Clinical and Translational Research Open Access
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. May 16, 2024; 12(14): 2359-2369
Published online May 16, 2024. doi: 10.12998/wjcc.v12.i14.2359
Genetically predicted fatty liver disease and risk of psychiatric disorders: A mendelian randomization study
Wei-Ming Xu, Department of Medicine, The First People's Hospital of Fuyang, Hangzhou 311400, Zhejiang Province, China
Hai-Fu Zhang, Yong-Hang Feng, Shuo-Jun Li, Bi-Yun Xie, Department of Internal Medicine, The First People's Hospital of Fuyang, Hangzhou 311400, Zhejiang Province, China
ORCID number: Wei-Ming Xu (0009-0003-6162-049X); Hai-Fu Zhang (0000-0003-3654-2226); Yong-Hang Feng (0009-0005-8077-4771); Shuo-Jun Li (0009-0008-5557-7786); Bi-Yun Xie (0009-0001-5508-0306).
Co-first authors: Wei-Ming Xu and Hai-Fu Zhang.
Author contributions: Zhang HF and Xu WM conceived and designed the study; Li SJ and Feng YH collected data and performed data analysis; Zhang HF and Xu WM wrote the draft of this manuscript; Xu WM and Xie BY edited the manuscript.
Institutional review board statement: This study employed a Mendelian randomization design, and all the data were sourced from an open-access database; hence, these regulations were not applicable.
Informed consent statement: This study used only publicly available data, especially summary level data from GWAS, did not involve sensitive personal information, did not cause harm to individuals, and did not compromise their privacy; hence, these regulations were not applicable.
Conflict-of-interest statement: All authors have no conflicts of interest to disclose.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hai-Fu Zhang, MD, Doctor, Department of Internal Medicine, The First People's Hospital of Fuyang, No. 429 Beihuan Road, Fuchun Street, Hangzhou 311400, Zhejiang Province, China. 1375100541@qq.com
Received: January 8, 2024
Revised: February 18, 2024
Accepted: April 2, 2024
Published online: May 16, 2024
Processing time: 118 Days and 3 Hours

Abstract
BACKGROUND

Non-alcoholic fatty liver disease (NAFLD) and alcohol-related liver disease (ArLD) constitute the primary forms of chronic liver disease, and their incidence is progressively increasing with changes in lifestyle habits. Earlier studies have documented a correlation between the occurrence and development of prevalent mental disorders and fatty liver.

AIM

To investigate the correlation between fatty liver and mental disorders, thus necessitating the implementation of a mendelian randomization (MR) study to elucidate this association.

METHODS

Data on NAFLD and ArLD were retrieved from the genome-wide association studies catalog, while information on mental disorders, including Alzheimer's disease, schizophrenia, anxiety disorder, attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder, multiple personality disorder, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), and schizophrenia was acquired from the psychiatric genomics consortium. A two-sample MR method was applied to investigate mediators in significant associations.

RESULTS

After excluding weak instrumental variables, a causal relationship was identified between fatty liver disease and the occurrence and development of some psychiatric disorders. Specifically, the findings indicated that ArLD was associated with a significantly elevated risk of developing ADHD (OR: 5.81, 95%CI: 5.59-6.03, P < 0.01), bipolar disorder (OR: 5.73, 95%CI: 5.42-6.05, P = 0.03), OCD (OR: 6.42, 95%CI: 5.60-7.36, P < 0.01), and PTSD (OR: 5.66, 95%CI: 5.33-6.01, P < 0.01). Meanwhile, NAFLD significantly increased the risk of developing bipolar disorder (OR: 55.08, 95%CI: 3.59-845.51, P < 0.01), OCD (OR: 61.50, 95%CI: 6.69-565.45, P < 0.01), and PTSD (OR: 52.09, 95%CI: 4.24-639.32, P < 0.01).

CONCLUSION

Associations were found between genetic predisposition to fatty liver disease and an increased risk of a broad range of psychiatric disorders, namely bipolar disorder, OCD, and PTSD, highlighting the significance of preventive measures against psychiatric disorders in patients with fatty liver disease.

