There have been many studies on the correlation between diet and tumors of the digestive system other than the liver, but few studies have been conducted on the influence of dietary habits and nutritional intake in the development of HCC, and no definite nutritional factors have been identified to play a role in the formation of HCC. For example, studies in alcoholics and HBV-infected patients found that vit-A and serum carotene levels were negatively associated with the development of HCC, and that vit-A and its derivatives deficiency may increase the development of HCC. Another study found that folate deficiency was associated with the occurrence of HCC, which was tentatively confirmed in animal models. Folic acid is a metabolite of adenosylmethionine (S-adenosylmefhionine: SAM), which acts as a donor of methyl in DNA methylation, which is an important regulator of gene expression, and methyladenosylmethionyltransferase, an intrahepatocellular enzyme, has decreased activity in alcoholic cirrhosis, which leads to a decrease in the synthesis of SAM in experimental ( animal) models, SAM deficiency leads to reduced DNA methylation and decreased stability, thereby increasing the risk of HCC development. Folic acid deficiency may reduce SAM levels in hepatocytes and cause DNA demethylation, and previous studies of DNA oncogene overexpression did find overall hypomethylation levels in HCC patients and hypermethylation in DNA associated with tumor suppressor genes. Essential fatty acids (EFAs) play a very important role in the complex metabolic processes of the body. Poly-unsaturated fatty acids (PUFA) contain multiple molecular types, and the absolute amounts and ratios of their various molecular types are significantly altered during the development of insulin resistance and metabolic syndrome, and these changes in amounts and ratios may be an important part of metabolic factors promoting tumorigenesis, and may become the most important potential link in tumor-related metabolism. The most important potential target sites in complex metabolism, and alterations in fatty acid composition may affect cell structure and function. Investigators have found correlations between different fatty acid compositions and HCC through the evaluation of different diets, but no consistent conclusions have been obtained. Conversely, some studies have suggested dietary habits that may protect the liver or even prevent the development of HCC, such as a high intake of vegetables and long-term coffee consumption. Metabolic factors and HCC Recent studies have shown that obesity, diabetes and metabolic syndrome can all contribute to the development of HCC. Currently, overweight is a major worldwide public health problem and is often closely associated with the metabolic syndrome. Overweight individuals often have abnormalities in indicators such as elevated arterial blood pressure, high triglycerides, low HDL, insulin resistance (with or without diabetic metabolic syndrome), and abnormalities in three of these indicators often lead to nonalcoholic steatohepatitis and associated cirrhosis. Overweight and diabetes similarly increase the risk of cirrhosis in patients with hepatitis C and alcoholic liver disease. In men, obesity increases the risk of HCC, pancreatic cancer, colorectal cancer and other gastrointestinal tract tumors; in women, obesity also increases the risk of gynecologic tumors, in addition to the same high risk of tumor development as in men. There are clear data showing that the incidence of HCC is significantly higher in obese patients with cirrhosis, and the incidence of HCC is higher in patients with diabetes combined with cirrhosis. The mechanism of obesity and tumorigenesis is unclear, but may be related to metabolic dysregulation due to obesity. Levels of insulin and insulin like growth factor-1 (ZG-1) are elevated in obese people and stimulate the growth of normal and tumor cells. Serum leptin is one of the major components of adipokines secreted by adipose tissue, and epidemiological studies have found that leptin may be associated with breast, endometrial, prostate, colorectal, and pancreatic carcinogenesis. Cell cultures have shown that leptin promotes cell growth through specific receptors in the cell membrane can stimulate the body to secrete MMP-2 and enhance MMP-6 activity, both MMP-6 and MMP-2 are metabolism-related regulatory factors that play an important role in tumorigenesis and metabolic disorders. In addition, many obese patients have increased levels of pro-angiogenic factors, most of which are based on over-secretion under leptin regulation, while some are secreted directly by adipose tissue, and the increase of pro-angiogenic factors will in turn stimulate tumor cell formation.