Fatty liver disease affects approximately one in three UK adults and occurs when excess fat accumulates in liver cells. Whilst obesity, type 2 diabetes, and metabolic syndrome are well-established causes, emerging evidence suggests hormonal imbalances may also play a significant role. Conditions such as polycystic ovary syndrome (PCOS), hypothyroidism, and hormonal changes during menopause have been linked to increased fatty liver risk. Hormones regulate crucial metabolic processes including insulin sensitivity and lipid metabolism, which directly influence hepatic fat accumulation. Understanding this connection is essential for identifying at-risk patients and implementing early interventions to prevent disease progression.

Understanding Fatty Liver Disease and Its Causes

Fatty liver disease, medically termed hepatic steatosis, occurs when excess fat accumulates in liver cells. The liver naturally contains some fat, but when fat is present in 5% or more of liver cells (hepatocytes), it becomes pathological. This condition has become increasingly common in the UK, affecting approximately one in three adults to some degree.

There are two main categories of fatty liver disease. Non-alcoholic fatty liver disease (NAFLD) develops in people who drink little or no alcohol and is strongly associated with metabolic factors such as obesity, type 2 diabetes, and high cholesterol. (You may also see the newer term metabolic dysfunction-associated steatotic liver disease, or MASLD, used alongside NAFLD in some settings.) Alcohol-related liver disease (ARLD) results from excessive alcohol consumption over time. NAFLD has emerged as the most common chronic liver condition in developed countries, reflecting rising rates of obesity and metabolic syndrome.

The causes of fatty liver are multifactorial. Primary risk factors include:

• Obesity, particularly central (abdominal) adiposity

• Insulin resistance and type 2 diabetes

• Dyslipidaemia (abnormal blood lipid levels)

• Metabolic syndrome

• Rapid weight loss or malnutrition

• Certain medications (corticosteroids, tamoxifen, methotrexate, amiodarone, valproate, some antiretroviral medicines)

The risk from medicines varies by dose and duration of treatment. In many cases, fatty liver disease progresses silently without symptoms. However, if left unmanaged, it can advance to non-alcoholic steatohepatitis (NASH), where inflammation damages liver cells, potentially leading to fibrosis, cirrhosis, or hepatocellular carcinoma. Understanding the underlying causes—including emerging evidence about hormonal influences—is essential for prevention and early intervention. NICE guidance and NHS resources emphasise lifestyle modification as the cornerstone of management, focusing on weight reduction, dietary changes, and increased physical activity.

Can Hormonal Imbalance Cause Fatty Liver?

Emerging research suggests that hormonal imbalances may contribute to the development and progression of fatty liver disease, though the relationship is complex and not yet fully understood. Hormones regulate numerous metabolic processes, including glucose metabolism, lipid storage, and insulin sensitivity—all of which influence hepatic fat accumulation. Whilst hormonal imbalance alone may not directly 'cause' fatty liver in isolation, it can create metabolic conditions that significantly increase susceptibility. Most evidence linking hormones and fatty liver is observational, and UK management focuses on addressing metabolic risk factors through lifestyle changes and treatment of underlying conditions.

Insulin and metabolic hormones play a particularly crucial role. Insulin resistance, often driven by hormonal dysregulation, impairs the liver's ability to process fats and sugars efficiently. When cells become resistant to insulin's effects, the pancreas produces more insulin to compensate (hyperinsulinaemia). This excess insulin promotes fat synthesis in the liver whilst simultaneously reducing fat breakdown, creating a perfect environment for hepatic steatosis. This mechanism explains why conditions characterised by insulin resistance frequently coexist with fatty liver disease.

Sex hormones also influence liver fat metabolism. Oestrogen appears to have protective effects on liver health, which may explain why premenopausal women have lower rates of NAFLD compared to men of similar age. After menopause, when oestrogen levels decline, women's risk increases substantially. Conversely, testosterone deficiency in men has been associated with increased visceral adiposity and hepatic fat accumulation, though these associations are observational and confounded by body composition and metabolic factors. Thyroid hormones regulate basal metabolic rate and lipid metabolism; hypothyroidism (underactive thyroid) slows metabolic processes and can contribute to fat accumulation in various tissues, including the liver.

Whilst there is no official link establishing hormonal imbalance as a sole cause of fatty liver disease, the evidence increasingly supports hormones as important modifying factors that influence disease risk and progression, particularly when combined with other metabolic risk factors.

Which Hormonal Conditions Increase Fatty Liver Risk?

Several specific hormonal disorders have been associated with increased prevalence of fatty liver disease, though the strength of association varies. Understanding these conditions helps identify patients who may benefit from liver health monitoring.