Key Words: Non-alcoholic fatty liver disease; Alcohol-related liver disease; Psychiatric disorders; Mendelian randomization; Single nucleotide polymorphisms

Core Tip: Non-alcoholic fatty liver disease and alcohol-related liver disease are the predominant forms of chronic liver diseases, with their incidence gradually increasing due to changing lifestyle habits. Observational studies have indicated a potential association between fatty liver and psychiatric disorders, necessitating Mendelian randomization studies to elucidate this relationship. The findings revealed significant associations between genetic susceptibility to hepatic steatosis and an elevated risk of a wide spectrum of psychiatric disorders, including bipolar disorder, obsessive-compulsive disorder, and post-traumatic stress disorder. These results underscore the imperative for preventive measures targeting mental health conditions in individuals with fatty liver disease.
INTRODUCTION

As is extensively documented, non-alcoholic fatty liver disease (NAFLD) and alcohol-related liver disease (ArLD) have emerged as the most important causes of hepatic injury, and their incidence is steadily increasing due to changes in lifestyle habits[1]. The former is a chronic liver condition associated with obesity and metabolic syndrome, with a prevalence of approximately 15%-20% and 30%-40% in women and men, respectively[2]. Existing evidence suggests that NAFLD not only affects the liver but is also a multi-system disease, influencing multiple extrahepatic organs and regulatory pathways[3]. ArLD is closely related to alcohol intake, with a prevalence ranging from 10% to 35% in individuals engaged in long-term heavy drinking[4]. The prevalence of NAFLD and ArLD has escalated, establishing them as the most prevalent forms of chronic liver disease and imposing a substantial clinical and economic burden[5].

While psychiatric disorders can be treated via various approaches, according to the World Health Organization (WHO), their incidence increases on a yearly basis[6]. Although the relationship between fatty liver and psychiatric disorders remains elusive, a higher prevalence of metabolic syndrome is observed in patients with psychiatric disorders[7]. Common psychiatric disorders, such as bipolar disorder, depressive disorder, or schizophrenia, may be associated with metabolic syndrome or substance abuse[8]. Elwing et al[9] observed a higher prevalence of major depression as well as anxiety disorders in NAFLD patients. At the same time, the incidence of ArLD is closely associated with excessive and chronic alcohol consumption, with addictive misuse of alcohol considered a highly prevalent psychiatric disorder[10]. For instance, anxiety is a common comorbidity in patients with alcohol abuse, causing significant discomfort and cognitive impairment[11].

Mendelian randomization (MR) is an approach for investigating causality between exposures and outcomes of interest[12] that utilizes single nucleotide polymorphisms (SNPs) as unconfounded proxies for exposures, thereby circumventing residual confounders and reverse causality commonly present in conventional observational studies[13]. The MR design represents a crucial strategy for causal inference without randomized clinical trials (RCTs), given that genetic variants are randomly assorted during meiosis, mimicking an RCT[14]. There is a non-negligible relationship between fatty liver and mental disorders, necessitating a comprehensive understanding of their shared characteristics to facilitate the development of appropriate assessments and interventions. Therefore, this MR study was conducted to determine the association between fatty liver and mental disorders.

MATERIALS AND METHODS

In this study, all data were derived from the Genetic Alliance's publicly available compilation of statistical data from genome-wide association studies (GWAS). All original studies underwent a thorough ethical review process and obtained informed consent from participants.

Study design

Summary statistics on fatty liver disease and psychiatric disorders were collected from published GWAS to explore the causal effect of fatty liver disease on the risk of psychiatric disorders using two-sample MR.

The MR Approach was constructed based on three primary assumptions: (1) Genetic variants as instrumental variables (IVs) should be significantly associated with the risk factor of interest; (2) the genetic variants used should not be associated with potential confounding factors; and (3) selected genetic variants influence the risk of outcome only via risk factors and not via other pathways (Figure 1).

Figure 1
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Figure 1 The overall design of Mendelian randomization analyses in the present study. SNPs: Single nucleotide polymorphisms.
Outcome and exposure data source

Summary statistics on fatty liver disease were downloaded from published GWAS. The GWAS Catalog database is publicly available for download and accessible at https://www.ebi.ac.uk/gwas/. Data on psychiatric disorders were retrieved from the psychiatric genomics consortium (https://pgc.unc.edu/). Among them the exposure groups were ArLD[15] and NAFLD[16], the outcome groups were psychiatric disorders (including Alzheimer’s disease[17], anorexia nervosa[18], anxiety disorder[19], attention deficit hyperactivity disorder[20], bipolar disorder[21], major depressive disorder[22], multiple disorders[23], obsessive-compulsive disorder[24], post-traumatic stress disorder[25], schizophrenia[26]). Details of the psychiatric disorders are presented in Table 1. The entire cohort consisted exclusively of individuals with European heritage.

