Magnesium deficiency increases the risk of metabolic dysfunction-associated fatty liver disease, with both moderate and severe deficiency raising the odds significantly, according to a recent study.
Researchers conducted a study that examined the association between magnesium deficiency, dietary magnesium intake, and metabolic dysfunction-associated fatty liver disease (MAFLD). Using data from 3,377 participants in the National Health and Nutrition Examination Survey 2017 to 2020 dataset, the researchers assessed magnesium deficiency with the magnesium depletion score (MDS), a tool incorporating renal function, diuretic and proton pump inhibitor use, and alcohol consumption. Participants were classified into three categories based on MDS: no magnesium deficiency, moderate magnesium deficiency, and severe magnesium deficiency. Hepatic steatosis was measured using vibration-controlled transient elastography, with MAFLD defined as hepatic steatosis (CAP≥274 dB/min) combined with either overweight/obesity, type 2 diabetes mellitus, or evidence of metabolic dysregulation.
The analysis, published in Scientific Reports, revealed that both moderate and severe magnesium deficiency were associated with increased risk of MAFLD. Compared to those without deficiency, participants with moderate deficiency had 32% higher odds (OR: 1.32, 95% CI: 1.05-1.66, p<0.05), while those with severe deficiency had 69% higher odds (OR: 1.69, 95% CI: 1.16-2.46; p for trend < 0.001). The researchers estimated that eliminating magnesium deficiency could reduce MAFLD cases by 11.1% (95% CI: 0.043-0.179).
Subgroup analyses demonstrated an inverse relationship between dietary magnesium intake and MAFLD risk only among participants without magnesium deficiency (p for trend < 0.01). Among participants with moderate or severe magnesium deficiency, increasing dietary magnesium intake did not significantly mitigate the risk of MAFLD.
Structural equation modeling identified inflammation, oxidative stress, and aging as mediators of the association between magnesium deficiency and MAFLD. For example, markers of inflammation, such as segmented neutrophils, mediated 13.41% of the total effect (p < 0.01), while markers of oxidative stress, including γ-glutamyl transferase, mediated 13.21% (p < 0.01). Accelerated aging was the most substantial mediator, accounting for 36.81% of the association (p < 0.001).
These findings suggest that magnesium deficiency, as assessed by MDS, is an independent risk factor for MAFLD. The researchers concluded that simply increasing dietary magnesium intake is insufficient to address MAFLD risk in participants with magnesium deficiency. Targeted interventions to correct deficiency may be necessary. This study highlights the importance of using comprehensive measures, such as MDS, over serum magnesium levels for evaluating deficiency and its clinical implications.
The researchers noted several limitations, including that the study population was predominantly white American, limiting generalizability to other populations. The cross-sectional design prevented establishment of causal relationships, and the researchers were unable to compare MDS with serum magnesium levels due to data limitations.
Full disclosures can be found in the published study.