By Ana Espino | Published on June 11, 2026 | 4 min read
Present in the environment as a result of industrial
activities, certain agricultural fertilizers, and tobacco smoke, cadmium
is a heavy metal of significant concern for human health. A recent review
published in iScience examines the mechanisms through which this
contaminant disrupts hepatic lipid metabolism and may contribute to the
development of metabolic liver diseases.
Also read: Pesticides: Securing Fields, Saving Health!
A Metal That Accumulates in the Body Over Time
Cadmium enters the body primarily through contaminated food
and the inhalation of polluted particles. Its exceptionally long biological
half-life, estimated at 10 to 30 years, promotes its gradual
accumulation in several organs, particularly the liver and kidneys. Once
stored within hepatocytes, cadmium disrupts cellular function and contributes
to the development of chronic tissue damage.
A Profound Disruption of Fat Metabolism
The authors show that cadmium alters the delicate balance
between the synthesis, storage, and breakdown of hepatic lipids. Exposure to
the metal promotes the production of triglycerides while reducing their
clearance, leading to an abnormal accumulation of fat within the liver.
This process is associated with the activation of genes
involved in lipogenesis, including SREBP-1c and fatty acid
synthase (FAS), as well as the inhibition of pathways responsible for fatty
acid oxidation.
Oxidative Stress and Inflammation: Key Drivers of
Toxicity
Cadmium markedly increases the production of reactive
oxygen species (ROS) while weakening the body's natural antioxidant defense
systems. This imbalance promotes oxidative stress, mitochondrial damage,
and the activation of inflammatory pathways such as NF-κB.
These mechanisms contribute to the progression of liver
injury and the development of metabolic dysfunction-associated steatotic
liver disease (MASLD).
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The Emerging Role of the Gut Microbiota
One of the most innovative aspects of this review concerns
the gut–liver axis. Cadmium impairs intestinal barrier function and
alters the composition of the gut microbiota, facilitating the translocation of
inflammatory molecules to the liver.
This interaction may amplify the metabolic disturbances
induced by cadmium and could represent a promising therapeutic target for
future interventions.
Also read: Gut–microbiome dialogue: the unexpected role of epithelial cells
Potentially Amplified Effects Through Microplastic
Exposure
The authors also highlight that simultaneous exposure to cadmium
and microplastics may increase the absorption and accumulation of the metal
within the body.
Several experimental studies have reported worsening
intestinal damage, enhanced hepatic inflammation, and greater metabolic
dysfunction when both contaminants are present together.
Also read: Microplastics and cardiovascular risk
What Are the Therapeutic Perspectives?
Currently, no specific treatment exists for chronic cadmium
toxicity. Investigational approaches include the use of antioxidants, natural
compounds, epigenetic modulators, and therapies targeting the gut
microbiota.
However, most of the available evidence still comes from
animal models, and clinical studies are needed to confirm the effectiveness of
these strategies in humans.
A Growing Public Health Concern
This review highlights cadmium as an environmental factor
that may contribute to the development of metabolic liver diseases. Given the
persistence of this contaminant in the environment and its gradual accumulation
within the body, the authors call for further research into the long-term
effects of low-level chronic exposure and its interactions with other emerging
pollutants such as microplastics.
About the author – Ana Espino
PhD in Immunology, specialized in Virology
As a scientific writer, Ana is passionate about bridging the gap between research and real-world impact. With expertise in immunology, virology, oncology, and clinical studies, she makes complex science clear and accessible. Her mission: to accelerate knowledge sharing and empower evidence-based decisions. 
