The ABCs of MAFLD
Dr. Gareth Morris-Stiff
AUGUST 2025
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The term fatty liver disease refers to the deposition of fat in the liver cells (hepatocytes) and occurs as a response to inflammation. It has several causes and, for the purpose of this overview, I will concentrate on disease related to metabolic imbalances within the liver—a condition known as metabolism dysfunction-associated fatty liver disease (MAFLD) or metabolism dysfunction-associated steatotic liver disease (MASLD) if you prefer to be cosmopolitan and return to the Greek origin of the word “fat.”
It has long been known that fatty changes are observed in alcohol-related liver disease (ALD), but it was not until 1980 that the term non-alcoholic fatty liver disease (NAFLD) was coined to describe near-identical changes in patients who did not consume alcohol. MAFLD was officially proposed as a replacement for NAFLD in 2020, and MASLD joined the debate in 2023, although for some aficionados, the debate is not over.
Regardless of which letters are chosen, the hallmarks of the condition are hepatic steatosis, along with at least one of the following: overweight/obesity, type 2 diabetes mellitus, or metabolic dysregulation even in the absence of overweight or obesity. Furthermore, the definition of metabolic dysregulation consists of the presence of at least two metabolic risk abnormalities, such as elevated waist circumference, high blood pressure, high triglyceride levels, low HDL cholesterol, prediabetes, high HOMA-IR (insulin resistance score), or high-sensitivity CRP levels. As such, with a large number of options, there are a significant number of people with fatty MAFLD.
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How common is common?
Well, if you look at the latest data, it would appear that just shy of 40% of the adult population in the U.S. has MAFLD, and this figure is likely to top 50% within the decade. But this is not just a disease of adults — pediatric and adolescent MAFLD is a major problem and is growing. Furthermore, there is reason to believe that MAFLD may be even more common than data suggests. If we take the over-18 population, national statistics indicate that 2/3 are overweight or obese, and without a national screening program, we don’t know how many have fatty liver disease.
What causes MAFLD?
The main culprit is ultra-processed foods. These items consist predominantly of substances extracted from foods, such as fats, starches, sugars, and hydrogenated fats, as well as additives such as artificial colors, flavors, and stabilizers. Collectively, they induce systemic inflammation, which is particularly badly felt in the liver, as all items consumed are processed first by this organ. Other factors, such as excess alcohol consumption, stress, poor sleep, and indeed many medications and supplements, may damage the liver and contribute to MAFLD, as all put stress on the liver.
So, with a MAFLD pandemic already present, how do we go about establishing the diagnosis and initiating treatment? Unfortunately, for the vast majority with MAFLD, there are no symptoms, at least nothing pathognomonic. When directly questioned, many do identify brain fog and fatigue, but these are frequently attributed to overwork, aging, or stress. Once the light bulb turns on and an individual or medical practitioner contemplates the diagnosis of MAFLD, what’s next? Unfortunately, from the perspective of confirming MAFLD, routine liver panels are not beneficial since 80% or more of those with uncomplicated MAFLD have normal liver tests.
The two main enzymes I look to evaluate in relation to MAFLD are aspartate aminotransferase (AST) and alanine aminotransferase (ALT). When elevated, and in the presence of indicators of metabolic dysfunction, they are highly indicative of MAFLD as they indicate inflammation of the liver cells (hepatocytes) by the time the liver tests are abnormal it often means that the MFLD is progressing or has reached the next stage in its evolution, namely metabolism dysfunction-associated steatohepatitis (MASH).
As MAFLD is associated with metabolic dysfunction, patients frequently show elevations in plasma total cholesterol, low-density lipoprotein, and triglyceride levels, as well as an increased hemoglobin A1c. Furthermore, there is a reduction in the levels of high-density lipoprotein, the so-called “good cholesterol.”
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In terms of imaging, many patients have steatosis identified as an incidental finding on ultrasound or computed tomography (CT) scans performed for other indications. Neither modality is good at quantifying the degree of fatty replacement, and as a result of the presence of fat being an incidental finding, the importance of its presence is often not conveyed. In many cases, this is because clinicians have traditionally not understood its importance, and since radiologists don’t know the full history, they do not relate the fat to MAFLD.
One very useful diagnostic test is transient elastography, which allows computation of a stiffness score that relates to scarring due to fibrotic damage in the liver and also a fat score that relates to the proportion of fat infiltration. Elastography performed by a dedicated machine (FibroScan→ or Hepatus→) is superior to that obtained by conventional ultrasound. As such, transient elastography represents an optimal means of screening populations for MAFLD, which is why The Liver Clinic is making liver scans more widely available and accessible.
Magnetic resonance imaging using a dedicated protocol to detect fat and fibrosis is a very good means of assessing MAFLD, but cost, lack of portability, and claustrophobia limit its screening potential. Still, it is ideal for confirming findings of transient elastography and allows a full evaluation for other non-MAFLD conditions that could be identified by the former during screening. The other reason to consider screening is that, unlike most liver diseases, where hepatocellular cancer occurs after the development of cirrhosis, in MAFLD, cancers can develop as soon as there is inflammation in the liver.
The obvious next question is, what do we do after detecting MAFLD? For allopathic practitioners, the answer is simple, namely diet (usually advised a Mediterranean diet) and exercise, as there is currently no FDA-approved approach to treat the majority of MAFLD patients that do not have marked fibrosis or cirrhosis. The literature would suggest that diet and exercise can benefit stage I MAFLD, but beyond that, it is unlikely to be of much benefit.
Furthermore, most individuals fail to stick to diet and exercise programs.
For all other practitioners, there are a number of options. Education is certainly a key component so that patients change their lifestyles to avoid ultra-processed foods, as the first step involves reducing the oxidant attack on the liver. Supporting the antioxidant defense of the liver is also key, as is reducing the inflammation in the liver, the force that drives the fibrosis. Other elements in plant-based medicines like de-liver-ance® can help reduce inflammation in the liver and assist in boosting the detoxification system within the liver. These maneuvers allow resolution of MAFLD over time and return of the liver to optimal health.
BIO:
Dr. Gareth Morris-Stiff is Global Chief Medical Officer of The Liver Clinic, advancing early screening and intervention for metabolism dysfunction-associated fatty liver disease (MAFLD). A former HPB surgeon with 28 years of experience in the UK and at the Cleveland Clinic, he also drives innovation in biopharma, developing therapies for liver and pancreatic cancers. Dr. Morris-Stiff holds an MBBCh, MD, MCh, and PhD, and is a Fellow of both the Royal College of Surgeons and the American College of Surgeons. He is currently earning a Doctor of Science in Ayurvedic medicine and has authored over 250 publications.
