Liver Steatosis: A Growing Concern in Our Community
Liver steatosis, commonly known as fatty liver disease, is rapidly gaining attention in our medical community. This lifestyle-related condition stems from poor diet and lack of physical activity, leading to an increase in metabolic dysfunction. Metabolic dysfunction is closely associated with obesity, dyslipidemia (elevated LDL, low HDL, and high triglycerides), hypertension, and elevated fasting plasma glucose levels (Antunes et al., 2025).
It’s important to note that fatty liver disease can develop without excessive alcohol consumption, a condition referred to as Non-Alcoholic Fatty Liver Disease (NAFLD). Liver damage in this context can be categorized into two groups: Non-Alcoholic Fatty Liver (NAFL) and Non-Alcoholic Steatohepatitis (NASH) (Antunes et al., 2025). The key difference between NAFL and NASH lies in whether liver cells (hepatocytes) have sustained actual damage. NAFL shows no hepatocyte damage, while NASH involves liver inflammation and damage.
The Impact of Fatty Liver Disease on Metabolism
The primary concern with fatty liver disease is the metabolic dysfunction it triggers throughout the body. Fatty liver disease is strongly linked to insulin resistance, where insulin’s ability to suppress the enzyme lipase is impaired. This allows free fatty acids (FFAs) to be released from fat tissue (Antunes et al., 2025), leading to a never ending cascade of triglyceride formation within the liver.
As insulin fails to unlock cells for sugar uptake, blood glucose levels remain elevated, initiating a cascade of inflammatory events that damage organs and the endothelial lining of blood vessels. Interestingly, cholesterol plays a protective role in this process, trying to repair tissue damage within the circulatory system. However, in individuals with fatty liver disease, elevated blood sugar and dyslipidemia (abnormal cholesterol levels) contribute to cholesterol being deposited where it shouldn’t be—along the blood vessel walls.
Current Treatments for Fatty Liver Disease
Present treatments for fatty liver disease primarily focus on lifestyle changes aimed at reducing dyslipidemia, obesity, and blood sugar imbalances. It’s essential to reduce contributors to liver damage, such as alcohol consumption and certain medications known to harm the liver (Antunes et al., 2025). Common pharmacological treatments for fatty liver include:
- Metformin (though it carries rare risks of liver damage)
- Gastric bypass (which doesn’t address the root cause of the disease, such as ECS dysfunction)
- Vitamin E and Orlistat (a gastric and pancreatic lipase inhibitor)
- Sibutramine (an appetite suppressant)
However, certain treatments like Orlistat have been shown to cause liver damage, ranging from acute liver injury to liver failure, sometimes even requiring a liver transplant (Orlistat, 2020). In that case, if it were me, I would search for a healthier alternative. I don't want to cause a problem on a problem!
Cannabinoids as a Potential Treatment for Fatty Liver
The Endocannabinoid System (ECS) plays a vital regulatory role in maintaining homeostasis across various tissues, including the liver, cardiovascular system, and pancreas (Lu & Mackie, 2021). This system makes the ECS a promising therapeutic target for conditions like fatty liver disease, which is linked to metabolic disorders such as obesity and type 2 diabetes.
While research on cannabinoids and their effects on the liver is still mixed, some studies suggest that CB1 agonists like THC (tetrahydrocannabinol) may induce lipogenesis (fat formation) in the liver when used acutely, potentially worsening liver function. However, chronic cannabis use has been associated with decreased lipogenesis, lower BMI, and improved metabolic parameters such as fasting insulin levels and waist circumference (Sansone & Sansone, 2014). This is kind of confusing because the results are contradicting each other. This puts emphasis on the fact we need further research to be conducted so we can get a better understanding of these exact mechanisms of action.
A study published in the Journal of Clinical Medicine found that chronic treatment with THC improved glucose tolerance, cholesterol levels, and overall insulin production in diabetic rats (Wikinski et al., 2023).
