Anorexia Nervosa
Anorexia nervosa (AN) is a severe and complex neuropsychiatric disorder characterized by an intense fear of gaining weight, a distorted body image, and dangerously low body weight[1]. This condition is associated with significant physical and psychological health consequences, often leading to chronic illness and high mortality rates.
Research consistently demonstrates a strong genetic component to anorexia nervosa. Family and twin studies have estimated the heritability of AN to be around 56%, with non-shared environmental factors accounting for a substantial portion of the remaining variance[1]. Recent genome-wide association studies (GWAS) have identified multiple genetic risk loci, highlighting a “metabo-psychiatric” origin for the disorder [2]. These findings suggest that AN is not solely a psychiatric condition but also involves metabolic dysfunction, with genetic variants influencing both psychiatric and metabolic pathways. Efforts are underway to further understand how these identified GWAS loci connect to specific genes through regulatory chromatin interactions [2].
Clinically, anorexia nervosa typically manifests during adolescence[2], though the age of onset can vary [2]. Its severe impact on an individual’s physical health, including cardiovascular complications, bone density loss, and electrolyte imbalances, underscores the critical need for early diagnosis and effective treatment.
The pervasive nature of anorexia nervosa, its serious health risks, and its impact on individuals and their families make it a disorder of considerable social importance. Understanding the underlying genetic and biological mechanisms is crucial for developing targeted prevention strategies, improving diagnostic tools, and creating more effective, personalized treatments to alleviate the burden of this challenging condition.
Limitations
Section titled “Limitations”Understanding the genetic underpinnings of anorexia nervosa (AN) through genome-wide association studies (GWAS) has advanced significantly, yet several inherent limitations in study design, phenotypic definition, and population representation warrant consideration. These limitations impact the interpretability and generalizability of current findings, highlighting areas for future research.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”Genome-wide association studies for complex psychiatric conditions like anorexia nervosa frequently encounter challenges related to statistical power and replication. While efforts to aggregate large cohorts have led to meta-analyses including thousands of AN cases, such as one study with 2,907 AN cases and 14,860 controls, studies can still be underpowered to detect all relevant genetic variants, especially those with smaller effect sizes. Understanding how these variants modulate gene activity provides insight into the molecular underpinnings of this severe disorder.
A number of identified variants, including rs11209950 and rs7531118 (LINC02796), rs10465868 (LINC01360 - LINC02238), rs1592757 , rs12658451 , rs254013 (NIHCOLE - RNU6-334P), and rs9834970 (HSPD1P6 - LINC02033), are located within or near genes encoding long intergenic non-coding RNAs (lncRNAs) or pseudogenes. LncRNAs, such as LINC02796 and LINC02033, do not produce proteins but serve as crucial regulators of gene expression, influencing processes like chromatin remodeling, transcription, and RNA stability. Pseudogenes, like RNU6-334P and HSPD1P6, are non-functional copies of protein-coding genes that can sometimes acquire regulatory roles, affecting the expression of their functional counterparts or other genes. Genetic variations in these non-coding regions can disrupt critical regulatory networks, potentially leading to dysregulation of genes involved in neuronal signaling, stress response, or metabolic adaptation, all of which are implicated in the development and persistence of anorexia nervosa[3].
Other variants, such as rs13093385 near BSN (Bassoon) and APEH (Acylaminoacyl-peptidase), highlight genes with diverse cellular functions. BSN encodes a key protein at the presynaptic terminal, essential for neurotransmitter release and synaptic communication, while APEH is involved in protein degradation processes. The variant rs4298967 is associated with CACNA1C, a gene encoding a subunit of an L-type voltage-gated calcium channel (CaV1.2), which is vital for neuronal excitability and synaptic plasticity and is a known risk gene for several other psychiatric disorders. Furthermore, rs1351394 is linked to HMGA2, a transcriptional regulator known to influence cell proliferation, development, and anthropometric traits like height and body mass index (BMI)[2]. Disruptions in calcium signaling via CACNA1Ccan profoundly affect mood, anxiety, and reward pathways, while alterations in synaptic function byBSN or metabolic regulation by HMGA2could contribute to the severe weight loss and distorted body image characteristic of anorexia nervosa[4]. Studies have revealed significant genetic correlations between anorexia nervosa and metabolic traits, including BMI and fat mass, underscoring the importance of genes likeHMGA2 in the disorder’s complex etiology [2].