Table 1 Detailed information on genome-wide association studies.
Ref.OutcomePMID
Sample size
Cases
Controls
Bellenguez et al[17], 2022Alzheimer’s disease3537999239106401577
Watson et al[18], 2019Anorexia nervosa313085451699255525
Schoeler et al[19], 2023Anxiety disorder37106081282802
Demontis et al[20], 2023Attention deficit hyperactivity disorder3670299738691186843
Stahl et al[21], 2019Bipolar disorder310437562035231358
Howard et al[22], 2019Major depressive disorder30718901246363561190
Cross-Disorder Group of the Psychiatric Genomics Consortium[23], 2019Multiple disorders31835028232964494162
IOCDF-GC, OCGAS[24], 2018Obsessive-compulsive disorder2876108326887037
Nievergelt et al[25], 2019Post-traumatic stress disorder3159494930000170000
Trubetskoy et al[26], 2022Schizophrenia3539658076775243649
Genetic variants selection criteria

The genetic instruments for each exposure trait or disease were meticulously chosen from the corresponding GWASs, surpassing the threshold of genome-wide significance (P < 5 × 108). Independent SNPs were defined by R2 < 0.001 and clump window > 10 kb without linkage disequilibrium (LD) were proposed as instrumental variables. LD among SNPs for each risk factor was calculated based on 1000 genomes LD reference panel European population[27] using the PLINK clumping approach (PLINK: a tool set for whole-genome association and population-based linkage analyses)[28].

Statistical analysis

The variance in fatty liver disease explained by the IVs was calculated, and weak IVs bias was analyzed using F-statistics. R2 was calculated based on the effect estimates (β) and allele frequencies (EAF) of each single SNP using the following formula: R2 = 2× EAF (1-EAF) × β2[29]. The F value was further calculated according to the formula F = R2 × (N-2)/(1-R2)[30]. F value > 10 was considered a strong genetic IV; otherwise, the SNP was discarded.

An assessment of heterogeneity across SNPs was conducted using Cochran's Q statistics. The primary analytical method used to examine causal associations was the random-effect inverse-variance-weighted model[31]. The MR-Egger method was used to determine the pleiotropic effects of the instrumental SNPs[32].

RESULTS
Selection of instrumental variables

F values for each SNP were individually calculated, and SNPs with values greater than 10 were retained, suggesting a low risk of bias due to weak IVs. Consequently, all SNPs in this study had F-statistics larger than 10 (Table 2).

Table 2 Details of variance explained by the selected instruments and F-statistics for the mendelian randomization analysis based on the sample size of autoimmune diseases.
Exposure/Outcome
SNPs
R2
F-statistic
Alcohol-related liver disease
Alzheimer’s disease///
Anorexia nervosa, anxiety disorder, attention deficit hyperactivity disorder, bipolar disorder, major depressive disorder, multiple disorders, obsessive-compulsive disorder, post-traumatic stress disorder, schizophreniars7384080.1157352.08
Non-alcoholic fatty liver disease
Alzheimer’s diseasers28601761, rs3747207, rs73001065 0.0435089.81
Anorexia nervosa, anxiety disorder, attention deficit hyperactivity disorder, bipolar disorder, major depressive disorder, multiple disorders, obsessive-compulsive disorder, post-traumatic stress disorder, schizophreniars3747207, rs4293580.0226942.59
SNPs: Single nucleotide polymorphisms.
Mendelian estimations

