With the continuous development of society, the improvement of people’s living standard and the change of diet structure, the incidence of liver disease is increasing, among which fatty liver and alcoholic liver disease are the two prominent diseases. The liver is the largest chemical plant of the human body, undertaking important functions such as digestion, detoxification and secretion, and human life activities are always inseparable from it. The nutrients we eat three meals a day must rely on the liver for processing, in order to provide the body with the needs of life activities. Without the liver, there is no life in the human body, the liver is damaged, health is compromised, so love and care for the liver is to care for life, so how do these two diseases of the liver occur, how do we face the occurrence of the disease? Fatty liver: known as the modern “rich disease”, it is not a disease but a domestic incidence has increased significantly in recent years, of which men aged 30 to 40 years account for 25%. Of particular concern is the trend of the onset of fatty liver at a younger age, and many hospitals have even identified patients with fatty liver at the age of 14 or 15. A survey shows that the prevalence of fatty liver in Guangzhou is 20%-30% in people around 30 years old, 8.8% in a college in Shanghai, and 11% in a college in Beijing. Under normal conditions, the liver maintains a dynamic balance in a series of delicate and complex operations of decomposition, synthesis, detoxification and fat metabolism of substances in the body. On the one hand, the liver absorbs free fatty acids in the body and synthesizes them into triglycerides, while on the other hand, it slowly delivers the synthesized triglycerides to the blood in the form of lipoproteins, making them an important energy source for human activities. Once the process of lipid uptake and transport by the liver becomes impaired, it causes fat to accumulate in the liver. Normal human liver tissue contains small amounts of fats, such as triglycerides, phospholipids, glycolipids and cholesterol, which weigh about 4 to 5 percent of the liver weight. If, for some reason, too much fat accumulates in the liver, exceeding 10% or even 15% of the liver’s weight, it is called a fatty liver. We are all at risk of developing fatty liver, but there are some groups of people who are at greater risk of developing fatty liver, which we call high-risk groups. The main groups at risk for fatty liver include obesity, especially visceral obesity; diabetes mellitus, especially adult non-insulin-dependent diabetes mellitus; chronic heavy drinkers; hyperlipidemia, especially those with elevated blood triglycerides; long-term users of liver-damaging drugs; and individuals with a family history of obesity, diabetes mellitus, and fatty liver. The clinical manifestations of fatty liver: The clinical manifestations of fatty liver are diverse, and mild fatty liver has no clinical symptoms and is easily ignored. It has been documented that more than 25% of patients with fatty liver can be clinically asymptomatic. Some only have fatigue, and most patients with fatty liver are fat, so it is more difficult to detect mild self-conscious symptoms. Therefore, at present, most patients with fatty liver are found incidentally during physical examination. Moderately severe fatty liver has similar manifestations to chronic hepatitis, including loss of appetite, fatigue, nausea, vomiting, weight loss, and vague pain in the liver or upper right abdomen. Mild enlargement of the liver may be painful to the touch, with a slightly tough texture, blunt edges and smooth surface, and a few patients may have splenomegaly and liver palms. When there is excessive fat deposition in the liver, it can cause severe pain or pressure pain in the right upper abdomen, fever, leukocytosis, and easy to be misdiagnosed as acute abdomen and operated by caesarean section. When the fat vesicles rupture, the fat particles enter the blood can also cause brain and lung vascular fat embolism and sudden death. If hepatocellular fat accumulation compresses the hepatic sinusoids or small bile ducts, the portal blood flow and bile excretion are blocked, resulting in portal hypertension and biliary stasis. Because of acute chemical poisoning, drug poisoning or acute fatty liver in pregnancy, the clinical manifestations are mostly acute or subacute hepatic necrosis, which can be easily confused with severe hepatitis. In addition, patients with fatty liver also often have changes of peripheral neuritis such as tongue inflammation, stomatitis, skin bruising, numbness in the extremities, and abnormal sensation in the extremities. A small number of patients may also have gastrointestinal bleeding, gum bleeding, and epistaxis. Patients with severe fatty liver can have ascites and lower limb edema, electrolyte disorders such as hyponatremia and hypokalemia, etc. The manifestations of fatty liver are varied, and in case of diagnostic difficulties, liver biopsy can be done to confirm the diagnosis. Treatment of fatty liver: Once fatty liver is found, we must pay attention to it, otherwise it will cause serious consequences and delay the treatment. Because the causes of fatty liver are different, the treatment will also be very different, first of all, we must find the root cause of the disease, and the targeted treatment is different from person to person. 