INL Education - Non-Alcoholic Fatty Liver and Nutraceutical Intervention
New ideas on Non-Alcoholic Fatty Liver and its treatment with nutraceutical intervention
Nonalcoholic fatty liver disease (NALFD) affects about 30% of adults and over half those over 50 and some 70% of those with diabetes. It is now estimated in 2020 to have a worldwide prevalence of 25%.(1)
CUHK published the world’s largest study on Epidemiology of NAFLD in Diabetic Patients shows fatty liver causing NASH or Cirrhosis in 1 out of 5 patients. It is worth noting that 19% of the non-obese subjects also suffered from NAFLD. The non-obese NAFLD patients had lower markers of liver injury and fibrosis, suggesting that the severity of their disease was less.(4)
Moreover, the study findings identified enlarged waist circumference, elevated blood sugar (HbA1c), insulin resistance, higher ferritin level, and the presence of polymorphism of the PNPLA3 gene as risk indicators of NAFLD in non-obese patients.
Recent studies emphasize the role of insulin resistance, triglyceride accumulation, adipokines, oxidative stress to LDL and subsequent lipid peroxidation as well as smaller LDL particle size and infiltration to the endothelium, release of pro-inflammatory cytokines, plus mitochondrial dysfunction in the development and progression of NAFLD into CVD. The pathogenesis of NAFLD and metabolic syndrome has common pathophysiological mechanisms, with insulin resistance as a key factor.(5)
Initial theories regarding its development have been based on the ‘2-hit hypothesis’, where the “first hit” involves hepatic lipid accumulation, and insulin resistance is proposed to be the key contributing factor for steatosis development.
Oxidative stress followed by lipid peroxidation, as well as the action of proinflammatory cytokines (e.g. tumor necrosis factor [TNF]-α), adipokines and mitochondrial dysfunction initiate the second hit, which progresses from simple steatosis to nonalcoholic steatohepatitis (NASH). A “third hit”, also caused by oxidative stress, inhibits the replication of mature hepatocytes resulting in the over population of the hepatic oval cells.(6)
Another key hallmark of NALFD is the variable prevalence, presentation and causation over different populations, most of which are attributable to the PNPLA3 gene mutation but also environmental and microbiome-oriented factors. The table below highlights the extent of these vary factors and their associated evidence bases.
On the other hand, probiotics can strengthen the intestinal wall, reducing its permeability, bacterial translocation, and endotoxemia according to animal and human studies. They can also reduce oxidative and inflammatory liver damage, while improving the histological state in certain situations. Research that has been conducted on probiotics and NAFLD, highlights their efficacy as a novel therapeutic option for the treatment of this condition.
I find berberine to be the most potent phytonutrient for correction of metabolic syndrome-induced NAFLD.
Dietary deficiency of choline can be corrected via supplementation and is an important consideration in fatty liver
Graeme's Dose: 500mg initially tid, reducing to bid after 6 months
Berberine is a potent plant-derived alkaloid that offers a wide range of benefits.* Traditionally, Berberine been used to support regular and normal bowel function in healthy individuals*
Graeme's Dose: 2 capsules tid initially, reducing to 2 capsules as maintenance after 6 months.
Phosphatidylcholine softgels are excellent for emulsifying fat, making this nutrient extremely valuable for liver health.** It is ideal for supporting absorption of all fat soluble nutrients.
Graeme's dose: 25-50 billion daily
Ther-Biotic® Complete is a robust, broad-spectrum, hypoallergenic blend of 12 probiotic species in a base of inulin. Designed to supply a complete component of synergistic and complementary species, each capsule provides 25 billion CFU protected by our proprietary InTactic® technology for maximum viability throughout the intestinal tract.