Breaking the silence on liver myths: a call for evidence-based practice

Highlights

• •Misconceptions in chronic liver disease (CLD) persist among both patients and non-hepatologist clinicians.
• •Common myths affect diagnosis, nutrition, medication use, and transplant referral timing.
• •This review presents a dual-perspective approach, contrasting myths with evidence-based realities.
• •Structured care pathways, visual tools, and early multidisciplinary involvement are emphasised.
• •Educational interventions targeting clinicians and patients are essential to improve outcomes.

Abstract

Chronic liver disease (CLD) is increasingly prevalent and represents a major global health burden. Despite advances in diagnosis and management, both patients and non-hepatologist clinicians continue to hold misconceptions that adversely impact care quality and outcomes. Common myths include misunderstandings about the causes of liver disease, protein restriction in hepatic encephalopathy, and the risks of procedures like paracentesis. These beliefs often stem from limited hepatology exposure and unverified public health information. This narrative review identifies and categorises prevalent misconceptions in CLD, highlighting their real-world clinical consequences. By contrasting these myths with evidence-based guidance, we aim to promote awareness and improve multidisciplinary management. We advocate for targeted continuing medical education, structured care pathways, enhanced patient education and early transplant planning. Addressing these gaps is essential for delivering high-quality, equitable liver care and aligning clinical practice with current hepatology standards.

Graphical abstract

Key practice implications:

• •Clinicians should avoid outdated practices such as protein restriction in hepatic encephalopathy and unnecessary correction of INR before paracentesis.
• •Misconceptions like relying solely on liver enzymes to assess liver health must be addressed through education.
• •Early referral for liver transplant, even in the absence of decompensation, should be normalised.
• •Ascitic fluid should be routinely tested, even in asymptomatic patients, to avoid missed SBP.
• •Patient education tools and visual infographics should be integrated into routine care to combat myths and improve adherence
• •Structured care pathways involving multidisciplinary teams should be implemented for comprehensive liver care.

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Introduction

Chronic liver disease (CLD) is a significant global health challenge, contributing to considerable morbidity, mortality, and healthcare costs.¹ With aetiologies ranging from viral hepatitis and alcohol-related liver disease (ARLD) to the increasingly prevalent MASLD (metabolic dysfunction-associated steatotic liver disease), formerly known as non-alcoholic fatty liver disease (NAFLD), the burden of CLD is escalating worldwide.² According to the World Health Organization (WHO), liver cirrhosis is among the leading causes of death globally, with millions affected by its complications, including hepatic encephalopathy (HE), ascites and hepatocellular carcinoma (HCC).³ Despite growing awareness and advancements in hepatology, widespread misconceptions continue to compromise the timely diagnosis, appropriate management and outcomes of patients with liver disease.⁴

Misconceptions in liver disease often stem from cultural beliefs, anecdotal experiences and online misinformation among patients, and from outdated training and limited hepatology exposure among clinicians. These can lead to suboptimal care, including misinterpreted tests, inappropriate treatments and delayed referrals for specialist assessment.

Patient reliance on herbal tonics and misconceptions about alcohol also delay effective care. These entrenched myths have real-world consequences. Inappropriate dietary advice can exacerbate malnutrition and sarcopenia;⁵ delayed spontaneous bacterial peritonitis (SBP) diagnosis due to missed ascitic fluid analysis may lead to sepsis; reliance on ammonia levels rather than clinical grading for encephalopathy can obscure diagnosis;⁶ and withholding beta blockers or diuretics due to mild hypotension may leave portal hypertension inadequately treated.⁷ Moreover, failing to engage in early end-of-life care discussions with patients having decompensated cirrhosis can deny them and families the opportunity to plan with dignity.⁸

Liver disease care requires a multidisciplinary approach, especially in low-resource settings with limited specialist access. Combating patient misinformation needs culturally sensitive, accessible education beyond clinic visits. Tools like digital platforms, support groups and community outreach can help debunk myths and empower patients to engage actively with their care teams.⁹

This review represents the first structured effort to address common liver disease myths among patients and non-specialist providers. Misconceptions are grouped into patient- and physician-led myths and countered with evidence-based guidance to bridge the gap between everyday practice and hepatology standards.

