], with less apparent case reports ( n = 5, 14%) [ 27 , 31 , 32 , 42 , 44 ]. Primarily, the studies ( n = 20, 56%) [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 32 , 33 , 35 , 38 , 39 , 40 , 45 , 46 , 47 , 48 , 49 ] explored disordered eating or eating behaviours in dementia or Alzheimer's disease, with only one included study focusing on amyotrophic lateral sclerosis (ALS).
Tools Used to Identify Disordered Eating Behaviours
Each study identified and classified disordered eating behaviours in a different way. Collectively, validated tools were most commonly utilised, including the Appetite and Eating Habits Questionnaire (APEHQ), ( n = 5, 14%) [ 28 , 37 , 38 , 39 , 40 ], the Eating Disorder Examination Questionnaire (EDE‐Q), ( n = 2, 6%) [ 36 , 47 ] and the Eating Attitudes Test (EAT), ( n = 3, 8%) [ 51 , 52 , 53 ]. The tools were used to identify the individual risk of having or developing an eating disorder. Some tools were used concurrently with these, such as Mini Mental State Examination (MMSE), Cambridge Behavioural Inventory (CBI) or Neuropsychiatric Inventory (NPI). Other studies did not highlight the use of a validated tool, or caregiver questionnaires for individuals living with dementia or AD were created by the researchers. The four disease types, apparent eating behaviours and frequency of tools used are described below (see Figure 2 and Supporting Information S1: Table S3 ).
Identified Disordered Eating Behaviours Across Neurodegenerative Diseases
A variety of eating behaviours were present in people living with the four neurodegenerative disease types studied. Outcomes of all 36 included studies indicate a range of disordered eating behaviours. The most common eating behaviours identified from these studies were eating disorders ( n = 11, 31%) [ 26 , 30 , 33 , 36 , 41 , 42 , 43 , 47 , 49 , 50 , 52 ], hyperphagia and overeating ( n = 10, 28%) [ 22 , 24 , 29 , 35 , 36 , 38 , 40 , 46 , 48 , 52 ] and appetite‐related changes ( n = 10, 28%) [ 23 , 25 , 27 , 28 , 34 , 37 , 39 , 44 , 45 , 54 ] and food addiction ( n = 4, 11%) [ 31 , 50 , 55 , 56 ]. Figure 3 identifies the range of disordered eating behaviours present among the studies and across diseases. It is evident that there are neurodegenerative disease types that have not yet been studied in this area including prion and motor neuron diseases.
Overeating‐related issues were presented as the most common theme among the included evidence sources. Seven dementia or AD‐related studies (7/20, 35%) reported the presence of hyperphagia or excessive eating [ 22 , 24 , 35 , 38 , 39 , 46 , 48 ]. The frequency of hyperphagia was dependent on the type of dementia diagnosed, with five studies reporting that it was more apparent in dementia (bvFTD and frontotemporal dementia) than Alzheimer's disease [ 23 , 28 , 29 , 32 , 49 ]. Non‐validated caregiver surveys and APEHQ were the most frequently used tools to identify abnormal eating behaviours, deemed by 10 studies as an appropriate method of data collection, given the cognitively deteriorating nature of dementia. Only one study attributed a less precise measure of appetite control in individuals with dementia and increasing age, evidenced by a test meal that indicated greater meal intake for hyperphagic patients [ 24 ]. However, five dementia‐related studies (5/20, 25%) attributed the aetiology of disordered eating behaviours such as hyperphagia to damage, atrophy or tissue loss to the right frontal lobe [ 28 , 29 , 33 , 35 , 38 ]. The remaining studies (15/20, 75%) did not comment on the aetiology of dementia‐related overeating. Hyperphagia or overeating specifically were not reported for any other neurodegenerative diseases, apart from dementia and AD.
Appetite‐related changes were the second most common eating behaviours identified. One study explored eating behaviours in ALS. This study employed the APEHQ tool to assess the severity of change in appetite, associating severe changes to appetite with decreased survival, which was statistically significant ( p = 0.031) [ 37 ]. This study did not investigate the pathophysiology behind the change in appetite experienced in ALS. One PD case report recognised two cases of bulimia (increased appetite) [ 34 ]. Appetite‐related changes were the second highest cause of altered eating behaviours in dementia and AD, with six studies (6/20, 30%) concluding these changes [ 23 , 27 , 28 , 39 , 40 , 48 ]. Three of these studies reported increased appetite [ 27 , 28 , 39 ], one of which determined 4/15 patients experienced increased appetite [ 27 ], with another stating the ‘increased likelihood that these appetite changes reflect the involvement of the ventral, frontal lobe, temporal pole and amygdala’ [ 23 ]. Only one dementia‐related study reported anorexia (decreased appetite) [ 48 ]. Appetite changes were not explored in any MS‐related studies.