ArLD: In the ArLD population, one SNP (rs738408) was retained following screening and filtering. The findings indicated that ArLD significantly elevates the likelihood of developing attention deficit hyperactivity disorder (ADHD) (OR: 5.81, 95%CI: 5.59-6.03, P < 0.01), bipolar disorder (BD) (OR: 5.73, 95%CI: 5.42-6.05, P = 0.03), obsessive-compulsive disorder (OCD) (OR: 6.42, 95%CI: 5.60-7.36, P < 0.01), and post-traumatic stress disorder (PTSD) (OR: 5.66, 95%CI: 5.33-6.01, P < 0.01). In contrast, there was no evidence suggesting that ArLD increased the risk of anorexia nervosa (OR: 0.97, P = 0.37), anxiety disorder (OR: 1.00, P = 0.14), major depressive disorder (MDD) (OR: 1.00, P = 0.88), multiple personality disorders (OR: 0.96, P = 0.47), and schizophrenia (OR: 0.97, P = 0.14) (Figure 2). Considering that only one SNP was included, tests for heterogeneity and pleiotropy could not be performed.

Figure 2
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Figure 2 Mendelian randomization analysis of alcohol-related liver disease with psychiatric disorders risk.

NAFLD: In the NAFLD population, 3 SNPs (rs28601761, rs3747207, and rs73001065) were included in the analysis of their association with Alzheimer's disease. At the same time, 2 SNPs (rs3747207 and rs429358) were analyzed for their association with other mental disorders. The results revealed that NAFLD was associated with a significantly increased risk of developing bipolar disorder (OR: 55.08, 95%CI: 3.59-845.51, P < 0.01), OCD (OR: 61.50, 95%CI: 6.69-565.45, P < 0.01), and PTSD (OR: 52.09, 95%CI: 4.24-639.32, P < 0.01). On the other hand, there was no evidence implying that ArLD increased the risk of Alzheimer’s disease, anorexia nervosa, anxiety disorder, ADHD, MDD, multiple personality disorders, and schizophrenia (Figure 3). Due to significant heterogeneity, the random-effects model was used.

Figure 3
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Figure 3 Mendelian randomization analysis of the relationship between non-alcoholic fatty liver disease and the risk of psychiatric disorders.
DISCUSSION

As fatty liver disease has emerged as a leading cause of chronic liver disease worldwide, and with a deeper understanding of its pathogenesis, attention has increasingly focused on its impact on the extrahepatic system, particularly psychiatric disorders. Indeed, exposing their relationship is conducive to the prevention of related diseases. Herein, publicly available GWAS data were obtained and analyzed using two-sample MR. Interestingly, the results uncovered that ArLD significantly elevates the likelihood of developing ADHD, BD, OCD, and PTSD, whilst NAFLD significantly increased the risk of BIP, OCD and PTSD.

According to the WHO, 5.1% of the global burden of disease can be attributable to alcohol misuse, ranking it as the seventh leading risk factor globally[33]. Of note, persistent alcohol use disorder is strongly correlated with progressive hepatic damage and increased mortality[34]. Among patients diagnosed with fatty liver disease, non-interrupted consumption of alcohol results in cirrhosis in 8% to 20% of cases. Furthermore, ongoing alcohol use significantly increases mortality rates in those already suffering from cirrhosis[35]. It is worthwhile emphasizing the close correlation between alcohol dependence and other neuropsychiatric disorders such as non-alcoholic substance abuse, bipolar disorder, and ADHD[36]. The lifetime prevalence of PTSD in Western countries is estimated to be 8%, showing a strong correlation with substance use disorders, particularly alcohol addiction[37]. The reward-seeking processes that drive alcohol-seeking in alcohol-dependent patients are also implicated in some patients with OCD[38]. Moreover, alcohol use disorder results in higher recurrence rates and worse prognosis in OCD[39]. Additionally, alcohol use disorder with comorbid PTSD generates a mutually reinforcing cycle that exacerbates the risk of trauma[40]. Besides, the rewarding effects of alcohol may aggravate cognitive impairments and attention deficits associated with ADHD[41].