Methodology

This narrative review highlights common misconceptions in CLD management from both patient and non-hepatologist perspectives. Myths were identified through clinical experience, patient interactions, peer discussions and a targeted literature review, focusing on those with significant impact and lacking guideline support.

A structured literature search was conducted through PubMed and Google Scholar using terms such as ‘liver disease myths’, ‘cirrhosis misconceptions’, ‘hepatic encephalopathy knowledge gaps’, ‘ascites management errors’ and ‘non-hepatologist liver management’. The search was limited to articles published in English between 2000 and 2024. Relevant guidelines from leading hepatology societies, including the American Association for the Study of Liver Diseases (AASLD), the European Association for the Study of the Liver (EASL) and the National Institute for Health and Care Excellence (NICE), were reviewed to extract evidence-based recommendations that counter commonly held myths.

Inclusion criteria for selecting myths included: (1) relevance to CLD; (2) frequent observation in clinical practice or literature; (3) potential to impact clinical outcomes if not addressed; and (4) availability of clear evidence or guideline statements that refute the misconception. Myths without sufficient clinical relevance or supporting counterevidence were excluded.

The collected misconceptions were then categorised into two primary domains: those commonly encountered among patients and those predominantly seen in clinical practice among generalist physicians. Each myth was accompanied by an explanation of the underlying belief, clarification based on current evidence, and references to authoritative guidelines or peer-reviewed studies. The objective of this methodological approach was to ensure a pragmatic, experience-informed and evidence-backed review that addresses real-world clinical challenges in hepatology.

Patient-centric misconceptions

Patients with CLD frequently hold misconceptions that can delay care and negatively influence health outcomes. Several patient-centric misconceptions are not merely benign misunderstandings; they contribute directly to avoidable harm. For instance, reliance on unproven herbal supplements can lead to drug-induced liver injury (DILI), a well-documented cause of acute liver failure.¹⁰ Addressing patient-centric misconceptions is crucial, as evidenced by qualitative research and patient surveys. For instance, a UK-based study involving 250 patients with CLD found that over 40% believed herbal tonics could serve as a substitute for medical treatment.¹¹ One prevalent myth is that liver disease only affects individuals who consume alcohol.¹² MASLD, viral hepatitis and autoimmune liver disorders are common in non-drinkers.¹³ Similarly, many patients believe that if their liver enzyme levels are normal, their liver must be healthy. However, it is well known that fibrosis and cirrhosis can progress silently, even with normal liver function tests.¹⁴ There also remains a widespread but dangerous belief that moderate or ‘social’ alcohol consumption is acceptable in patients with CLD or compensated cirrhosis. For these patients, no amount of alcohol is safe, as even minimal intake can worsen fibrosis and raise the risk of decompensation and cancer.¹⁵ Complete abstinence is frequently neglected in clinical practice. Fatty liver is also frequently perceived as harmless, despite its potential to progress to cirrhosis and liver cancer.

Many patients assume that treating the underlying cause, such as hepatitis C or autoimmune hepatitis, eliminates all long-term risks. However, complications like HCC and portal hypertension can still occur, particularly in those with cirrhosis, highlighting the need for ongoing surveillance and education.

Another misunderstanding is that once jaundice resolves, the liver has recovered. In fact, jaundice may fluctuate, and its resolution does not necessarily reflect true hepatic improvement.¹⁶ The use of herbal tonics and liver detox cleanses is also widespread, despite a lack of scientific evidence and potential for liver injury.¹⁷ Specific examples include green tea extract, kava, and traditional Chinese or Ayurvedic remedies containing ashwagandha or bupleurum, which are often used in ‘liver detox’ formulations. Studies have shown higher prevalence of such practices in South Asian, East Asian and Middle Eastern communities where traditional medicine use is common.¹⁸

Patients often attribute ascites to excessive water intake, overlooking the actual cause, portal hypertension and hypoalbuminaemia to seek timely advice. Nutritional misconceptions are particularly harmful. Patients commonly avoid extra protein out of concern for ammonia build-up, not realising that adequate protein is essential to prevent sarcopenia and that restriction can worsen HE.¹⁹ The term ‘added salt’ can be misinterpreted, as some individuals may restrict only visible salt intake while still consuming processed foods that are high in sodium, which may affect fluid management strategies for ascites.