In another study, rats fed a sucrose-rich diet—known to induce liver and lipid dysfunction—developed liver damage and oxidative stress, which is common in fatty liver disease. When these rats were treated with cannabis oil (a 2:1 ratio of CBD to THC), they showed improvements in liver damage, lipid metabolism, and oxidative stress, indicating that cannabinoids could potentially play a role in treatment. Specifically, NrF2 expression increased, and NF-kB p65 expression decreased in the liver, indicating protection against oxidative stress and reduced inflammation (Degrave et al., 2023).
Additionally, a neutral CB1 antagonist like THCV shows promise as a potential treatment for fatty liver disease. This cannabinoid is a CB1 antagonist, shown to reduce appetite, regulate blood sugar and leptin levels, decrease body weight, and improve energy metabolism—all of which can help alleviate symptoms of fatty liver disease, obesity, and diabetes (Abioye et al., 2020).
Conclusion: The Role of the ECS in Fatty Liver Disease
The Endocannabinoid System (ECS) is integral to both the development and potential treatment of fatty liver disease. While the data is mixed—particularly regarding the effects of different cannabinoids and the timing of exposure—the ECS’s involvement in fatty liver disease is undeniable. THC’s acute effects may exacerbate fat accumulation in the liver, but chronic use appears to improve dyslipidemia, liver damage, and oxidative stress, offering potential therapeutic benefits.
As research continues, we will gain a clearer understanding of how different cannabinoids, dosages, and treatment durations influence fatty liver disease. By exploring the ECS as a treatment target, we may discover new ways to combat this growing health issue.
Bee Well,
Brandon Farless
*This information is for educational purposes only, as I am simply sharing information pertaining to these studies. No medical advice or claims are being made on my behalf.
References
1. Abioye, A., Ayodele, O., Marinkovic, A., Patidar, R., Akinwekomi, A., & Sanyaolu, A. (2020). Δ9-Tetrahydrocannabivarin (THCV): a commentary on potential therapeutic benefit for the management of obesity and diabetes. Journal of cannabis research, 2(1), 6. https://doi.org/10.1186/s42238-020-0016-7
2. Antunes C, Azadfard M, Hoilat GJ, et al. Fatty Liver. [Updated 2023 Jan 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441992/
3. Degrave, V., Vega Joubert, M. B., Ingaramo, P., Sedan, D., Andrinolo, D., D'Alessandro, M. E., & Oliva, M. E. (2023). Effects of Full-Spectrum Cannabis Oil with a Cannabidiol:Tetrahydrocannabinol 2:1 Ratio on the Mechanisms Involved in Hepatic Steatosis and Oxidative Stress in Rats Fed a Sucrose-Rich Diet. Medical cannabis and cannabinoids, 6(1), 170–183. https://doi.org/10.1159/000534610
4. Lu, H. C., & Mackie, K. (2021). Review of the Endocannabinoid System. Biological psychiatry. Cognitive neuroscience and neuroimaging, 6(6), 607–615. https://doi.org/10.1016/j.bpsc.2020.07.016
5. Sansone, R. A., & Sansone, L. A. (2014). Marijuana and body weight. Innovations in clinical neuroscience, 11(7-8), 50–54.
6. U.S. National Library of Medicine. (2020, January 21). Metformin. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. http://www.ncbi.nlm.nih.gov/books/NBK548726/#
7. U.S. National Library of Medicine. (2020, June 4). Orlistat. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK548898/
8. Wiciński, M., Fajkiel-Madajczyk, A., Kurant, Z., Gryczka, K., Kurant, D., Szambelan, M., Malinowski, B., Falkowski, M., Zabrzyński, J., & Słupski, M. (2023). The Use of Cannabidiol in Metabolic Syndrome-An Opportunity to Improve the Patient's Health or Much Ado about Nothing?. Journal of clinical medicine, 12(14), 4620. https://doi.org/10.3390/jcm12144620
