The term fatty liver is derived from pathology and refers to diffuse fatty infiltration of the liver, which is classified as simple fatty liver, steatohepatitis and fatty cirrhosis depending on the presence or absence of inflammation, necrosis and fibrosis. Fatty liver disease, on the other hand, is a clinical concept that can be divided into alcoholic and non-alcoholic fatty liver disease based on the presence or absence of a history of excessive alcohol consumption, the latter being mainly associated with obesity, diabetes mellitus and hyperlipidemia. Fatty liver is a common clinical phenomenon rather than an independent disease.
There are many causes of fatty liver, and its clinical manifestations are asymptomatic in the milder cases and aggressive in the more severe ones, mainly manifesting as liver damage. Steatohepatitis refers to hepatitis secondary to steatosis of large vesicular hepatocytes, which can be divided into two categories: alcoholic hepatitis and non-alcoholic steatohepatitis, depending on the cause. The histological changes of the liver are similar in both cases, as they are characterized by ballooning of hepatocytes and a mixed inflammatory cell infiltrate with neutrophil predominance in the lobules on the basis of hepatic steatosis. Some steatohepatitis is also associated with Mallory vesicles and pericellular fibrosis and pericentral venous fibrosis. Fatty liver is common in alcoholics, whereas alcoholic hepatitis occurs only in some severe alcoholics, and the prevalence of alcoholic fatty liver and alcoholic hepatitis is much higher in Europeans and Americans than in Easterners.
The main morphological changes of the liver in patients with alcoholic hepatitis are.
1, the main body of the lesion is degenerative necrosis of hepatocytes in the central part of the lobules, and the hepatocytes are obviously swollen and balloon-like;
2.Necrosis of hepatocytes of different degrees and nature;
3, Inflammatory cells focal infiltration, usually neutrophil-based, the degree of inflammation in the confluent area is often lighter than the inflammation in the lobules;
4, Malory bodies;
5, varying degrees of hepatocellular steatosis;
6, pericellular fibrosis forming a lattice-like structure. In alcoholics, hepatocellular steatosis may not be obvious, which is called alcoholic liver fibrosis, otherwise it is called alcoholic fatty liver combined with liver fibrosis. Alcoholic liver fibrosis is more common in patients with alcoholic liver disease in China and Japan. When the inflammation, necrosis, Mallory vesicles and fibrosis of alcoholic hepatitis involve the central vein of the lobules, it can lead to sclerotic hyaline necrosis, which is one of the reasons for portal hypertension in alcoholic hepatitis without cirrhosis. The histological changes in nonalcoholic steatohepatitis are similar to those in alcoholic hepatitis, but the detection rate of severe hepatocellular steatosis and glycogen nuclei is relatively high, and simple nonalcoholic steatohepatitis usually requires steatohepatitis as a basis for liver fibrosis and cirrhosis to occur. Generally speaking, fatty liver is a reversible disease early diagnosis and timely treatment can often restore normalcy. Therefore, community guidance is important for the recovery of fatty liver.
Etiology
Common causes of fatty liver
The immune status, nutritional factors, genetic background, lifestyle, and age and gender all play a significant role in the development of fatty liver, especially steatohepatitis and liver fibrosis, and can be considered as conditional factors in the development of fatty liver. Broadly divided into the following categories.
1, obesity disease: the degree of fat accumulation in the liver is proportional to body weight, and about half of the obese patients are seen to have mild fatty liver. In patients with severe obesity the incidence of fatty liver can be as high as 60%-90%. It can be seen that obese patients have a clear tendency to develop fatty liver. The fatty infiltrate is also reduced or disappears in obese individuals when their weight is controlled. Obesity caused by inappropriate increase in nutrition and lack of exercise after hepatitis is one of the most common causes of fatty liver in China.
2, alcohol: according to long-term alcoholics liver puncture biopsy 75%-95% have fat infiltration, research shows that there is a quantitative relationship between the consumption of alcohol and the incidence of fatty liver, more than 80-160 grams of alcohol per day, the incidence of ethanolic fatty liver increased 5-25 times. The pathogenesis is currently thought to be the result of a combination of factors. First of all, a large amount of ethanol in the body can inhibit the synthesis of mitochondrial proteins and reduce the ability of mitochondria to oxidize fat, causing the accumulation of fatty acids in liver tissues, the accumulation of ketone bodies in the body, the increase of lactic pyruvic acid ratio in the body, the excess of lactic acid inhibits the excretion of uric acid by the kidneys, causing hyperuricemia, reducing the hepatic glycogen anisotropy, leading to hypoglycemia, and in some patients, sudden death. In addition, the metabolites of ethanol, such as acetaldehyde, also have a direct toxic effect on the liver tissue itself, causing liver tissue steatosis.
