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studies conducted in Italy and Greece, indicating patients with alcoholic liver disease.
that strong adherence to the Mediterranean diet
may be protective against HCC (approximately a 50% Red meat
reduction in risk), with potential benefits also in Red meat consumption has been reported to be
[14]
patients with chronic viral hepatitis. As for patients associated with an increased risk of HCC. Meat
[4]
with established chronic liver disease, nutritional processing, e.g. curing and smoking, can in fact
interventions to support sufficient energy intake result in the formation of carcinogenic chemicals,
significantly improve patient survival. [5-8] A better including N-nitroso-compounds and polycyclic
knowledge of the detrimental or beneficial effects of aromatic hydrocarbons. cooking, especially if high-
foods is therefore important in the prevention and temperature, can also produce known or suspected
management of HCC, and the evaluation of dietary carcinogens, including heterocyclic aromatic amines
[15]
supplements potentially able to reduce the risk and/ and polycyclic aromatic hydrocarbons. The
or the progression of cirrhosis and steatosis is of the International Agency for Research on Cancer has
highest interest. recently classified red meat and processed meat as
“probably carcinogenic to humans” (Group 2A) and
The potential protective and therapeutic mechanisms “carcinogenic to humans” (Group 1), respectively.
[15]
of natural compounds in the prevention and However, the strongest association appears to
treatment of hepatotoxicity and HCC have been be with colorectal cancer, pancreatic cancer and
recently reviewed. The aim of the present review is prostate cancer, and currently available evidence
[15]
[9]
to provide an insight on the clinically relevant effects- supporting a causative role for red meat in HCC is
either beneficial or detrimental-of natural products inconsistent. [16,17]
consumed by humans on HCC risk and management.
Pickled foods
DETRIMENTAL NATURAL PRODUCTS A possible carcinogenic effect of pickled vegetables
was first reported in 1992. Traditionally, pickled
[18]
Foods and beverages vegetables are prepared by packing moist vegetables
Alcohol in a jar for weeks to months, allowing fermentation
The detrimental effects of alcohol on the liver are and growth of fungi and yeasts. This process can
well known; ethanol exerts toxic effects that can potentially yield carcinogenic compounds such as
cause cell injury and a reactive response culminating the N-nitroso compound Roussin’s red (dimethylthiot
in alcohol-induced hepatic cirrhosis. More in detail, etranitrosodiiron). Consistently, a large systematic
[19]
reactions catalyzed by the main enzymes involved in review and meta-analysis revealed that those who
alcohol metabolism, namely alcohol dehydrogenase consume pickled vegetables/foods have an about
and aldehyde dehydrogenase, lead to the production 50% increase in risk of gastric cancer vs. those who
of reactive oxygen species (ROS) that can exert consume little or no pickled vegetables/foods. An
[20]
toxic effects such as lipid peroxidation, enzymes association between pickled food and HCC has also
inactivation, DNA mutations, and destruction of cell been reported. [21]
membranes; in addition, in conditions of chronic
alcohol abuse there is an increased production Sugar
of acetaldehyde from ethanol, due to induction Non-alcoholic fatty liver disease (NAFLD) is
of the microsomal system and in particular of considered as the hepatic manifestation of the
the Cytochrome P450 enzyme Cytochrome P450 metabolic syndrome. It is characterized by an
2E1. Acetaldehyde is one of the main mediators increase in intrahepatic triglyceride content (i.e.
[10]
of alcohol-induced fibrogenesis in the liver, as it can steatosis), with or without inflammation and fibrosis
stimulate synthesis of fibrillar-forming collagens [i.e. non-alcoholic steatohepatitis (NASH)]. Hepatic
and structural glycoproteins of extracellular matrix de novo lipogenesis (DNL) has been suggested to be
in hepatic stellate cells, and increase the secretion abnormally increased in NAFLD, and to contribute to
of transforming growth factor-β. Eventually, these its development. As glycolysis and the metabolism
[22]
events may lead to hepatic cirrhosis, which is of carbohydrates are the main providers of substrates
associated with a 5-year cumulative risk for HCC of for DNL, a high-carbohydrate diet can prime the DNL
8%. The immunosuppressive effects of alcohol [11,12] pathway with a large substrate load and increase rates
[10]
and alcohol-induced epigenetic modifications [13] of DNL. Dietary fructose may contribute to NAFLD
[23]
may also contribute to the development of HCC in by promoting DNL, insulin resistance, oxidative
54 Hepatoma Research | Volume 2 | March 9, 2016