Polycystic ovary syndrome (PCOS) represents one of the strongest hormonal links to NAFLD. This common endocrine disorder, affecting approximately 10% of women of reproductive age in the UK, is characterised by insulin resistance, hyperandrogenism (excess male hormones), and irregular menstrual cycles. Studies indicate that women with PCOS have a significantly elevated risk of developing fatty liver disease—prevalence estimates commonly range from 20–50% overall, with higher rates in those with obesity and insulin resistance. The insulin resistance inherent to PCOS appears to be the primary mechanistic link.

Hypothyroidism (underactive thyroid) has been associated with NAFLD in multiple studies. Thyroid hormones regulate lipid metabolism, and their deficiency can lead to elevated cholesterol, reduced metabolic rate, and weight gain—all risk factors for hepatic steatosis. Patients with subclinical hypothyroidism (mildly elevated TSH with normal thyroid hormone levels) may also face increased risk, though evidence remains somewhat inconsistent.

Cushing's syndrome, caused by prolonged exposure to excess cortisol, creates a metabolic profile strongly associated with fatty liver. Whether from endogenous overproduction or exogenous corticosteroid therapy, elevated cortisol promotes central obesity, insulin resistance, and dyslipidaemia. Long-term or high-dose therapeutic corticosteroid use can increase fatty liver risk; monitoring of metabolic factors and liver function tests may be clinically indicated in these patients.

Growth hormone deficiency in adults has been linked to increased visceral adiposity and metabolic dysfunction, potentially contributing to NAFLD development, though evidence is largely observational and confounded by body composition. Similarly, hypogonadism (low testosterone in men) correlates with increased liver fat content, likely mediated through effects on body composition and insulin sensitivity. Menopausal women experiencing declining oestrogen levels also face increased risk, highlighting the protective role of female sex hormones in liver health.

Recognising Symptoms of Hormone-Related Fatty Liver

Fatty liver disease typically progresses silently in its early stages, with most patients experiencing no specific symptoms. This asymptomatic nature makes opportunistic detection through blood tests or imaging particularly important, especially in patients with obesity, type 2 diabetes, or metabolic syndrome. Fatty liver is often detected incidentally on ultrasound scans performed for other reasons, and liver function tests can be entirely normal in NAFLD. When symptoms do occur, they are often non-specific and may be attributed to the underlying hormonal condition rather than liver involvement.

Early-stage symptoms, when present, may include:

• Persistent fatigue or malaise

• Vague discomfort or fullness in the right upper abdomen

• General feeling of being unwell

• Unexplained weight changes

These symptoms overlap considerably with those of many hormonal imbalances, making clinical correlation essential. For instance, fatigue is common in both hypothyroidism and early liver disease, whilst abdominal discomfort might be dismissed as related to PCOS or menstrual irregularities.

Signs suggesting disease progression warrant more urgent attention. As fatty liver advances to steatohepatitis or fibrosis, patients may develop:

• Jaundice (yellowing of skin or eyes)

• Persistent nausea or loss of appetite

• Abdominal swelling (ascites)

• Easy bruising or bleeding

• Confusion or difficulty concentrating (hepatic encephalopathy)

• Spider naevi (small, spider-like blood vessels on the skin)

Laboratory abnormalities often provide the first clue to liver involvement. Routine blood tests may reveal elevated liver enzymes (ALT, AST, GGT), though normal liver function tests do not exclude fatty liver disease. When NAFLD is suspected, your GP may calculate a simple score called FIB-4 using your age and blood test results to estimate the risk of liver scarring (fibrosis). Depending on the result, further tests such as the Enhanced Liver Fibrosis (ELF) blood test or a liver elastography scan may be arranged to guide management and determine whether specialist referral is needed.

It is important to recognise that symptoms attributed to hormonal imbalance—such as weight gain, fatigue, or menstrual irregularities—may coexist with developing liver disease. Patients with diagnosed hormonal conditions who experience worsening symptoms or new abdominal complaints should discuss liver health screening with their GP.

Treatment Options for Hormone-Linked Fatty Liver Disease

Management of fatty liver disease associated with hormonal imbalance requires a dual approach: addressing the underlying hormonal disorder whilst implementing liver-specific interventions. NICE guidance emphasises lifestyle modification as the foundation of NAFLD treatment, regardless of contributing factors.

Lifestyle interventions remain the most effective treatment for fatty liver disease. Evidence demonstrates that:

• Weight loss of 7–10% of body weight can significantly reduce liver fat, inflammation, and fibrosis in patients with NAFLD. Even modest weight reduction (3–5%) provides measurable benefits.

• Dietary modifications should focus on reducing refined carbohydrates, saturated fats, and added sugars whilst increasing consumption of vegetables, whole grains, and lean proteins. The Mediterranean diet pattern has shown particular promise in improving liver health.