3, protein-calorie deficiency: malnutrition, lack of protein: such as gassica disease. It is an important cause of fatty liver. Mostly seen in insufficient food intake or digestive disorders can not synthesize apolipoproteins, so that triglycerides accumulate in the liver to form fatty liver. Increased serum free fatty acids during starvation can lead to fatty liver formation, and the mechanism may be related to lack of glucose acquisition, increased growth hormone and increased sympathetic excitability. And the degree of hepatic steatosis depends on the length of starvation, and increased fat mobilization in the body after jejuno-ileal colectomy and gastric segmentation can also lead to fatty liver.
4, diabetes mellitus: diabetes mellitus can occur in an average of 50% of patients with fatty liver, especially 40 to 50 years of age, diabetes mellitus, more likely to appear intrahepatic fatty deposits. The pathogenesis is not yet well understood, and may be related to increased plasma insulin levels and increased concentrations of unesterified fatty acids in the plasma.
5, drugs, according to statistics, there are at least two hundred kinds of drugs can cause different degrees of fatty liver: such as tetracycline, rifampin, isoniazid, adrenocorticotropic hormone, puromycin, cyclamate, thujone alkaline and antibiotics, central nervous system drugs, testosterone hormones, etc. According to statistics, the incidence of drug fatty liver in all cases of adverse drug reactions in the third. The mechanism is complex. For example, tetracycline can bind to the RNA of hepatocytes, damage the synthetic function of hepatocytes, so that the preprotein of very low density lipoprotein, very low density lipoprotein triacylglycerol synthesis is reduced, the oxidation of fatty acids in the mitochondria and the role of fatty acid uptake by hepatocytes are impaired and fatty liver occurs.
6, toxins: common fatty liver toxins are carbon tetrachloride, yellow phosphorus, isopropyl alcohol, cyclohexylamine, emetine, arsenic, lead, mercury, etc. Its pathogenesis is more complex. Such as carbon tetrachloride through the inhibition of intrahepatic protein synthesis, reduce the rate of fatty acid oxidation in the liver, so that the liver triglyceride release barriers, resulting in the formation of fatty liver. Yellow phosphorus mainly leads to impaired protein apolipoprotein synthesis in the liver, while reducing lipid secretion and fat accumulation in the liver, resulting in the formation of fatty liver. Isopropyl alcohol can make the liver 2-phosphoglycerol increase, fat cells decomposition of fat increased, unesterified fatty acids into the liver also increased, so that too much triacylglycerol synthesis in the liver to form a fatty liver.
7. Endocrine metabolic factors such as cortisolism, hyperthyroidism, pregnancy, hyperuricemia, hyperlipoproteinemia, etc. can cause hepatocyte steatosis and fatty liver.
Fatty liver diagnosis
Symptoms: Light fatty liver can have no symptoms and is only detected by B-mode ultrasound or CT examination, etc. After the formation of fatty liver, most of them show loss of appetite, nausea, vomiting, weight loss, weakness, abdominal distension, discomfort or vague pain in the liver area, and a few patients may develop mild jaundice.
Physical examination: an enlarged liver can be palpated (usually within 2-3 cm below the right rib cage) with smooth surface, rounded edges, soft or moderate hardness and mild pressure pain, some patients have percussion pain, and severe patients may show signs of cirrhosis.
Laboratory tests: normal or elevated liver function ALT, manifestations of hyperlipidemia, elevated triglycerides, elevated serum γ-GT activity, elevated protein electrophoresis plasma globulin. Ultrasound and CT B-mode ultrasound shows enlarged liver parenchyma with dense strongly reflective light spots deep tissue echogenic attenuation CT scan shows low liver density compared to other parenchymal organs (e.g. spleen)
Liver biopsy: Liver biopsy is the basis for confirmation.
Differential diagnosis
Severe fatty liver is a fatty liver with aggressive clinical symptoms and poor prognosis; strictly speaking it is a pathological process of certain critical diseases. It mainly includes acute fatty liver in pregnancy and encephalopathy fatty liver syndrome. It is significantly different from general fatty liver in terms of clinical symptoms, signs and disease prognosis.