Food addiction and binge eating were identified as a prominent theme. Impulsive compulsive disorders were the main investigation for PD, of which binge eating or food addiction were reported within all nine PD studies [ 31 , 34 , 36 , 50 , 53 , 54 , 55 , 56 , 57 ]. From six of the PD studies with 1240 participants, 137 participants met the food addiction criteria or were binge eaters, without adhering to the full diagnostic criteria for binge eating disorder [ 36 , 37 , 39 , 55 , 56 , 57 ]. Five PD‐related studies (5/9, 56%) found no significant association between dopamine agonists and impulsive compulsive disorders or binge eating specifically [ 34 , 36 , 53 , 54 , 57 ]. One of these studies had identified a higher prevalence of food addiction in females rather than males with no other studies commenting on the difference between sexes [ 57 ]. Four studies did not comment on the aetiology of disordered eating behaviours or the impact of dopamine agonists on food addiction and binge eating in PD [ 31 , 50 , 55 , 56 ]. One case report observed two cases of sleep‐related eating disorders, demonstrating nocturnal binge eating [ 31 ]. Binge eating was also identified in one dementia study with six patients who demonstrated this behaviour [ 35 ].
Eating disorders were reported across all six MS‐related studies with a total sample of 461 participants, 76% female [ 41 , 42 , 43 , 47 , 51 , 52 ]. From this sample, 260 people were exhibiting disordered eating behaviours or classified at risk of an eating disorder (56.4%), according to the EAT and EDE‐Q. The EAT and EDE‐Q were used to identify disordered eating behaviours and patterns in 4/6 MS‐related studies, with the remaining two studies being case reports [ 42 , 47 , 51 , 52 ]. From the two MS case reports, binge eating disorder and anorexia nervosa were diagnosed post‐disease [ 41 , 43 ]. One PD study identified one case of bulimia and two cases of binge eating disorder [ 53 ]. Another PD study also reported that 3.9% of participants adhered to the full criteria for binge eating disorder [ 57 ]. One case report focusing on two cases of food aversion within semantic dementia concluded that anorexia and eating disorders should be considered in older adults with a neurodegenerative disease [ 26 ]. No studies determined or suggested the aetiology of these eating disorders for MS. Eating disorders were not reported in ALS or AD studies. See Supporting Information S1: Table S2 , for the included study characteristics.
Disordered Eating Behaviours and Health‐Related Outcomes
The implications of disordered eating behaviours significantly impact overall health outcomes, including QoL, in adults living with neurodegenerative diseases. Negative implications and reduced QoL were consistently reported across included studies where disordered eating behaviours were present. However, only four studies (11%) considered this [ 31 , 37 , 51 , 56 ]. One study determined reduced survival rates (three times less likely to survive) where changes in eating behaviours were reported, for people living with ALS [ 37 ]. Two MS‐related studies considered the impact of disordered eating behaviours on QoL and reported reduced QoL concurrent with disordered eating behaviours [ 43 , 51 ]. There was a positive association between social anxiety and disordered eating in MS in one study [ 47 ]. Additionally, one study highlighted a lower QoL for people living with PD who have an impulsive compulsive disorder, including binge eating and food addiction [ 55 ]. Interestingly, one case report investigated the correlation between PD and sleep‐related eating disorders in two participants and reported that it affects patients' QoL. [ 31 ] However, all other studies failed to address QoL or associated implications, such as depression and social anxiety. QoL was not considered in any dementia or AD‐related studies.
Discussion
Our scoping review highlighted the limited research that investigates disordered eating behaviours among people living with a neurodegenerative disease. To our knowledge, this is the first scoping review to investigate this relationship across multiple neurodegenerative diseases. The age range of participants across the included studies was 24.0–84.1 years, however, most studies reported on neurodegenerative diseases in adults over 65 years, given ageing is a primary risk factor [ 57 ]. More than half of the included studies that reported sex included higher rates of female than male participants. While some diseases, such as MS, report a 3:1 female‐to‐male ratio this may not be common to all disease types [ 58 ]. However, it is known that females are more likely to participate in clinical research studies and a recent review also reports higher enrolment of males in studies potentially to counter a potential for sex bias [ 59 ]. To confirm if females living with neurodegenerative diseases are more likely to have disordered eating behaviours than males, as found in the general population [ 60 ], more studies are needed.