Core Definition and Conceptualization
Section titled “Core Definition and Conceptualization”Anorexia nervosa (AN) is precisely defined as a complex neuropsychiatric disorder characterized by dangerously low body weight[1]. This condition is often conceptualized as an “extreme weight condition” [5], highlighting the severe physical manifestation alongside psychological components. Emerging research also implicates “metabo-psychiatric origins” [2], suggesting a complex interplay between metabolic and psychiatric factors in its etiology. This framework moves beyond purely psychological interpretations, emphasizing biological underpinnings and a broader conceptualization of the disorder.
Diagnostic Frameworks and Criteria
Section titled “Diagnostic Frameworks and Criteria”The classification and diagnosis of anorexia nervosa rely on standardized criteria established by major nosological systems. A lifetime diagnosis is typically established through comprehensive methods such as hospital or register records, structured clinical interviews, or online questionnaires[2]. These diagnostic approaches are based on criteria from successive editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R, DSM-IV, and the 5th edition, DSM-5) [2], as well as the International Classification of Diseases (ICD-8, ICD-9, and ICD-10) [2]. These systems provide categorical definitions, outlining specific clinical criteria and thresholds for diagnosis, which are crucial for both clinical practice and research studies.
Associated Terminology and Clinical Context
Section titled “Associated Terminology and Clinical Context”Anorexia nervosa is categorized under the broader umbrella of “eating disorders,” a group of conditions involving severe disturbances in eating behaviors and related thoughts and emotions[6]. A significant aspect of its clinical presentation is its high comorbidity with other psychiatric conditions, notably anxiety disorders[7] and major depression [8], indicating shared underlying vulnerabilities. The age of onset for anorexia nervosa is a key demographic and clinical characteristic, frequently investigated in genetic studies to understand its developmental trajectory and potential genetic variations[2]. This comprehensive understanding of AN within its clinical context is essential for effective diagnosis, treatment, and ongoing research into its complex nature.
Anorexia nervosa is a serious neuropsychiatric disorder characterized by a restrictive eating pattern that leads to significantly low body weight, accompanied by a profound fear of gaining weight and a distorted perception of body shape or size. The condition involves a complex interplay of psychological, behavioral, and physiological symptoms.
Core Clinical Features and Presentation
Section titled “Core Clinical Features and Presentation”Anorexia nervosa is fundamentally defined by a dangerously low body weight, which is maintained through restrictive eating behaviors, excessive exercise, or other compensatory actions. Individuals with the disorder often experience an intense and persistent fear of gaining weight or becoming fat, even when they are severely underweight[1]. This fear is frequently coupled with a disturbance in the way one’s body weight or shape is experienced, leading to an overemphasis on body shape and weight in self-evaluation, or a denial of the seriousness of the current low body weight. These core psychological and behavioral patterns are central to establishing a lifetime diagnosis of the condition . These variations highlight the importance of detailed assessment to capture the full spectrum of the disorder’s presentation.
Associated Medical and Psychiatric Manifestations
Section titled “Associated Medical and Psychiatric Manifestations”Anorexia nervosa is associated with a range of medical complications largely stemming from malnutrition, prominently including distinct patterns of menstrual disturbance[9]. Beyond physical symptoms, the disorder often co-occurs with other psychiatric conditions, showing clinical correlations such as a shared genetic basis with obsessive-compulsive disorder [7]. Emerging research suggests that anorexia nervosa may have metabo-psychiatric origins, implicating a complex interaction between metabolic and psychological pathways in its development[2]. These severe prognostic indicators underscore the critical need for early detection, comprehensive intervention strategies, and a holistic approach that addresses both the psychological and physiological aspects of the illness.
Causes
Section titled “Causes”Anorexia nervosa is a complex disorder influenced by a combination of genetic predispositions, environmental factors, and their intricate interactions. Research indicates a multifactorial etiology, highlighting the importance of understanding these diverse contributing elements.
