01/05/2026
The condition once called NASH (non-alcoholic steatohepatitis) is now called MASH (metabolic dysfunction-associated steatohepatitis), and it sits within a broader category called MASLD (metabolic dysfunction-associated steatotic liver disease), formerly NAFLD (non-alcoholic fatty liver disease). These new names were introduced because fatty liver disease is now understood to be part of a wider metabolic disorder rather than just a liver problem defined by the absence of alcohol. These name changes are relevant in the context of CKD (chronic kidney disease), because the same underlying factors, such as insulin resistance, obesity, inflammation and vascular damage, can affect both the liver and the kidneys. In other words, MASH and CKD often occur together not because one directly causes the other, but because both develop from the same underlying metabolic stress.
The incidence of both MASH and CKD has been rising steadily worldwide in parallel with the epidemics of obesity and type 2 diabetes. In Australia, fatty liver disease overall affects about one in four adults, and it is estimated that around 4 to 6% of adults have MASH, the inflammatory and more progressive form. Biomedical evidence of CKD is present in roughly 11% of Australian adults (about 1.7 million people), with rates increasing sharply with age. In the United States, MASH is estimated to affect about 5 to 6% of adults, within a much larger group with fatty liver disease, and CKD affects roughly one in seven adults (around 35 million people).
Given this rather alarming epidemiological context, a recent clinical trial of bioavailable curcumin in patients with MASH and CKD is highly noteworthy. In this double blind trial, 52 patients with biopsy-confirmed MASH were studied. Most had moderate to advanced liver scarring (71% had stage F2 fibrosis or worse), and more than half also had moderate CKD (58% had stage 2 or 3). They were randomised 1:1 to receive 2 g/d of a curcumin phytosome (containing 400 mg/day curcumin) or placebo for 72 weeks.
The primary endpoint was NASH resolution with no worsening of fibrosis. The secondary endpoints included a ≥1 stage liver fibrosis improvement with no MASH worsening; regression of significant fibrosis and CKD; and improvement in renal, glucose lipid, and inflammatory parameters. The scientists also explored the treatment effect on hepatic activation of NF-kB, a key proinflammatory transcription factor and a major target of curcumin.
Fifty-one patients (26 on curcumin and 25 on placebo) completed the trial. Sixteen (62%) patients on curcumin versus 3 (12%) patients on placebo had MASH resolution (relative risk, RR = 5.33; p = 0.003). Thirteen (50%) patients on curcumin versus 2 (8%) patients on placebo had ≥1 stage fibrosis improvement (RR = 6.50; p = 0.008). Eleven (42%) patients on curcumin versus 0 (0%) on placebo had regression of significant liver fibrosis (RR = 18.01; p = 0.02). Hepatic NF-kB inhibition predicted MASH resolution and fibrosis improvement. Thirteen (50%) patients on curcumin versus 0 (0%) on placebo had CKD regression (RR = 10.71; p = 0.004). Compared with placebo, curcumin improved eGFR (difference in adjusted eGFR change: +3.59; p = 0.009), fasting glucose, HbA1c, LDL-cholesterol, triglycerides, HDL-cholesterol and inflammatory markers. Adverse events were rare, mild, and evenly distributed.
These are truly amazing results that make me wonder why findings like this receive such little attention, and why studies like this are so often overlooked by mainstream medicine and the general media, especially when we are talking about one of the central epidemics in modern healthcare.
For more information see: https://pubmed.ncbi.nlm.nih.gov/38809154/