Many believe that liver disease is always fatal, whereas several chronic liver conditions are manageable if detected and treated early. There is further confusion surrounding liver transplantation. Some assume it is only available to people with alcohol use disorder or drug users, and others mistakenly believe that transplantation guarantees full recovery, regardless of disease severity or comorbidities.²⁰

Patients often underestimate the genetic component of liver disease, overlooking conditions such as haemochromatosis, Wilson’s disease or alpha-1 antitrypsin deficiency, which may affect asymptomatic family members and necessitate screening (Table 1).

Table 1.

Patient centric misconceptions.

Myth	Reality
I don’t drink, so I can’t have liver disease.	MAFLD, viral hepatitis and autoimmune liver diseases are common in non-drinkers.
I can still drink under safe limits with cirrhosis.	Complete abstinence is the safest option.
If my liver enzymes are normal, my liver must be fine.	Many cirrhosis patients have normal LFTs; fibrosis may still be present.
Once jaundice goes away, I’m cured.	Jaundice can fluctuate and its resolution does not indicate recovery.
Herbal tonics and liver cleansers can cure liver disease.	Many of these are hepatotoxic and not evidence based.
Ascites is because I drank too much water.	Ascites is due to portal hypertension and low oncotic pressure.
I should avoid extra protein because of high ammonia.	Protein is necessary; restriction worsens sarcopenia and HE.
Liver disease is always fatal.	Many liver diseases are treatable or manageable if diagnosed early.
Fatty liver is harmless.	MAFLD can progress to cirrhosis and liver cancer.
Liver transplant is only for alcoholics or drug users.	Transplant is indicated for many liver conditions, including autoimmune and genetic.
‘Added salt’ only means salt sprinkled on food.	It includes hidden sodium in processed foods; total intake must be controlled.
No matter how sick I am, a liver transplant will make me completely well.	Outcomes depend on timing, functional status, and comorbidities.

Physician-centric misconceptions

Among non-hepatologist clinicians, several persistent misconceptions continue to impact the quality of CLD management. Viral hepatitis is often misunderstood, although hepatitis C is now curable, and hepatitis B manageable with long-term care. Diagnosis should go beyond basic serology, incorporating confirmatory tests (eg HBV DNA, HCV RNA), fibrosis assessment and ongoing monitoring, as normal enzymes or antibody positivity alone can be misleading.

Many assume that ALT and AST elevations always reflect hepatic inflammation, ignoring that these enzymes can be non-specifically elevated without a primary liver aetiology²¹ or even normal in advanced fibrosis.²² On the other hand, signs like mildly fluctuating ALT are often overlooked. Conditions such as viral hepatitis, autoimmune hepatitis, haemochromatosis and alpha-1 antitrypsin deficiency may present silently for years, underscoring the need for greater awareness and proactive investigation in primary care. Simple tests such as ELF and FibroScan provide non-invasive, scalable methods for assessing liver fibrosis and hold significant potential for community-based screening initiatives.

MASLD is often dismissed as benign, yet it can progress to advanced fibrosis or HCC, necessitating appropriate follow-up. Mild hepatomegaly on imaging is often ignored, despite it potentially indicating steatosis or fibrosis. Statins are frequently withheld in patients with MASLD due to concerns over mildly elevated liver enzymes. However, clinical evidence supports the safety and cardiovascular benefit of statins in this population, with discontinuation only necessary if transaminases exceed three times the upper limit of normal.²³

Proton pump inhibitors (PPIs) are frequently prescribed for patients with cirrhosis without a valid indication just for GI prophylaxis, a practice associated with an increased risk of infections such as SBP and Clostridium difficile.²⁴ Non-selective beta-blockers (NSBBs) are often inappropriately withheld based on low systolic blood pressure alone. However, current guidance recommends that their use should be individualised, considering mean arterial pressure (MAP), clinical symptoms and overall haemodynamic stability. Evidence supports continued NSBB use in patients with MAP ≥65 mmHg unless symptomatic hypotension or acute decompensation occurs, as they confer benefits in reducing portal hypertension and preventing variceal bleeding.⁷

Nutritional myths also persist, such as enforcing strict no-salt diets in all patients with cirrhosis, which can lead to poor caloric intake and worsened malnutrition.²⁵ There’s also a misconception that patients with cirrhosis should avoid protein due to concerns about ammonia, when in fact adequate protein intake is vital to prevent sarcopenia and worsen HE.²⁶ Skipping meals is perceived as trivial, yet fasting worsens catabolism in patients with cirrhosis and should be avoided through small, frequent meals.^27,28 A late-evening carbohydrate-rich snack may reduce overnight catabolic drive and maintain muscle mass.

