Liver disease accounts for approximately 2 million deaths per year worldwide, 1 million due to complications of cirrhosis and 1million due to viral hepatitis and hepatocellular carcinoma.
About 2 billion people consume alcohol worldwide and upwards of 75 million are diagnosed with alcohol-use disorders and are at risk of alcohol-associated liver disease.
Approximately 2 billion adults are obese or overweight and over 400 million have diabetes; both of which are risk factors for non-alcoholic fatty liver disease and hepatocellular carcinoma.
Over the past few days, I have been looking at an area that has become a global public health issue – non alcoholic fatty liver disease (NAFLD).
The tremendous progress in antiviral agents and treatment strategies, vigorous national vaccination program for hepatitis B has resulted in a gradual decrease in end-stage liver disease caused by chronic viral hepatitis.
There is, on the other hand, an increase in NAFLD which has become a major cause of the chronic liver disease (CLD).
One can therefore appreciate the Proceedings of the Nutrition Society, Volume 75, Issue 1 February 2016, pp. 47-60 as authored by Rodriguez-Ramiro et al. 2015 DOI: https://doi.org/10.1017/S0029665115004218 and published online by Cambridge University Press: 23 November 2015. it is titled “Polyphenols and non-alcoholic fatty liver disease: impact and mechanisms”.
The term non-alcoholic fatty liver disease (NAFLD) refers to a condition defined by fat accumulation in the liver when it accounts for more than 5 % of the total organ weight.
NAFLD encompasses a wide spectrum of liver damages, ranging from simple tri-acyl-glycerol(TAG) accumulation in hepatocytes (liver cells)-steatosis to non-alcoholic steatohepatitis (NASH), which is characterized by the additional presence of inflammation and tissue injury.
NASH can lead to fibrosis, which can progress to cirrhosis with a high risk of liver failure and hepatocellular carcinoma (liver cancer).
NAFLD is a major public health issue. Most NAFLD patients are clinically asymptomatic. About 10–25 % progress to NASH and 5–8 % of these will be susceptible to develop cirrhosis within 5 years.
About 12·8 % of patients with liver cirrhosis will develop hepatocellular carcinoma (liver cancer) within 3 years.
NAFLD is considered to be the hepatic component of the metabolic syndrome, which is characterized by insulin resistance, obesity (>90 % of NAFLD patients are overweight), hyperinsulinaemia, dyslipidaemia and hypertension.
The metabolic syndrome is a significant risk factor for cardiovascular disease (CVD), which is the most prevalent clinical feature of NAFLD.
Although a persistent elevation of plasma transaminase enzymes (liver enzymes) can be used as an early indication of liver damage, the accurate diagnosis of NAFLD presence and severity is not possible by routine blood tests.
For an accurate and sensitive diagnosis of NAFLD, a liver biopsy accompanied by histological staining and NAFLD activity scoring is considered the gold standard, but its use in clinical practice is limited by its invasive nature.
NAFLD has a high prevalence and represents an important economic burden lifestyle. Strategies such as dietary and exercise regimens focused on weight reduction and insulin sensitisation have been the primary therapeutic approach.
Regular consumption of polyphenol-rich foods reduces the risk of a number of metabolic diseases, including obesity, insulin resistance, hypertension and CVD.
New evidence supports the use of polyphenol-rich diet as important in the prevention and treatment of NAFLD.
NAFLD has a complex pathophysiology, which is described by the two-hit model. In this model, the first hit describes the accumulation of fatty acids (FA) and tri-acyl-glycerols (TAG) in liver cells leading to steatosis, which results from multiple mechanisms.
These include increased hepatic delivery and uptake of FA associated with increased lipolysis (fat breakdown) in adipose tissue and/or increased intake of dietary fat.
There is also decreased FA oxidation and increased hepatic lipogenesis (fat formation) together with decreased hepatic lipid export.
The inability to regulate lipid (fat) partitioning leads to the second hit. In this case, the excessive FA oxidation produces increased reactive oxygen species (ROS) resulting in sustained oxidative stress and a depletion of the antioxidant defences.
There is production of inflammatory mediators, and dysregulated insulin action leading to the progression from benign steatosis to NASH. Chronic inflammation and oxidative stress induce liver cell death, injury and progression to liver fibrosis.
Polyphenols have been identified as powerful antioxidants. NAFLD has been correlated with visceral adiposity/fat (abdominal obesity) and dysregulation of a variety of adipokines. Adipokines are cell-signalling proteins secreted by adipose tissues.
The first of its kind to be discovered is leptin in 1994. Increased serum leptin levels are found in NAFLD patients and are correlated with the severity of fatty liver disease.
Adiponectin hampers the excess lipid storage in the liver. There is decreased levels of adiponectine in NASH patients. Adiponectin is a protein hormone produced by fat cells. It reduces inflammation and deposition of fat in the arteries (atherosclerosis).
An imbalance between lipogenesis and fatty acid (FA) oxidation is central to the development and progression of steatosis/NASH.
Polyphenols have been identified as activators of key signalling proteins and regulator in the prevention of non alcoholic fatty liver disease (NAFLD).
NAFLD is characterised by oxidative stress and a redox imbalance generated in part as a consequence of insulin resistance and an accumulation of FA in liver cells.
Elevated free radicals, lipid peroxidation and reduced antioxidants have been observed in NAFLD patients. All these are counteracted by polyphenols.
Cocoa is the richest food source of polyphenols on a weight basis. Supplementation with foods high in polyphenols reduces lipid peroxidation in both the liver and blood of persons with NAFLD.
NAFLD is the major cause of chronic liver disease. Some individuals with NAFLD can develop non alcoholic steato hepatitis (NASH).
NASH is an aggressive form of fatty liver disease marked by liver inflammation and may progress to advanced scarring (cirrhosis)and liver failure. The damage inflicted on the liver is similar to the damage caused by heavy alcohol use.
I like the concluding remarks of the authors. NAFLD is essentially a condition of over-nutrition, and there is a current lack of effective therapies. There is a great need to identify dietary approaches for NAFLD prevention and treatment.
Taken together, there is evidence that polyphenols can prevent infiltration of liver cells with fat and its progression to non alcoholic steato hepatitis (NASH).
Until then, daily or regularly consume polyphenol-rich cocoa to among others prevent non-alcoholic fatty liver disease (NAFLD).
The consumption of a warm mug of unsweetened natural cocoa powder drink, without sugar or milk, every morning and night helps your body prevent liver disease, hypertension and several other diseases. Make it a lifestyle for a long healthy life.