• Physical activity of at least 150 minutes of moderate-intensity exercise weekly improves insulin sensitivity and reduces hepatic fat, independent of weight loss.

• Alcohol guidance aligns with UK Chief Medical Officers' recommendations: to keep health risks low, do not regularly drink more than 14 units per week, spread drinking over 3 or more days, and have several alcohol-free days each week. Many liver specialists advise complete abstinence if steatohepatitis or fibrosis is present.

Hormonal treatment optimisation plays a crucial complementary role. For patients with hypothyroidism, achieving optimal thyroid hormone replacement may improve metabolic parameters and support liver health. Women with PCOS may benefit from metformin, which addresses insulin resistance—a key driver of both PCOS and NAFLD. However, metformin is not licensed specifically for NAFLD treatment in the UK. Hormone replacement therapy in menopausal women requires individualised assessment, balancing potential metabolic benefits against other health considerations.

Pharmacological options for NAFLD itself remain limited. Currently, no medications are specifically licensed by the MHRA for treating fatty liver disease. Pioglitazone and vitamin E have shown some benefit in research settings for patients with biopsy-proven NASH, but their use is restricted to selected cases under specialist supervision due to potential adverse effects, and the risks and benefits must be carefully discussed. Management of associated conditions—hypertension, dyslipidaemia, and diabetes—follows standard guidelines. Statins are safe in NAFLD and should not be withheld when indicated for cardiovascular disease risk reduction; they are an important part of managing lipid levels in patients with fatty liver disease.

Monitoring and specialist referral are essential components of care. Patients should have regular assessment of liver function tests, metabolic parameters, and non-invasive markers of fibrosis. Your GP may use the FIB-4 score (with age-specific cut-offs: for those under 65, <1.3 suggests low risk and >2.67 high risk; for those 65 and over, <2.0 suggests low risk) to guide further testing. If FIB-4 is in the intermediate range or elevated, an Enhanced Liver Fibrosis (ELF) blood test or liver elastography may be arranged. An ELF score of 10.51 or above suggests advanced fibrosis and typically prompts hepatology referral. Those with evidence of advanced fibrosis or progressive disease require specialist assessment and consideration of emerging therapies.

If you experience side effects from any medicine or medical device, you can report them via the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk.

When to See Your GP About Fatty Liver Concerns

Knowing when to seek medical advice about potential fatty liver disease is important for early detection and intervention, particularly for patients with hormonal imbalances or metabolic risk factors. Several scenarios warrant GP consultation.

You should arrange a routine GP appointment if you:

• Have been diagnosed with a hormonal condition (PCOS, hypothyroidism, Cushing's syndrome) alongside obesity, type 2 diabetes, or metabolic syndrome

• Have multiple metabolic risk factors (obesity, type 2 diabetes, high cholesterol) alongside hormonal imbalance

• Experience persistent fatigue, unexplained weight changes, or vague abdominal discomfort

• Have a family history of liver disease combined with personal hormonal or metabolic concerns

• Are taking long-term or high-dose medications that may affect liver function (corticosteroids, certain hormonal treatments, or other steatogenic medicines)

Your GP can arrange appropriate blood tests (liver function tests, lipid profile, HbA1c, thyroid function) and assess whether imaging studies such as ultrasound are warranted. Non-invasive scoring systems like the FIB-4 index may be calculated to estimate fibrosis risk, and if needed, further tests such as the Enhanced Liver Fibrosis (ELF) blood test or elastography can help determine whether specialist referral is appropriate.

Seek urgent same-day medical attention (urgent GP appointment or NHS 111) if you develop:

• Yellowing of the skin or whites of the eyes (jaundice)

• Severe or persistent abdominal pain

• Significant abdominal swelling

• New confusion or altered mental state

• Dark urine combined with pale stools

Call 999 or go immediately to A&E if you experience:

• Vomiting blood or material that looks like coffee grounds

• Passing black, tarry stools (melaena)

• Unexplained severe bruising or bleeding that will not stop

These symptoms may indicate advanced liver disease, acute liver injury, or gastrointestinal bleeding requiring urgent assessment.

Preventive screening is particularly important for high-risk groups. If you have obesity, type 2 diabetes, or metabolic syndrome—with or without a hormonal disorder—discuss with your GP whether liver health monitoring should be part of your ongoing care. Early detection of fatty liver disease, when the condition is still reversible through lifestyle changes, offers the best opportunity for preventing progression to more serious liver damage. Your GP can provide personalised advice based on your individual risk profile and coordinate care between endocrinology and hepatology services when necessary.

Frequently Asked Questions