A commonly held belief is that performing paracentesis in patients with elevated INR is unsafe. However, evidence shows that diagnostic in most cases and therapeutic paracentesis in some cases is safe even in the presence of coagulopathy,^29,30 as INR is not a reliable marker of coagulation status in these patients.³¹ Similarly, albumin is often administered based solely on low serum levels, whereas its clinical use is primarily indicated for volume expansion in settings such as large-volume paracentesis (LVP), SBP or hepatorenal syndrome (HRS).³² Furthermore, clinicians may neglect to sample ascitic fluid in the absence of overt signs of infection, overlooking that SBP can present asymptomatically.³³ Some clinicians routinely prescribe midodrine for ascites, despite its limited evidence-based role in hypotensive diuretic-resistant ascites.³⁴

Another misconception is that all patients with HE require enemas; in reality, oral lactulose remains the first-line therapy, with enemas reserved for severe or unresponsive cases.³⁵ A greater clinical concern lies in the failure to identify underlying precipitants, exclude alternative causes of altered mental status, and counsel patients on fitness to drive. These lapses are frequent in HE management and can have serious safety, diagnostic and medicolegal consequences. Moreover, recognising subclinical or covert HE is equally important, as it can significantly impair quality of life and daily functioning, and increase the risk of progression to overt HE if left unaddressed.³⁶ Many clinicians overlook that hyponatraemia should be corrected in HE, as low serum sodium can exacerbate cerebral oedema and worsen outcomes. Contrary to popular belief, 0.9% saline can be safely used in cirrhosis when judiciously administered, while 5% dextrose may worsen hyponatraemia and fluid overload.³⁷ Routine ammonia monitoring and albumin replacement based solely on lab values remain common misconceptions. Ammonia levels, though limited in their correlation with clinical severity of HE, retain diagnostic utility for their negative predictive value and may offer prognostic insights in selected inpatient and outpatient contexts, reflecting an evolving area of hepatology research,³⁸ and albumin should be used only for evidence-based indications such as LVP, SBP or HRS, not merely in response to low serum levels.³⁹

Referral for liver transplantation is often postponed until advanced decompensation, yet evidence suggests that timely evaluation, particularly in patients with progressive liver disease, can optimise outcomes. While transplant is not curative, early specialist input allows for risk stratification, psychosocial assessment and anticipation of complications. A structured hub-and-spoke referral model ensures appropriate triage from non-tertiary centres to specialised transplant services.⁴⁰

A common misconception among clinicians is that end-of-life planning is only relevant in the final hours or days of life. This belief leads to missed opportunities for timely goals-of-care discussions and involvement of the palliative care team in patients with advanced liver disease.⁴¹

Some clinicians continue to believe that biopsy is necessary to diagnose HCC; however, characteristic imaging findings are often sufficient, enabling earlier curative options such as resection or liver transplantation.⁴² (Table 2).

Table 2.

Physician centric misconceptions.

