Can Hashimoto's cause fatty liver? Whilst no direct causal link is officially established, observational studies suggest that Hashimoto's thyroiditis—an autoimmune condition causing hypothyroidism—may increase the risk of non-alcoholic fatty liver disease (NAFLD). Thyroid hormones regulate hepatic lipid metabolism, and when thyroid function is impaired, the liver's ability to process fats efficiently may be compromised. This article explores the association between Hashimoto's and fatty liver, the mechanisms linking thyroid dysfunction to hepatic fat accumulation, and practical strategies for managing liver health in individuals with Hashimoto's thyroiditis.

Understanding Hashimoto's Thyroiditis and Liver Health

Hashimoto's thyroiditis is an autoimmune condition in which the immune system mistakenly attacks the thyroid gland, leading to chronic inflammation and, over time, reduced thyroid hormone production (hypothyroidism). It is the most common cause of an underactive thyroid in the UK, affecting approximately 1–2% of the population, with women being significantly more susceptible than men (NHS, NICE NG145).

The thyroid gland produces hormones—primarily thyroxine (T4) and triiodothyronine (T3)—that regulate metabolism, energy production, and numerous bodily functions. When thyroid hormone levels fall, metabolic processes slow down, which can have wide-ranging effects on cardiovascular health, weight regulation, cholesterol metabolism, and liver function.

Non-alcoholic fatty liver disease (NAFLD) is characterised by excessive fat accumulation in the liver (hepatic steatosis) in individuals who consume little to no alcohol. In the UK, NAFLD is defined as hepatic steatosis in people drinking ≤14 units of alcohol per week (in line with UK Chief Medical Officers' low-risk drinking guidelines). NAFLD has become increasingly prevalent, affecting an estimated 20–30% of UK adults (NHS, NICE NG49). Risk factors include obesity, type 2 diabetes, dyslipidaemia, and metabolic syndrome. Emerging evidence suggests that thyroid dysfunction, particularly hypothyroidism associated with Hashimoto's thyroiditis, may also contribute to the development or progression of fatty liver disease.

Note: The term metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly used internationally, though NAFLD remains the term commonly used in current NHS and NICE guidance.

The liver plays a central role in lipid metabolism, glucose regulation, and detoxification. Thyroid hormones influence hepatic lipid synthesis, oxidation, and clearance. Consequently, when thyroid function is impaired, the liver's ability to process fats efficiently may be compromised, potentially leading to fat accumulation within hepatocytes. Understanding this relationship is essential for clinicians managing patients with both Hashimoto's thyroiditis and liver concerns, as optimising thyroid hormone replacement may positively influence liver health.

The Link Between Hashimoto's and Fatty Liver Disease

While there is no direct causal link officially established between Hashimoto's thyroiditis and fatty liver disease, observational studies have identified a notable association between hypothyroidism and an increased prevalence of NAFLD. Research suggests that individuals with untreated or inadequately treated hypothyroidism may be at higher risk of developing hepatic steatosis compared to those with normal thyroid function, though the evidence is mainly observational and heterogeneous.

Several population-based studies have demonstrated that thyroid-stimulating hormone (TSH) levels—often elevated in hypothyroidism—correlate positively with the presence and severity of fatty liver disease. Conversely, adequate thyroid hormone replacement therapy may improve liver enzyme profiles in some patients, though evidence for reduction in hepatic fat content is limited and not definitive. It is important to note that these associations do not prove causation, and fatty liver disease is multifactorial, with obesity, insulin resistance, and metabolic syndrome being primary drivers.

Autoimmune mechanisms may also play a role. Hashimoto's thyroiditis is associated with systemic inflammation and the presence of thyroid autoantibodies (anti-thyroid peroxidase and anti-thyroglobulin antibodies). Chronic low-grade inflammation is a recognised contributor to metabolic dysfunction and may indirectly promote hepatic fat accumulation. Additionally, individuals with one autoimmune condition are at increased risk of developing others. Rarely, autoimmune liver diseases such as primary biliary cholangitis (PBC) or autoimmune hepatitis may coexist with Hashimoto's; if cholestatic liver function tests or other autoimmune features are present, these conditions should be considered.

It is also worth considering that both Hashimoto's thyroiditis and NAFLD share common risk factors, including obesity, insulin resistance, and dyslipidaemia. These overlapping metabolic disturbances may explain much of the observed association. Therefore, while Hashimoto's may contribute to fatty liver development through metabolic and hormonal pathways, it is rarely the sole cause, and a comprehensive assessment of metabolic health is essential (NICE NG49, BSG NAFLD guideline).

How Thyroid Dysfunction Affects Liver Fat Accumulation

Thyroid hormones exert profound effects on hepatic lipid metabolism through multiple mechanisms. Triiodothyronine (T3), the active thyroid hormone, regulates the expression of genes involved in lipid synthesis, oxidation, and transport. In hypothyroidism, reduced T3 levels lead to decreased hepatic lipid oxidation and impaired clearance of triglycerides and low-density lipoprotein (LDL) cholesterol from the bloodstream. This results in elevated serum lipid levels and increased delivery of fatty acids to the liver, promoting fat accumulation.

Furthermore, thyroid hormones influence insulin sensitivity and glucose metabolism. Hypothyroidism is associated with insulin resistance, a key pathophysiological feature of NAFLD. Insulin resistance promotes lipolysis in adipose tissue, releasing free fatty acids into circulation, which are then taken up by the liver. Concurrently, insulin resistance stimulates hepatic de novo lipogenesis (the synthesis of new fatty acids), further contributing to hepatic steatosis.