Disordered eating behaviours were identified using several different tools across the neurodegenerative disease types. Due to the multifaceted nature of these tools, each using differing questions and methods to identify disordered eating, it was challenging to compare the outcomes across all studies. In contrast, non‐validated tools were frequently used in the identification process. For example, caregiver questionnaires were commonly used to gather information on participants’ eating behaviours. Both the unvalidated tools and validated tools were completed by a participant or caregiver, presenting the potential for response bias, underreporting or overreporting of eating behaviours. Thus, there is a need for a standardised tool to assess disordered eating behaviours specifically for neurodegenerative diseases to aid in the earlier detection of disordered eating behaviours and prevent their progression.
Previous research has highlighted the negative effect of disordered eating and neurodegenerative diseases on QoL as individual areas of research [ 61 , 62 ]. However, studies addressing the association between the two are lacking. This was apparent as few ( n = 4, 11%) studies included in this review considered QoL. Those that did, reported eating behaviours to have a negative impact on QoL among neurodegenerative diseases, which coincides with the previously mentioned studies. Of the four studies that did consider QoL, two (50%) were MS‐focused and associated with reduced QoL, depression and social anxiety. The presence of mental health as a comorbidity should also be considered when assessing QoL. The remaining two studies highlighted reduced QoL in PD and ALS. The impact of disordered eating on QoL was not reported within dementia or AD. The studies that did explore QoL used disease‐specific tools. Thus, QoL between disease types could not be compared due to heterogeneity of the tools.
Overeating‐related issues, such as hyperphagia, emerged as frequent disordered eating behaviours present for dementia and AD. The frequency and severity of hyperphagia appeared to correlate with the type of dementia, with bvFTD and frontotemporal dementia exhibiting more pronounced symptoms than AD in multiple studies. However, there are also additional contributing factors behind the aetiology of these behaviours in dementia and AD. For example, as dementia and AD cause memory impairment, behavioural factors can also contribute to hyperphagia as an individual may have forgotten that they have already eaten, thus causing excessive eating. A potential neurological basis for hyperphagia in dementia was identified, which was supported by 30% of dementia‐focused studies included in this review, attributing this to right frontal lobe damage or atrophy. This aligns with the previous studies that connect frontal lobe function with self‐regulation [ 63 ]. However, 15 studies did not address the aetiology of these behaviours, an area for further research. Hyperphagia was only reported for dementia and AD with no other neurodegenerative diseases reported hyperphagia, specifically. This could suggest a possible mechanism that is not well supported in the current evidence. Underlying mechanisms in dementia could be further explored, to understand the health implications or comorbidities that may result.
Appetite‐related changes constituted a significant theme among dementia, AD and PD‐focused studies. This was the eating behaviour investigated in the one ALS study that was included in this review and was related to decreased survival. This suggests that disease progression has a significant impact on appetite. As found by Ngo et al. [ 64 ] increased appetite and anorexia (decreased appetite) were present across studies. However, increased appetite was more apparent in these diseases. This could also contribute to a reason behind hyperphagia in dementia as aforementioned suggesting that neurodegeneration may relate to appetite fluctuations. However, the aetiology of appetite‐related changes remains uncertain and requires further investigation to confirm this association. Identifying appetite changes early in the disease may aid in further understanding the disease progression and a standardised tool would assist in identifying appetite fluctuations as well as other disordered eating behaviours.
Food addiction and binge eating were common behaviours within neurodegenerative diseases, specifically PD and dementia. Binge eating in this context was explored similarly to compulsive eating rather than aligning with the diagnostic criteria for binge eating disorder as an eating disorder. The concept of food addiction as an impulsive compulsive disorder has previously been researched for PD. However, despite previous research attributing dopamine agonists to food addiction as an impulsive compulsive disorder, the more recent findings of this review are contradictory [ 65 ]. Five out of nine PD‐focused studies investigated the association; however, they found no significant correlation and concluded that dopamine agonists do not impact food addiction or binge eating in PD, respectively. Only one PD study considered sex as an influencing factor in food addiction and binge eating, which concluded a higher prevalence in females. Although the eating behaviours of food addiction and binge eating are more often investigated in PD, research considering the potential impact of sex on eating behaviours will contribute to further understanding the aetiology of these disordered eating behaviours. Binge eating was reported in one dementia‐related study, which supports similar findings to hyperphagia, as previously mentioned. However, binge eating did not consistently align with binge eating disorder as an eating disorder and were a fluctuating eating behaviour.