Myth	Reality
Paracentesis is dangerous in patients with high INR or low platelets.	Paracentesis, especially diagnostic fluid aspiration, can be done in most cases with coagulopathy and thrombocytopenia.
No signs of infection = no need to test ascites.	SBP can be asymptomatic; diagnostic paracentesis is essential.
Ascitic drains can remain longer with intermittent drainage safe as compared to drain to dryness approach.	Prolonged drainage increases infection risk; removal should be done as soon as possible with large-volume paracentesis under albumin cover.
Midodrine is useful for all types of ascites.	Midodrine is only used for selective diuretic-resistant cases.
Albumin should be given if the serum albumin level is low.	Albumin is used for volume expansion in specific indications–not lab correction.
A mildly enlarged liver on ultrasound is insignificant.	May indicate steatosis or fibrosis and warrants further evaluation.
Fatty liver doesn’t require follow-up.	MAFLD needs risk stratification and monitoring.
Normal AST and ALT means, normal liver.	Transaminases may not be present event in advanced cirrhosis.
Patients with cirrhosis should avoid extra protein due to ammonia production.	Adequate protein is critical; malnutrition worsens HE.
All patients with HE should be treated with enemas.	Oral lactulose is first line; enemas are for severe or unresponsive cases.
Frequent ammonia monitoring is needed to assess HE.	Ammonia levels correlate poorly with clinical status; not required for monitoring.
Skipped meals are not a concern in cirrhosis.	Fasting worsens catabolism; small, frequent meals are essential.
All cirrhosis patients need a no-salt diet.	Moderation is essential; over-restriction worsens nutrition.
All cirrhosis patients benefit from PPIs.	PPIs should be used only when indicated; overuse increases infection risk.
5% dextrose, rather than N-saline, should be used in patients with cirrhosis.	N-saline can be used judiciously, and 5% dextrose can make hyponatraemia worse.
Stop beta blockers and diuretics with low BP.	Should be based on mean arterial pressure and symptoms and clinical diagnosis – not absolute numbers.
End-of-life planning should wait until imminent death.	Early conversations improve care quality and family preparedness.
Referral for transplant should wait until severe decompensation.	Early referral improves outcomes specially for progressive conditions.
Statins can’t be used with abnormal liver enzymes.	Statins should only be stopped if liver enzymes are more than 3>ULN.

Discussion

Misconceptions in CLD have profound implications for patient outcomes, healthcare costs and the overall quality of care. These myths, when left unchallenged, contribute to misdiagnosis, delayed treatment and mismanagement of complications. From underappreciating the severity of MASLD to incorrectly interpreting liver function tests or withholding necessary treatments due to unfounded safety concerns, both patient and provider misconceptions pose substantial barriers to optimal care. While this review is aimed primarily at clinicians, addressing patient-centric misconceptions has clinical relevance for all providers. Misinformed patients may delay medical attention, self-medicate with hepatotoxic supplements, or adhere poorly to prescribed therapy. Healthcare professionals must recognise these knowledge gaps to better educate, counsel and protect their patients. Integration of culturally sensitive education-validated health literacy tools and patient-targeted interventions is essential.

One of the most critical consequences of these misconceptions is the delay in diagnosis. For example, the false belief that liver disease only occurs in people with alcohol use disorder often leads patients to ignore symptoms and delay medical evaluation. Similarly, the assumption that normal liver enzymes exclude liver pathology may lead physicians to miss early cirrhosis or fibrosis, particularly in MASLD.⁴³ Misguided therapeutic practices, such as unnecessary protein restriction in HE or indiscriminate use of PPIs, can exacerbate complications like sarcopenia or SBP.⁴⁴ Inaccurate interpretations of lab values, such as overreliance on ammonia levels in HE or serum albumin for fluid resuscitation, further illustrate how these misconceptions impact real-world clinical decision-making.

Several factors contribute to the persistence of these myths. For patients, cultural beliefs, anecdotal experiences and community narratives often play a central role in shaping perceptions of liver disease. These informal sources of information can strongly influence how individuals interpret symptoms, choose treatments and engage with medical advice.⁴⁵ In many communities, liver disease is still primarily associated with alcohol use, leading non-drinkers to dismiss early symptoms or delay seeking care. Additionally, widespread misinformation particularly from social media, wellness influencers and unregulated health websites promotes ineffective or even harmful practices, such as restrictive diets, excessive fasting, overuse of supplements and reliance on so-called ‘liver detox’ products.⁴⁶ These platforms often present simplified or sensationalised claims that appeal to fear or hope, but lack scientific grounding. As a result, patients may prioritise unproven alternative therapies over guideline-based medical treatment, discontinue prescribed medications, or avoid necessary procedures out of fear or misunderstanding. This environment of misinformation complicates physician–patient communication and makes evidence-based education and trust-building even more essential.