Thyroid dysfunction also affects the activity of enzymes involved in lipid metabolism. For example, hypothyroidism reduces the activity of lipoprotein lipase and hepatic lipase, enzymes responsible for breaking down triglyceride-rich lipoproteins. This impairment leads to hypertriglyceridaemia and increased hepatic fat deposition. Additionally, reduced thyroid hormone levels decrease the expression of genes involved in mitochondrial fatty acid oxidation, limiting the liver's capacity to burn fat for energy.

Another important consideration is the impact of hypothyroidism on body weight and composition. Weight gain is a common consequence of untreated hypothyroidism, primarily due to a reduced basal metabolic rate, fluid and salt retention, and reduced physical activity (NHS, British Thyroid Association). Appetite is typically normal or may even be reduced in hypothyroidism. The combination of metabolic slowing and reduced activity can lead to progressive weight gain, visceral adiposity, and worsening hepatic steatosis. Addressing thyroid dysfunction through appropriate hormone replacement therapy may help mitigate some of these metabolic disturbances and reduce the risk of fatty liver progression.

Managing Liver Health with Hashimoto's Thyroiditis

Effective management of liver health in individuals with Hashimoto's thyroiditis requires a multifaceted approach that addresses both thyroid function and metabolic risk factors. The cornerstone of treatment is optimising thyroid hormone replacement therapy, typically with levothyroxine, to restore euthyroidism (normal thyroid hormone levels). Regular monitoring of TSH and free T4 levels is essential to ensure adequate dosing, as both under-treatment and over-treatment can have adverse metabolic consequences.

According to NICE NG145, thyroid function should be assessed at least annually in patients on levothyroxine once stable, with dose adjustments made as necessary. Achieving optimal thyroid hormone levels may improve lipid profiles, enhance insulin sensitivity, and potentially reduce hepatic fat accumulation. Some studies suggest that normalising thyroid function can lead to improvements in liver enzyme levels (such as alanine aminotransferase, ALT), though evidence for reduction in hepatic steatosis is limited.

Lifestyle modifications are equally critical in managing fatty liver disease. Weight loss of 7–10% or more of body weight has been shown to significantly reduce hepatic fat content and improve liver histology, including inflammation and fibrosis, in patients with NAFLD (NICE NG49, BSG guideline). A balanced diet rich in vegetables, fruits, whole grains, and lean proteins, combined with regular physical activity (at least 150 minutes of moderate-intensity exercise per week, per UK Chief Medical Officers' guidelines), is recommended. Limiting intake of refined carbohydrates, saturated fats, and added sugars can help reduce hepatic lipogenesis and improve metabolic health.

Patients should also be screened for and manage other cardiovascular and metabolic risk factors, including:

• Dyslipidaemia: Statins are safe and effective in NAFLD and should not be withheld when clinically indicated for cardiovascular risk reduction, even in the presence of mildly raised liver enzymes (NICE NG238, BSG guideline). Thyroid optimisation often improves lipid profiles.

• Type 2 diabetes or prediabetes: Glycaemic control is essential, as insulin resistance drives NAFLD progression.

• Hypertension: Blood pressure management reduces cardiovascular risk, which is elevated in both hypothyroidism and NAFLD.

Avoidance of hepatotoxic substances, including excessive alcohol consumption (above 14 units per week), is important. Patients should be counselled on the risks of over-the-counter supplements and herbal remedies, some of which may have adverse hepatic effects. If you experience any suspected side effects from medicines, report them via the MHRA Yellow Card Scheme at yellowcard.mhra.gov.uk.

When to Seek Medical Advice for Liver Concerns

Patients with Hashimoto's thyroiditis should be vigilant for signs and symptoms that may indicate liver dysfunction or progression of fatty liver disease. While NAFLD is often asymptomatic in its early stages, certain clinical features warrant prompt medical evaluation. Persistent fatigue, unexplained weight changes, or abdominal discomfort—particularly in the right upper quadrant—should be discussed with a GP, as these may indicate worsening liver health or other complications.

Routine blood tests may reveal elevated liver enzymes (ALT, aspartate aminotransferase [AST], or gamma-glutamyl transferase [GGT]), which can suggest hepatic inflammation or steatosis. If liver enzyme abnormalities are detected, further investigation is typically warranted. In UK practice, many primary care services use simple scoring systems such as the FIB-4 score or NAFLD Fibrosis Score (NFS) as a first-line tool to assess the risk of advanced liver fibrosis. NICE NG49 recommends the Enhanced Liver Fibrosis (ELF) test to assess for advanced fibrosis in adults with NAFLD. Transient elastography (FibroScan) is also widely used as a second-line non-invasive assessment. Typical FIB-4 thresholds are <1.3 (low risk) and >2.67 (high risk; >2.0 if aged over 65). Referral to a hepatologist may be appropriate if advanced fibrosis or cirrhosis is suspected (BSG NAFLD guideline).

Patients should seek urgent medical attention if they develop signs of advanced liver disease, including:

• Jaundice (yellowing of the skin or eyes)

• Ascites (abdominal swelling due to fluid accumulation)

• Confusion or altered mental state (hepatic encephalopathy)

• Easy bruising or bleeding (coagulopathy)

• Gastrointestinal bleeding (vomiting blood or passing black, tarry stools)

• Severe abdominal pain with fever

These features may indicate decompensated liver disease and require immediate specialist assessment. Additionally, individuals with Hashimoto's thyroiditis who have multiple metabolic risk factors (obesity, diabetes, dyslipidaemia) should discuss liver health screening with their GP, as early detection and intervention can prevent progression to more serious liver conditions. Regular follow-up, adherence to thyroid hormone replacement, and proactive lifestyle management remain the best strategies for maintaining both thyroid and liver health (NHS, NICE NG49).

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