Diagnosed eating disorders were prevalent across multiple neurodegenerative diseases. MS‐related studies reported the highest prevalence of eating disorders, which emphasises a junction between neurological and psychological health, exposing the need for strategies to aid eating disorder treatment for neurodegenerative diseases. Eating disorders present in MS‐related studies included anorexia nervosa and binge eating disorder. In the MS studies included in our review, 56% of participants from six studies had an eating disorder or were at risk of an eating disorder. This indicates a higher prevalence of eating disorders in comparison to the general population [ 66 ]. This aligns with various studies concluding increased vulnerability to disordered eating among individuals with chronic illnesses [ 67 , 68 ]. Sex was noted in MS‐related studies as females had a higher prevalence of disease and eating disorders concurrently. MS is, however, more common in females, suggesting that sex may not be the only factor to consider. This reiterates the critical nature of early eating disorder detection to improve behaviour management for these diseases.
Interestingly, one case of bulimia was present for PD highlighting participant adherence to the full binge eating disorder criteria. This aligns with overeating tendencies in PD that have been reported by others [ 36 ]. Additionally, this also supports the concept of vulnerability in those with a chronic illness [ 67 , 68 ]. Anorexia nervosa was identified in semantic dementia, raising further unanswered questions regarding the broader health implications of impaired cognition on eating behaviours. This suggests that disordered eating behaviours may manifest in older adults with a neurodegenerative disease though studies fail to explore the aetiology underscoring a need for further research.
Overall, the main findings of our review established a range of disordered eating behaviours within the most prevalent neurodegenerative diseases. PD is the second most prevalent neurodegenerative disease which was concurrently the second most researched disease in this review. There are a lack of studies that consider disordered eating behaviours within ALS and MS and prion diseases were not considered at all.
Limitations
Several limitations to this review should be acknowledged. First, despite the comprehensive search strategy employed, the exclusion of the grey literature, published reviews, conference reports and editorials may have impacted the extent of evidence analysed, as some relevant studies may not have been captured. Second, the exclusion of studies that were unable to be translated to the English language may have hindered the depth of the review, as data from non‐English publications may have been missed. Third, a quality appraisal of included studies was not conducted because it is not required for a scoping review [ 69 ]. This limited the ability to evaluate the reliability of the included evidence.
Finally, the included evidence base itself has notable limitations. The evidence is dominated by case reports and small observational studies across several disease groups. Also, many studies used non‐validated or inconsistent assessment tools, defined eating behaviours differently, and rarely include QoL measures. Additionally, there is limited investigation into underlying mechanisms or causes of disordered eating behaviours across diseases. These gaps highlight the need for future research to explore contributing biological, psychological, or social factors, rather than focusing only on describing disordered eating behaviours in neurodegenerative diseases. Future research should also assess the impact of disordered eating behaviours on QoL, as this relationship remains underexplored across neurodegenerative diseases.
Conclusion
Our review identified the range of disordered eating behaviours that were present within dementia, AD, PD, MS and ALS. However, further research needs to be conducted to understand the aetiology behind disordered eating behaviours within these populations. Additionally, a standardised eating behaviour tool for neurodegenerative diseases should be considered in the future to enhance comparability and understand the severity of these disordered eating behaviours. This will support recognising these behaviours earlier and provide guidance around person centred care in the context of neurodegenerative diseases for clinicians. Specifically, dietitians should consider screening for eating behaviours in populations living with neurodegenerative diseases, recognising their increased risk.
Author Contributions
Search strategy development (E.B., S.A. and Y.P.), search implementation (E.B.), study screening (E.B., S.A. and Y.P.), data extraction (E.B., S.A. and Y.P.), data synthesis (E.B.), draft manuscript (E.B.), manuscript review, writing and finalisation (E.B., S.A. and Y.P.).
Funding
The authors have nothing to report.
Conflicts of Interest
Yasmine Probst is a person living with MS. Yasmine has received honoraria from MS Australia and MS Plus, is supported by a fellowship funded by MS Australia, and contributes to MS Australia advisory panels. The remaining authors declare no conflicts of interest.
Supporting information
Supporting File
Acknowledgements
Open access publishing facilitated by University of Wollongong, as part of the Wiley ‐ University of Wollongong agreement via the Council of Australasian University Librarians.
Data Availability Statement
The data that support the findings of this study are available from the corresponding author upon reasonable request.
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Associated Data
Supplementary Materials
Supporting File
Data Availability Statement
The data that support the findings of this study are available from the corresponding author upon reasonable request.