Genetic Predisposition
Section titled “Genetic Predisposition”Anorexia nervosa is recognized as a highly heritable disorder, with genetic factors significantly contributing to an individual’s susceptibility[8]. Large-scale genome-wide association studies (GWAS) have been instrumental in identifying specific genetic vulnerabilities, revealing a polygenic architecture where numerous common genetic variants collectively increase risk [5]. Notably, recent research has pinpointed eight risk loci across the genome, strongly implicating a “metabo-psychiatric” origin for the condition, suggesting an intricate interplay between metabolic and psychiatric pathways [2]. These identified genetic loci are thought to influence various biological mechanisms, potentially through regulatory chromatin interactions that impact gene expression [2]. The common genetic variation also appears to influence the age at which anorexia nervosa typically manifests[10], further highlighting the role of inherited factors in the disorder’s presentation.
Interaction with Psychiatric Comorbidities
Section titled “Interaction with Psychiatric Comorbidities”A substantial aspect of anorexia nervosa’s etiology involves its significant genetic overlap with other psychiatric conditions, which can predispose individuals to the disorder or occur concurrently. Studies have revealed a shared genetic basis between anorexia nervosa and obsessive-compulsive disorder (OCD), indicating common underlying biological pathways that contribute to both conditions[7]. Furthermore, research has identified genetic correlations with other major psychiatric comorbidities, including attention-deficit/hyperactivity disorder (ADHD), schizophrenia, bipolar disorder, and major depressive disorder[5]. The presence of diagnosed anxiety disorders has also been shown to increase the risk of developing anorexia nervosa later in life, highlighting a sequential or cumulative risk factor[11]. These shared genetic underpinnings and comorbid relationships suggest that the genetic predisposition to anorexia nervosa often exists within a broader spectrum of psychiatric vulnerability.
Environmental Context and Developmental Timing
Section titled “Environmental Context and Developmental Timing”Beyond genetic predispositions, environmental factors are recognized as integral components in the development of anorexia nervosa, interacting with an individual’s genetic vulnerabilities. While specific environmental triggers such as lifestyle, diet, exposure, socioeconomic factors, or geographic influences are acknowledged as potential contributors, the precise mechanisms of their contribution are complex and varied[12]. The interplay between an individual’s genetic makeup and these external elements is crucial in determining the manifestation of the disorder. The timing of these influences throughout an individual’s life also plays a role, with common genetic variation impacting the age of onset for anorexia nervosa[10]. This suggests that developmental stages may present windows of increased vulnerability where environmental stressors or protective factors can interact with genetic predispositions to shape the trajectory of the illness.
Genetic Predisposition and Heritability
Section titled “Genetic Predisposition and Heritability”Anorexia nervosa (AN) is a complex condition with a significant genetic component, as evidenced by its high heritability[1]. Genome-wide association studies (GWAS) have been pivotal in uncovering specific genetic risk loci linked to AN [2]. These investigations have illuminated a multifaceted genetic architecture, encompassing common, low-frequency, and rare genetic variations that contribute to an individual’s susceptibility [1].
Recent research has pinpointed eight distinct risk loci associated with anorexia nervosa, and these genetic regions often interact with specific genes through regulatory chromatin interactions[2]. This mechanism suggests that genetic variants can modulate gene expression patterns by influencing how DNA is organized and accessed, thereby impacting cellular functions and regulatory networks. The discovery of these loci underscores the polygenic nature of AN, where numerous genes, each with a modest effect, collectively increase the risk of developing the disorder [2].
Neurobiological and Psychiatric Underpinnings
Section titled “Neurobiological and Psychiatric Underpinnings”The genetic findings for anorexia nervosa strongly suggest a “metabo-psychiatric” origin, highlighting a critical interplay between metabolic and psychiatric processes[2]. This perspective indicates that AN is not merely a disorder of metabolism or body weight but also involves substantial alterations in brain function and psychological traits. Studies have further revealed a shared genetic basis between anorexia nervosa and other psychiatric conditions, such such as obsessive-compulsive disorder (OCD)[7]. This shared genetic vulnerability implies common underlying neurobiological pathways that may predispose individuals to both AN and certain anxiety-related disorders.