(A) Acute fatty liver of pregnancy
This disease, also known as obstetric acute yellow liver atrophy, is a serious complication of pregnancy, which is relatively rare clinically and has a poor prognosis. It occurs in the last trimester of pregnancy (30-40 weeks) and is thought to be induced by large oral and tetracycline doses during pregnancy.
The main clinical symptoms: sudden onset of persistent nausea, vomiting, and even vomiting of blood, accompanied by epigastric pain, and jaundice for a week, often without pruritus. Later, jaundice deepens rapidly, followed by varying degrees of impaired consciousness or coma; serum bilirubin is mildly to moderately elevated, and if combined with DIC, vomiting of coffee-colored fluid or fresh blood, as well as blood in urine, blood in stool, purpura, bleeding from gums and injection sites, along with a decrease in platelets and fibrinogen, an increase in FDP values and prolonged prothrombin time, oliguria in half of the patients, metabolic acidosis, and other early renal failure manifestations.
(B) Encephalopathy fatty liver syndrome (Reye’s syndrome)
The disease mainly occurs in children and adolescents, and is often preceded by some kind of viral infection. After 2-3 days of improvement of cold-like prodromal symptoms and chickenpox infection, the disease suddenly appears with frequent vomiting and severe headache, and within a few hours enters delirium, spasms, rigidity and decortication, and finally enters coma, often accompanied by fever, hypoglycemia and abnormal liver function. This disease is dangerous and has a high mortality rate.
Liver cancer
Hepatocellular carcinoma is a malignant liver disease, which can be clinically associated with malignant fluid, elevation of methemoglobin, abnormal liver function and increased blood sedimentation. However, the distinction between early stage liver cancer and focal fatty liver is mostly made by CT examination and, if necessary, liver aspiration biopsy.
Complications of fatty liver
Fatty liver can be an independent disease or a complication of some systemic diseases, often complicated by other manifestations of alcoholism. For example, alcohol dependence, pancreatitis, peripheral neuritis, anemic linguitis, alcoholic hepatitis, and cirrhosis of the liver. Over-nutritional fatty liver often appears with other underlying diseases, such as obesity, diabetes, hyperlipidemia, hypertension, coronary atherosclerotic heart disease (referred to as coronary heart disease), gout, gallstone disease, etc. Malnutrition fatty liver often coexists with chronic wasting diseases, such as tuberculosis and ulcerative colitis. Acute fatty liver in pregnancy is often complicated by renal failure, hypoglycemia, pancreatitis, sepsis, and disseminated intravascular coagulation (DIC). Therefore, in patients who have been found to have fatty liver, further comprehensive investigations should be performed to clarify the nature of the fatty liver and the possible coexistence of other diseases.
Treatment of fatty liver
The principles of treatment are to remove the causes, adjust the diet, increase exercise, and use reasonable medication.
1.Remove the causesRemove all factors that can cause fatty liver, abstain from alcohol and apply high protein diet, which often can effectively reduce fat in the liver. Alcoholic fatty liver is mainly to abstain from alcohol and give a sufficient amount of protein diet, so that the fat accumulated in the liver can be effectively removed; obese people should lose weight; diabetic patients should treat the original disease.
2, adjust the diet This is an important part of the treatment of fatty liver, the diet needs to be high in protein, moderate amounts of fat and sugar.
3.Increase the amount of exercise according to the different primary diseases can be moderate exercise to accelerate the metabolism of fat.
4.Rational medication can be taken according to the drug instructions of some fat removal drugs and weight loss drugs, but the treatment effect is not very sure. Reasonable use of drugs can reduce the transaminases, so that liver function back to normal. However, most of these drugs have liver-damaging side effects and should be used with care.
Fatty liver prevention
1, reasonable diet three meals a day should be reasonable, to make coarse and fine match, nutritional balance. Adequate amount of protein can remove fat from the liver.
2, appropriate exercise every day to adhere to physical exercise, can be their own physical fitness to choose the appropriate exercise program. Such as: jogging, playing table tennis, badminton and other sports; to start with a small amount of exercise, step by step, gradually reach the appropriate amount of exercise to strengthen the consumption of body fat.
3, careful use of drugs liver is the body’s chemical plant, any drugs into the body are to be detoxified by the liver. Therefore, usually do not move to take drugs, especially do not just eat the so-called health care drugs advertised, the appearance of symptoms of fatty liver patients, in the choice of drugs more carefully, beware of the toxic side effects of drugs, especially on the liver damage drugs, absolutely not to use, to avoid further aggravation of liver damage.