Alcohol dependence and BD frequently coexist, with chronic alcoholism being associated with 24%-62% of BD cases worldwide[42]. Prolonged alcohol consumption can exert detrimental effects on both the immune system and nervous system while also increasing the frequency and severity of emotional episodes in individuals with BD[43]. Abnormalities in the N-methyl-d-asperate (NMDA) receptor play a critical role in the occurrence and development of BD. Conversely, ethanol acts on the brain to inhibit NMDA receptors, thereby elevating the risk of BD[44]. However, the risks of fatty liver appear to outweigh the risks associated with alcohol abuse, and patients with NAFLD seem to be at a higher risk compared with patients with ArLD[45]. The results of this study demonstrated that NAFLD patients had a higher risk of developing BD than ArLD (NAFLD: OR = 55.08; ArLD: OR = 5.73). Clinically, compared with other psychiatric disorders, BD patients are more likely to suffer from metabolic syndrome, which is also a characteristic of NAFLD[46]. Hence, the vulnerability of individuals with NAFLD to BD has been hypothesized to be associated with the presence of metabolic syndrome[45]. MiR-34a tightly regulates lipid metabolism by suppressing the expression of sirtuin 1 (Sirt1), contributing to hepatic steatosis[47,48]. Noteworthily, its level is elevated in the serum of patients with NAFLD. At the same time, miR-34a is also a component of the molecular network that mediates neurodevelopment and synaptogenesis, and its increased level is considered a risk factor for bipolar disorder[49].

NAFLD is closely linked to metabolic disorder syndrome that is characterized by obesity, insulin resistance, and hyperlipidemia[50]. Animal experiments have validated that metabolic syndrome can lead to astrogliosis and microgliosis, causing damage to adjacent neuronal processes and aggravating PTSD-like symptoms[51]. Furthermore, a long-term observational study noted a significant correlation between metabolic syndrome and OCD, suggesting a potential synergistic interaction between the two conditions[52]. In parallel, chronic inflammation also plays a key role in NAFLD, with the levels of several proinflammatory cytokines being significantly higher in NAFLD patients[53]. According to an earlier study, the levels of proinflammatory markers (such as interleukin-1β, interleukin-6, and tumor necrosis factor-α), which are closely related to the development of the disease, were elevated in PTSD patients[54]. Elevated levels of inflammatory factors can elicit neuroinflammation within the basal ganglia, leading to abnormalities in the cortico-striato-thalamo-cortical circuitry, which is a significant mechanism underlying OCD[55]. Therefore, metabolic syndrome and high levels of inflammatory factors in NAFLD patients play an instrumental role in the occurrence and development of OCD and PTSD.

The combination of fatty liver and persistent inflammation is associated with neuroinflammation, disruptions in neurotransmission, and hypothalamic-pituitary-adrenal axis dysfunction, which are important pathogenesis of mental diseases[56]. A high correlation was also observed between NAFLD and MDD, with chronic stress-mediated increase in glucocorticoid levels playing a vital role[57]. However, no association was observed between fatty liver disease and other psychiatric disorders in this study.

This is the first study to explore the causal relationship between psychiatric disorders and fatty liver disease using a two-sample MR analysis with pooled GWAS-level statistics, thereby minimizing potential confounding and reverse causality by aggregating a large amount of genetic data. However, this study has some limitations that merit acknowledgment. To begin, independent SNPs (P < 5 × 108) with genome-wide significance levels were utilized in this study, with F statistics being greater than 10 to avoid weak IVs from compromising the validity of the MR results. This ultimately resulted in a limited number of SNPs after screening, warranting future GWAS with larger sample sizes to identify more SNPs. Secondly, the results of our study may not be generalizable to the global population, given that the study population in this study was limited to individuals of European ancestry. Therefore, the conclusions of this study should be interpreted with caution.

CONCLUSION

In summary, this MR study provides genetic evidence supporting a causal relationship between fatty liver disease and psychiatric disorders. Our results collectively suggest that ArLD is a risk factor for ADHD, bipolar disorder, OCD, and PTSD. Moreover, our findings highlight a correlation between the presence of NAFLD and a higher risk of bipolar disorder, OCD, and PTSD. Thus, patients with fatty liver disease should be more vigilant to prevent the onset of mental disorders.

Footnotes

Provenance and peer review: Unsolicited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Gastroenterology and hepatology

Country/Territory of origin: China

Peer-review report’s scientific quality classification

Grade A (Excellent): 0

Grade B (Very good): 0

Grade C (Good): C

Grade D (Fair): 0

Grade E (Poor): 0

P-Reviewer: Khan MM, India S-Editor: Liu JH L-Editor: A P-Editor: Xu ZH

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