The molecular pathways connecting these genetic predispositions to neurobiological changes likely involve key biomolecules such as proteins, receptors, and signaling molecules within the central nervous system. These elements can influence neurotransmitter systems, neural circuits responsible for appetite regulation, reward processing, and emotional control. Furthermore, common genetic variations can influence the age of onset for anorexia nervosa, emphasizing the developmental impact of these genetic factors on brain development and function[10].
Metabolic and Homeostatic Dysregulation
Section titled “Metabolic and Homeostatic Dysregulation”The “metabo-psychiatric” framework for anorexia nervosa underscores profound disruptions in metabolic processes and the body’s homeostatic balance[2]. Genetic research has identified significant metabolic genetic correlations, indicating that genes involved in regulating metabolism contribute to AN susceptibility [1]. For instance, the Fat mass and obesity-associated gene (FTO), commonly linked to obesity, has also been associated with anorexia nervosa, suggesting an intricate connection between energy balance pathways and the pathology of eating disorders[5].
These genetic influences likely manifest as alterations in critical biomolecules, including hormones, enzymes, and metabolic signaling pathways that govern hunger, satiety, and energy expenditure. The condition can be understood as an extreme weight state with significant genetic implications for metabolic functioning[5]. Such disruptions can trigger compensatory responses within the body, which may inadvertently perpetuate the cycle of restricted eating and metabolic imbalance.
Systemic Consequences and Tissue Interactions
Section titled “Systemic Consequences and Tissue Interactions”Anorexia nervosa, though characterized primarily by severe weight loss and a distorted body image, leads to widespread systemic consequences that affect multiple tissues and organ systems throughout the body. The extreme nutritional deprivation and metabolic dysregulation trigger a cascade of physiological changes. These systemic effects can impact bone mineral density, cardiovascular function, endocrine systems, and overall cellular health[5].
The complex interplay among genetic predispositions, neurobiological alterations, and metabolic disruptions contributes to these broad effects across the body. For example, dysregulation of hormones involved in energy balance can have downstream effects on bone metabolism, while psychiatric comorbidities can influence neuroendocrine axes. Understanding these intricate tissue interactions and systemic consequences is vital for comprehending the full biological impact of anorexia nervosa beyond its psychiatric and weight-related symptoms.
Clinical Relevance
Section titled “Clinical Relevance”Anorexia nervosa is a complex and biologically influenced psychiatric disorder characterized by dangerously low body weight, an intense fear of weight gain, and a distorted perception of body image[5]. Affecting approximately 1% of the population, predominantly females, it has a significant public health impact due to its substantial morbidity, mortality, and personal and familial burden[5]. Understanding its clinical relevance is crucial for effective diagnosis, treatment, and prevention.
Prognostic Indicators and Disease Course
Section titled “Prognostic Indicators and Disease Course”Anorexia nervosa carries one of the highest mortality rates among all psychiatric disorders, highlighting the critical need for robust prognostic indicators[13]. While many individuals achieve recovery, a significant proportion, approximately 25%, experience a chronic and relapsing course, underscoring the challenges in long-term management [14]. The disorder also ranks among the ten leading causes of disability in young women, emphasizing its profound long-term implications for health and quality of life [15]. Further research into genetic factors, such as common genetic variations associated with the age of onset, may offer insights into predicting individual disease trajectories and informing early intervention strategies[10].
Diagnostic Utility, Risk Assessment, and Personalized Interventions
Section titled “Diagnostic Utility, Risk Assessment, and Personalized Interventions”The clinical application of knowledge regarding anorexia nervosa involves precise diagnostic utility, typically guided by standardized criteria from manuals such as DSM-III-R, DSM-IV, ICD-8, ICD-9, or ICD-10, often established through comprehensive clinical assessments[2]. Risk stratification efforts are significantly enhanced by the identification of genetic variants linked to disordered eating, which can aid in identifying individuals at higher risk and guiding targeted prevention strategies [16]. The discovery of specific risk loci and the implication of metabo-psychiatric origins for anorexia nervosa provide a foundation for developing personalized medicine approaches, potentially informing treatment selection and monitoring strategies tailored to an individual’s genetic and metabolic profile[2]. Furthermore, an understanding of genetic variations influencing the age of onset can facilitate the identification of individuals prone to earlier disease manifestation, allowing for more timely interventions and potentially mitigating severe outcomes[10].