1, non-pharmaceutical treatment: (1) through the adjustment of dietary structure, eat high protein, high vitamin, low sugar, low fat diet. Do not eat or eat less animal fats, sweets (including sugary drinks). Eat more green vegetables, fruits and fiber-rich foods, as well as lean meat, river fish and soy products with high protein, no snacking and no extra meals before bedtime. (2) Properly increase exercise to promote body fat consumption. Run every day, at least 6 km per hour to achieve weight loss. Sit-ups or fitness equipment exercise are very beneficial. 2, drug treatment: (1) according to the results of laboratory tests, under the guidance of doctors to choose the appropriate drugs for regular treatment, do not abuse. Commonly used drugs include hepatocyte protection, lipid removing drugs and antioxidants, such as vitamins B, C, E, lecithin, ursodeoxycholic acid, silymarin, inosine, coenzyme A, reduced glutathione, taurine, carnitine orotate, hepatale, and certain lipid-lowering drugs (e.g., hepatocyte), etc. (2) Chinese medicine treatment. If the disease is caused by liver and stomach disharmony, liver qi stagnation and phlegm stasis, the treatment should be based on draining liver qi, removing phlegm and eliminating stasis. In case of phlegm and stagnation, Qi stagnation and blood stagnation, stagnation of stagnation, we can benefit Qi and activate blood, remove phlegm and stagnation, eliminate swelling and disperse knots. In addition, acupuncture and electrophysiological therapy are also being researched and developed. Prevention of fatty liver: For high-risk groups, serious complications may occur if no attention is paid to prevention, such as liver fibrosis, cirrhosis, induced or aggravated hypertension, coronary heart disease, atherosclerosis, encephalopathy fatty liver syndrome, and even induced liver cancer. 1, to have a good state of mind, have good habits, have restraint, do not crave, do not overeat. 2.Pay attention to adhere to physical exercise, reduce the amount of food appropriately and control weight gain. 3.Consult your doctor promptly if you find any problem, do not take it lightly or use drugs blindly. 4.Although all patients with fatty liver need to receive treatment, the treatment means are not limited to drugs and surgery. For patients with obese fatty liver, the most important treatment is non-pharmacological treatment such as diet control, strengthening exercise and correction of bad habits. These non-pharmacological measures need to be implemented for life, otherwise the fatty liver will recur even if it is cured. Alcoholic liver disease: Alcoholic liver disease is a liver damaging disease caused by long-term heavy drinking (alcoholism). In western countries where alcoholism is worse, alcoholic cirrhosis accounts for 50% to 70% of patients with cirrhosis, and is one of the main causes of morbidity and mortality among young and middle-aged people. The more economically developed countries with high material living standards, the more their nationals drink alcohol, which has been a worldwide trend. In the past decade, with the improvement of people’s living standard and the expansion of social circle, the incidence of alcoholic liver disease due to alcohol consumption in China is also on the rise and has become a hidden killer that cannot be ignored. Alcoholic liver disease pathogenesis: Alcoholic liver disease occurs with the amount of alcohol and drinking time, ethanol into the liver cells, by the liver ethanol dehydrogenase, hydrogen peroxide decomposition enzyme and liver microsomal ethanol oxidase oxidation, the formation of acetaldehyde. Acetaldehyde has obvious toxic side effects on liver cells, causing obstruction of their metabolism and leading to degeneration and necrosis of liver cells. Long-term high alcohol intake can cause several different lesions in the liver, ranging from steatosis in mild cases to alcoholic hepatitis and liver fibrosis in severe cases, which can then lead to irreversible cirrhosis. In general, the average daily alcohol consumption of 80~150g for more than 10 years before developing alcoholic cirrhosis, and alcoholic hepatitis often occurs with short-term heavy alcohol consumption. There are also a few patients with alcoholic liver injury due to genetic predisposition, gender, primary liver disease and nutrition. We can calculate the amount of alcohol in the cited alcohol by using the following formula: alcohol amount (g) = volume of alcohol consumed (ml) × alcohol content (%) × 0.8. Diagnosis of alcoholic liver disease: Alcoholic liver disease lacks specific clinical manifestations, and most of them are asymptomatic or have mild