4, in addition, the mood should be cheerful, not angry, less irritated, pay attention to the combination of work and rest, etc. is also quite important.
Community education treatment.
Fatty liver does not require special drugs as already mentioned above, and a few points will be made on community prevention.
In terms of treatment, no special medication is needed for simple fatty liver, and the main focus is on proper diet, physical exercise, and proper behavior. The prevention and treatment of children is particularly important. Prevention should start with children. Diet is the first step in prevention and treatment.
Special attention should be paid to the following issues in the diet.
First, in the daily diet, pay attention to the rational structure of the diet, food with grains and cereals as the most, followed by vegetables, fruits and vegetables account for a larger proportion, can eat appropriate amounts of milk, fish, soy products and other protein-rich food, as little as possible to consume sugar, lard, fatty (butter, animal offal, chicken skin, roast goose, crab yellow, etc.) food.
Secondly, limit the total calories in your diet. When nutrients exceed your caloric and metabolic needs, they will also become fat storage.
Exercise is also an important part
In addition to diet, exercise is also an important part of controlling the development of fatty liver. Proper exercise burns excess calories, prevents fat accumulation, and strengthens the muscular and skeletal systems as well as the cardiopulmonary system. The following guidelines can be used as a reference for the regulation of exercise and behavioral patterns in children
General principles.
Children: choose exercises that children enjoy and are appropriate so that they can develop the habit of sticking to them for a long time; include different kinds of exercises in one exercise to avoid losing interest; cherish opportunities for activities in daily life, such as doing housework, to develop the habit of hard work; emphasize whole-body exercises, such as walking, swimming and cycling. In terms of intensity, let children exercise until they feel a little tired, but to an acceptable degree. Each exercise time to maintain a minimum of 30 minutes, beginners can begin to exercise in sections, such as three times, each time 10 minutes, etc.. Exercise frequency of 5 to 7 times per week (emphasis on daily exercise); the above recommended amount of exercise must be maintained for 18 weeks or more. Exercise should be step-by-step and gradual; encourage parents, other family members or friends to exercise with children; parents should appreciate and encourage children if they put in efforts and make progress, such as weight loss, fat loss, and increased exercise.
To modify behavioral habits, the purpose of behavior modification is to establish some new exercise habits to replace the previous inappropriate diet and exercise habits.
The following are some suggestions.
1.Establish good eating habits, eat three balanced meals every day, do not eat on the side, do not miss one of the meals, do not eat too much, do not let children develop the habit of snacking, can choose some moderate amount of healthy snacks in a regular period of time to eat.
2, establish healthy behavioral rewards, do not use food (such as taking children to McDonald’s and other large meals and so on) as a reward for good behavior, turn interest to other projects, such as going to the park, doing outdoor activities, etc.
For fatty liver that has developed liver function impairment, appropriate medication can be used in conjunction with treatment, but the choice of medication should be streamlined. While treatment remains focused on diet adjustment and moderate exercise, most children with fatty liver can be cured.
Adults: In recent years, the prevalence of non-alcoholic fatty liver disease in adults has been on the rise. 8 years ago, a survey was conducted in Shanghai among white-collar workers, and the detection rate of fatty liver was 12 or 9%; nowadays, the proportion of fatty liver detected among white-collar workers has reached more than 20%, and there is a tendency of gradual under-ageing. However, there are still many misconceptions about fatty liver, and some effective prevention and treatment methods are still not well implemented. Statistically, the common misconceptions are as follows.
One of the misconceptions: fatty liver is not a disease, it does not matter if you look at it or not
With the increase in the detection rate of fatty liver in the surrounding population, people have become unconcerned about it, and always think that fatty liver is at most a sub-healthy state, not a real disease, and no treatment is needed. So is fatty liver a disease or not, and should it be treated?
The medical profession used to believe that NAFLD is a pathological state of excessive fat accumulation in the liver and does not cause hepatitis or liver fibrosis. However, a large number of studies in recent years have shown that NAFLD is a chronic disease closely related to lifestyle behaviors for three reasons.