Comorbidity and Overlapping Phenotypes
Section titled “Comorbidity and Overlapping Phenotypes”Anorexia nervosa frequently co-occurs with a range of other psychiatric and somatic conditions, which can complicate its clinical presentation and management. Patients commonly experience comorbidities such as major depressive disorder and various anxiety disorders, underscoring the need for comprehensive mental health assessments[17]. Beyond psychiatric overlap, AN is associated with multiple somatic complications, and research indicates a shared genetic basis with conditions like obsessive-compulsive disorder, suggesting common underlying biological pathways that may contribute to overlapping phenotypes [7]. The identification of metabo-psychiatric origins further highlights the intricate interplay between metabolic dysregulation and psychiatric symptoms, necessitating a holistic and integrated approach to treatment that addresses the full spectrum of associated conditions in individuals with anorexia nervosa[2].
Ethical or Social Considerations
Section titled “Ethical or Social Considerations”The growing understanding of the genetic underpinnings of anorexia nervosa (AN) introduces a complex array of ethical and social considerations that require careful navigation. While genetic research holds promise for improved understanding and treatment, it also raises critical questions regarding individual rights, societal impact, and equitable access to care.
Ethical Implications of Genetic Research and Application
Section titled “Ethical Implications of Genetic Research and Application”The identification of genetic variants associated with anorexia nervosa raises significant ethical considerations, particularly concerning genetic testing and its potential applications. Ensuring robust informed consent is paramount when individuals participate in genetic studies or consider genetic testing for AN risk, given the complex and sensitive nature of the disorder[5]. This includes transparent communication about the probabilistic nature of genetic risk, the absence of definitive diagnostic tests, and the potential for psychological distress. Furthermore, the privacy of genetic information is a critical concern, necessitating stringent data protection measures to prevent unauthorized access or misuse.
The specter of genetic discrimination, where individuals might face prejudice in areas like employment or insurance based on their genetic predisposition to AN, poses a serious ethical challenge. Such discrimination could exacerbate the existing stigma surrounding mental health conditions. Additionally, as genetic understanding advances, discussions around reproductive choices may arise, prompting complex ethical dilemmas about the use of genetic information in family planning, which requires careful consideration of individual autonomy and societal values. Robust genetic testing regulations and research ethics frameworks are essential to navigate these challenges, ensuring that scientific progress benefits individuals without infringing upon their rights or well-being.
Social Impact, Stigma, and Health Disparities
Section titled “Social Impact, Stigma, and Health Disparities”Anorexia nervosa carries substantial morbidity and mortality, yet it is often accompanied by significant social stigma, which can be compounded by genetic findings if misinterpreted as deterministic[5]. This stigma, combined with socioeconomic factors, contributes to considerable health disparities in the prevalence and impact of AN. Access to care remains a major challenge, with effective treatment often described as “weak” and inpatient hospitalizations being costly [5]. Many individuals, especially those from vulnerable populations, face barriers to diagnosis and specialized treatment, highlighting inequities in healthcare provision.
Cultural considerations play a crucial role in the manifestation, recognition, and treatment-seeking behaviors for AN. Societal pressures and beauty standards can influence the presentation of the disorder, and cultural contexts may shape how genetic information is perceived and integrated into public understanding. Achieving health equity in AN care requires not only addressing financial and geographical barriers but also challenging deeply ingrained societal biases and ensuring that resource allocation prioritizes comprehensive and culturally sensitive interventions for all affected individuals.
Policy, Regulation, and Global Health Perspectives
Section titled “Policy, Regulation, and Global Health Perspectives”The evolving understanding of the genetic basis of anorexia nervosa necessitates robust policy and regulatory frameworks to guide research, clinical practice, and public understanding. This includes developing clear genetic testing regulations and comprehensive data protection protocols to safeguard sensitive genetic information gathered from large-scale studies[2]. Ethical research practices, including oversight boards and transparent reporting, are crucial to maintain public trust and ensure that genetic discoveries are translated responsibly into clinical guidelines for diagnosis, prevention, and treatment.