symptoms. Mild cases may present with weakness, loss of appetite, vague pain or discomfort in the right upper abdomen. In severe cases, there may be varying degrees of anemic appearance, occasional jaundice, spider nevus, liver palms, finger tremors, and more signs of moderate liver enlargement, ascites, and lower limb edema. Of course, the most important thing is a long history of heavy alcohol consumption, together with the above clinical symptoms and signs, and laboratory tests related to glutamic oxalacetic transaminase/glutamic alanine transaminase (AST/ALT) >1, mostly between 2-5, increased alkaline phosphatase (AKP), transpeptidase (GGT), decreased serum hemoglobin, increased globulin, prolonged prothrombin time and vitamin K cannot be corrected. In the fatty liver stage, blood triglycerides, pre-beta lipoproteins and cholesterol are mildly to moderately increased. In the alcoholic liver steatosis stage, cholesterol is normal, but the cholesteryl ester to total cholesterol ratio is decreased. Imaging examinations B-mode ultrasound and CT show phase changes of fatty liver or hepatic steatosis. AST/ALT>1, mostly between 2 and 5 AKP and GGT are increased, serum hemoglobin is decreased, globulin is increased, prolonged prothrombin time and vitamin K cannot be corrected. In the fatty liver stage, blood triglycerides, pre-beta lipoproteins and cholesterol are mildly to moderately increased. In the alcoholic liver steatosis stage, cholesterol is normal, but the cholesteryl ester to total cholesterol ratio is decreased. Imaging examinations: B-mode ultrasound and CT showed the phase change manifestation of fatty liver or hepatic steatosis. At the same time in the diagnosis of alcoholic liver disease at the same time need to exclude hepatophilic virus infection, drugs and toxic liver injury and so on so that the diagnosis can be basically confirmed, need to promptly go to the hospital for treatment. Treatment of alcoholic liver disease: 1. Abstinence from alcohol is the most important measure for the treatment of alcoholic liver disease. Withdrawal syndrome may occur during the process of alcohol withdrawal (more acute seizures, often with shaking limbs and sweating and other symptoms, severe cases have withdrawal convulsions or epileptiform seizures). 2.Nutritional support: Most patients with alcoholic liver disease are malnourished and need to provide good nutritional support. 3.Medication. Polyenyl phosphatidylcholine has a tendency to prevent histological deterioration in patients with alcoholic liver disease. Glycyrrhetinic acid preparations, silymarin and polyenyl phosphatidylcholine have different degrees of antioxidant, anti-inflammatory and hepatocyte membrane and organelle protection effects, and their clinical application can improve liver biochemical indexes. However, multiple anti-inflammatory and hepatoprotective drugs should not be applied at the same time, so as not to increase the burden on the liver. Adrenocorticosteroids have a role in improving the acute phase and cerebral symptoms in severe alcoholic hepatitis, but attention should be paid to co-infections, and propylthioxypyrimethamine, which may increase clinical recovery in mild and moderate alcoholic. Prognosis of alcoholic liver disease: Alcoholic fatty liver is usually considered a benign lesion, and although acute fatty liver can lead to portal hypertension, its lesions can be reversed after abstinence from alcohol. If patients with alcoholic fatty liver disease continue to drink alcohol, more severe liver injury can occur as confirmed by serial liver biopsies. It is now believed that alcoholic hepatitis has a higher independent risk factor for death than inactive cirrhosis. Based on liver biopsy histology, a group investigated the natural history of alcoholic liver disease and found that patients with fatty liver had the best prognosis, with a survival rate of 70%-80% over 4-5 years; patients with alcoholic cirrhosis with alcoholic hepatitis had the worst prognosis, with a survival rate of 30%-50% over 4-5 years; and patients with alcoholic hepatitis or cirrhosis had a prognosis in between, with a survival rate of 50%-75% over 4-5 years. 75%. When all patients with alcoholic liver disease were combined, the average survival rates at 1 and 5 years were 80% and 50%, respectively. In addition to alcohol consumption as an important factor affecting the prognosis of alcoholic liver disease, gender also has an impact on the prognosis of alcoholic liver disease, as women are more sensitive to alcohol than men, and even though the initial liver damage is mild and abstinence from alcohol is not uncommon, the development of cirrhosis is always inevitable. The combination of hepatitis B and C virus or other viral infections must also be taken into account in the prognosis determination. Alcoholics are immunocompromised and may have a reduced resistance to infection. The impact on alcoholic liver disease may be even more pronounced in China where the prevalence of hepatitis B virus infection is very high.