Among non-specialist clinicians, many misconceptions about CLD originate from outdated medical training and limited exposure to hepatology during residency or fellowship. Hepatology is often underrepresented in general medical education, resulting in gaps in understanding key principles such as portal hypertension management, nutrition in cirrhosis, and evidence-based use of albumin or PPIs. These gaps are further magnified in practice settings where access to hepatologists is scarce, or referral pathways are underdeveloped. In such environments, generalists including internists, emergency physicians and family practitioners are expected to manage complex liver conditions without sufficient support, structured protocols or updated clinical tools.

To bridge these gaps, a multifaceted approach is necessary. First, clinical education must be strengthened with emphasis on liver disease management across medical training programmes. Hepatology should be more prominently integrated into internal medicine and primary care curricula. Continuing medical education (CME) modules focused on common myths in CLD can also help practising physicians stay aligned with current guidelines. Institutions can support evidence-based care by embedding clinical decision support tools within electronic health records (EHRs), such as automated prompts for diagnostic paracentesis in patients with cirrhosis with ascites or alerts to avoid unnecessary PPI prescriptions. A practical example of this is the British Society of Gastroenterology (BSG) Cirrhosis Care Bundle, which provides a structured, checklist-based approach to the early management of decompensated cirrhosis.⁴⁷ The bundle includes recommendations for timely paracentesis, infection screening, nutritional assessment and early senior review, and has been shown to improve adherence to guidelines and reduce care variability.

Professional societies like AASLD and EASL have a pivotal role in developing concise, myth-busting clinical resources tailored to primary care and emergency settings. Quick-reference guides, flowcharts and mobile apps can make guideline-based practices more accessible.⁴⁸ In addition, quality improvement (QI) initiatives should focus on reducing low-value interventions driven by outdated beliefs.

Empowering patients with accurate, culturally sensitive and accessible information is key to addressing common misconceptions. Educational interventions should go beyond the brief physician encounter and include multimedia tools like videos, illustrated leaflets, patient portals and mobile applications that clarify diet, medication use and warning signs of decompensation.⁴⁹ Engaging dietitians, nurses and community health workers in education efforts can also reinforce consistent messages and support behavioural change.⁵⁰

Visual aids, infographics and multilingual content can enhance comprehension, particularly in populations with limited health literacy. Patient support groups, both in person and online, provide platforms for knowledge sharing and myth correction.⁵¹ Peer influence can be powerful, and hearing the experience of others who manage CLD effectively with evidence-based care can encourage healthier choices.⁵²

A cultural shift is needed to normalise early, proactive discussions on prognosis, goals of care and end-of-life planning in CLD. Early, structured conversations initiated during periods of clinical stability or following key decompensating events can lead to clearer care trajectories, fewer invasive interventions, and greater alignment with patients’ values and preferences.⁵³ Discussing topics such as transplant candidacy, palliative care integration and advance directives in a timely and compassionate manner enhances trust, reduces decisional conflict, and improves satisfaction for both patients and their families. Moreover, normalising these discussions as part of routine care helps dismantle the stigma surrounding palliative approaches and supports the shift from disease-centred to patient-centred care in hepatology.⁵⁴

Recommendations (Fig. 1).

Fig. 1.

Recommendation to combat the misconceptions.

Conclusion

Misconceptions in CLD remain a key barrier to timely diagnosis, effective treatment and better outcomes. Myths held by patients or non-specialist clinicians can lead to malnutrition, missed complications, avoidable admissions and delayed transplant referrals. Integrating evidence-based hepatology into routine care is vital, with a focus on correcting false beliefs around diet, diagnostics and medications. This requires targeted education for providers and accessible, culturally sensitive resources for patients.

Bridging the gap between belief and evidence calls for collaboration across hepatology societies, healthcare systems and frontline staff, fostering care grounded in science, education and compassion.

Declaration of generative AI and AI-assisted technologies in the writing process

During the preparation of this work, the author(s) used Grammarly and DeepSeek in order to correct language and grammar. After using this tool/service, the author(s) reviewed and edited the content as needed and take(s) full responsibility for the content of the publication.

CRediT authorship contribution statement

Syed A. Gardezi: Writing – review & editing, Writing – original draft, Validation, Supervision, Software, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Mohammed Al Jawad: Writing – review & editing, Writing – original draft. Muhammed Yossof Albahrani: Writing – review & editing, Writing – original draft.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.