From a global health perspective, the substantial public health impact of AN, coupled with its high mortality rate, demands equitable resource allocation for research, prevention, and treatment worldwide[5]. As genetic insights emerge, there is a risk that advanced genetic technologies may be disproportionately available in high-income countries, further exacerbating existing global health disparities. International collaboration and policy initiatives are vital to ensure that the benefits of genetic research on AN are accessible and applicable to diverse populations, acknowledging varying healthcare infrastructures and cultural contexts globally.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs2799079 | ZSCAN26 | anxiety, stress-related disorder, major depressive disorder hemoglobin measurement anorexia nervosa |
| rs9379897 | ABT1 - ZNF322 | MMP9/OLR1 protein level ratio in blood hemoglobin measurement anorexia nervosa |
| rs13217619 | ZSCAN31 | anorexia nervosa schizophrenia fatty acid amount saturated fatty acids to total fatty acids percentage |
| rs13093385 | BSN - APEH | PR domain zinc finger protein 1 measurement anorexia nervosa protein measurement |
| rs11209950 rs7531118 | LINC02796 | anorexia nervosa |
| rs10465868 | LINC01360 - LINC02238 | anorexia nervosa |
| rs1592757 rs12658451 rs254013 | NIHCOLE - RNU6-334P | attention deficit hyperactivity disorder insomnia measurement anorexia nervosa |
| rs4298967 | CACNA1C, CACNA1C-IT3 | bipolar disorder schizophrenia anorexia nervosa attention deficit hyperactivity disorder, schizophrenia neuroticism measurement, cognitive function measurement |
| rs1351394 | HMGA2 | body height body height at birth hip circumference BMI-adjusted hip circumference insulin measurement |
| rs9834970 | HSPD1P6 - LINC02033 | bipolar disorder attention deficit hyperactivity disorder, bipolar disorder, autism spectrum disorder, schizophrenia, major depressive disorder bipolar disorder, schizophrenia bipolar disorder, response to lithium ion bipolar I disorder |
Frequently Asked Questions About Anorexia Nervosa
Section titled “Frequently Asked Questions About Anorexia Nervosa”These questions address the most important and specific aspects of anorexia nervosa based on current genetic research.
1. My sister had AN. Does that mean I’m also at risk?
Section titled “1. My sister had AN. Does that mean I’m also at risk?”Yes, having a close family member with anorexia nervosa significantly increases your risk. Research shows AN has a strong genetic component, with heritability estimated around 56%, meaning genes play a substantial role in your susceptibility. However, it’s not a guarantee, as non-shared environmental factors also contribute.
2. Why do I feel so different about food compared to others?
Section titled “2. Why do I feel so different about food compared to others?”Your unique feelings about food might be influenced by your genetic makeup. Anorexia nervosa has been identified as having “metabo-psychiatric” origins, meaning genetic variations can affect both your brain’s processing of food cues and your body’s metabolism, making your experience distinct from others.
3. Is AN just “in my head,” or is something else going on?
Section titled “3. Is AN just “in my head,” or is something else going on?”It’s definitely not just “in your head.” While AN has significant psychological components, genetic studies show it also involves metabolic dysfunction. Your genes influence both psychiatric pathways (like distorted body image) and metabolic pathways (like how your body handles energy), making it a complex biological disorder.
4. Why did my struggles with food start in my teenage years?
Section titled “4. Why did my struggles with food start in my teenage years?”Anorexia nervosa commonly manifests during adolescence, and this age of onset can also have genetic influences. While the exact reasons are still being explored, genetic factors likely interact with developmental stages and environmental triggers during these formative years.
5. Why does my body resist gaining weight so much?
Section titled “5. Why does my body resist gaining weight so much?”Your body’s strong resistance to gaining weight could be linked to the “metabo-psychiatric” nature of AN. Genetic variants can influence metabolic pathways, affecting how your body processes energy and regulates weight, contributing to the dangerously low body weight characteristic of the disorder.
6. Why do some people stay thin without trying, but I struggle?
Section titled “6. Why do some people stay thin without trying, but I struggle?”Everyone’s genetic blueprint influences their metabolism and body weight regulation differently. For individuals with anorexia nervosa, genetic factors contribute to the “metabo-psychiatric” origins, influencing metabolic pathways that can make weight gain particularly challenging and contributing to the dangerously low body weight characteristic of the disorder.
7. Can healthy habits really prevent AN if it runs in my family?
Section titled “7. Can healthy habits really prevent AN if it runs in my family?”While genetics play a significant role, accounting for about 56% of AN risk, non-shared environmental factors also contribute substantially. Adopting healthy habits and seeking early support can be crucial in managing predispositions and potentially mitigating risk, as genes are not the sole determinant.
8. Does my non-European background change my AN risk?
Section titled “8. Does my non-European background change my AN risk?”Current genetic findings for anorexia nervosa are predominantly based on studies of individuals of European ancestry. This means the identified genetic risk profiles may not fully represent the genetic landscape in diverse ethnic populations, and your background could involve different or unique genetic variants.
9. Is there a link between my AN and how I feel emotionally?
Section titled “9. Is there a link between my AN and how I feel emotionally?”Yes, there’s a strong connection. Anorexia nervosa is a neuropsychiatric disorder, meaning it involves both brain function and mental health. Genetic studies have identified risk loci influencing both psychiatric pathways (like mood and anxiety) and metabolic functions, showing a clear biological interplay.
10. Could a DNA test tell me if I’m predisposed to AN?
Section titled “10. Could a DNA test tell me if I’m predisposed to AN?”While genome-wide association studies have identified multiple genetic risk loci for AN, a single DNA test cannot definitively predict your individual risk. The identified variants contribute to susceptibility, but AN is complex, involving many genes and environmental factors, so such tests aren’t currently diagnostic or fully predictive.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
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[3] Duncan, L. et al. “Significant Locus and Metabolic Genetic Correlations Revealed in Genome-Wide Association Study of Anorexia Nervosa.”Am J Psychiatry, vol. 174, no. 9, 2017, pp. 850–858.
[4] Wang, K. et al. “A genome-wide association study on common SNPs and rare CNVs in anorexia nervosa.”Mol Psychiatry, vol. 16, 2011, pp. 949–959.
[5] Boraska V et al. “A genome-wide association study of anorexia nervosa.”Mol Psychiatry, vol. 19, 2014, pp. 1085–1094. PMID: 24514567.
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[7] Yilmaz, Z. et al. “Examination of the shared genetic basis of anorexia nervosa and obsessive-compulsive disorder.”Molecular Psychiatry, vol. 24, no. 12, 2019, pp. 1787-1796.
[8] Bulik, C. M., et al. “Prevalence, heritability, and prospective risk factors for anorexia nervosa.”Archives of General Psychiatry, vol. 63, no. 3, 2006, pp. 305-312.
[9] Poyastro Pinheiro, A., et al. “Patterns of menstrual disturbance in eating disorders.” International Journal of Eating Disorders, vol. 40, no. 5, 2007, pp. 424–434.
[10] Watson HJ et al. “Common Genetic Variation and Age of Onset of Anorexia Nervosa.”Biol Psychiatry Glob Open Sci, vol. 2, 2022, pp. 368–378. PMID: 36324647.
[11] Meier, S. M., et al. “Diagnosed Anxiety Disorders and the Risk of Subsequent Anorexia Nervosa: A Danish Population Register Study.”European Eating Disorders Review, vol. 23, no. 6, 2015, pp. 524-530.
[12] Wade, T. D., Martin N. G., Neale M. C., Tiggemann M., Treloar S. A., Bucholz K., et al. “The structure of the genetic and environmental risk factors for three measures of disordered eating.” Psychological Medicine, vol. 29, no. 4, 1999, pp. 925-934.
[13] Arcelus J et al. “Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies.”Arch Gen Psychiatry, vol. 68, 2011, pp. 724–731. PMID: 21727255.
[14] Berkman ND, Lohr KN, Bulik CM. “Outcomes of eating disorders: a systematic review of the literature.” Int J Eat Disord, vol. 40, 2007, pp. 293–309. PMID: 17370291.
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[16] Wade, T. D., et al. “Genetic variants associated with disordered eating.” International Journal of Eating Disorders, vol. 46, no. 4, 2013, pp. 341-351.
[17] Katzman D. “Medical complications in adolescents with anorexia nervosa: a review of the literature.”Int J Eat Disord, vol. 37, 2005, pp. S52–S59. PMID: 15852321.