1, at least 20% of NAFLD is non-alcoholic steatohepatitis rather than simple fatty liver, and non-alcoholic steatohepatitis is now clearly an important precursor lesion to cryptogenic cirrhosis and hepatocellular carcinoma, and a rare cause of liver failure;
2, even if it is simple fatty liver, fatty liver is more vulnerable than normal liver, more vulnerable to drugs, industrial toxins, alcohol, ischemia and viral infection, which leads to higher incidence of other types of liver disease, and fatty liver as a donor liver for liver transplantation is very likely to transplantation liver non-functional;
3, for overweight and obese people, the appearance of fatty liver may indicate “malignant obesity”, because such people are prone to hyperlipidemia, diabetes and hypertension, and eventually the probability of coronary heart disease, stroke will also increase significantly. For this reason, whether from the perspective of liver disease or diabetes and cardiovascular disease prevention and control, non-alcoholic fatty liver disease should be considered as a disease, and its scientific name should be non-alcoholic fatty liver disease. Therefore, even asymptomatic fatty liver found in health checkups should not be taken lightly and should be treated in hospital in a timely manner.
Myth #2: Fatty liver is not curable at all
Clinically, many patients with fatty liver have visited many hospitals for a long time and tried a lot of drugs, but they do not see any improvement, so they pessimistically believe that fatty liver cannot be cured.
In fact, simple fatty liver is an early manifestation of various hepatotoxic injuries, and if the cause is removed and the primary disease is controlled in a timely manner, the fatty deposits in the liver can be completely eliminated within a few months. For example, alcoholic fatty liver is absolutely effective; most drugs and industrial toxic fatty liver can be recovered after timely discontinuation of the drugs or after leaving the toxic working environment; malnutrition fatty liver can be improved after supplementation of calories and protein; and obese fatty liver can be quickly eliminated if the weight can be effectively controlled and the waist circumference can be reduced. However, if simple fatty liver has developed into steatohepatitis, it often takes half a year or even more than a few years for the lesion to recover completely, and a few patients can progress to irreversible cirrhosis even if the cause is removed. Therefore, early diagnosis and treatment of fatty liver should be strengthened. Some patients with fatty liver may have difficulty recovering because of untimely treatment or inappropriate treatment methods and inadequate duration of treatment.
Myth No. 3: Treatment of fatty liver mainly relies on liver-protective drugs
Many patients often turn to major hospitals or pharmacies for special drugs to treat fatty liver. In fact, no panacea for fatty liver has been found at home and abroad, and it is more important to lose weight through diet and exercise than liver-protective drugs to prevent and treat obese fatty liver, especially simple obese fatty liver. For non-alcoholic steatohepatitis with elevated transaminases, weight loss is an important prerequisite to ensure the effectiveness of hepatoprotective drugs. In the past, weight loss has been taken lightly, and even many clinicians mistakenly believe that “no medication means no treatment”. In fact, in the comprehensive treatment of fatty liver, hepatoprotective drugs are only an adjunctive measure, mainly used for patients with steatohepatitis with elevated transaminases, and are a short-term reinforcement; what needs to be highly valued and adjusted in the long term is the patient’s diet, exercise and modification of bad behavior. These non-pharmacological measures need to be carried out for life, otherwise fatty liver will recur even after it is cured. Therefore, patients with fatty liver must understand the importance of active participation in treatment and strive to identify and correct their poor diet and lifestyle habits, rather than thinking that health can be achieved simply by spending money on medication.
Myth No. 4: With fatty liver, you have to take lipid-lowering drugs
Although hyperlipidemia and fatty liver are closely related, the two are usually not causally related, and there are no formal clinical trials at home and abroad on the effectiveness of lipid-lowering drugs in reducing fat deposits in the liver. For this reason, it is not always necessary to take lipid-lowering drugs when you have a fatty liver, and the improper application of lipid-lowering drugs can sometimes aggravate liver damage instead of reducing fatty liver. The reason for this may be that the appearance of fatty liver represents the limit of the liver’s ability to deal with disorders of lipid metabolism, at which point the use of lipid-lowering drugs is equivalent to “whipping a fast cow”, that is, the fatty liver’s tolerance to lipid-lowering drugs is reduced, and improper application is prone to drug-related liver disease.
The current belief is that fatty liver is not accompanied by hyperlipidemia, then do not use lipid-lowering drugs. If you have fatty liver and hyperlipidemia, you need to decide whether to use lipid-lowering drugs according to the cause and degree of hyperlipidemia and the probability of atherosclerotic cardiovascular lesions. If it is caused by alcoholism, then quitting alcohol is good for lowering blood lipids and reducing fatty liver; if it is caused by drugs, try to stop the drugs if you can, but if you can’t quit drinking or stop the drugs and the increase in blood lipids is not too obvious, don’t mind it, because if you “manage” it, it may increase the burden on the liver. For hyperlipidemia caused by obesity and diabetes, if the blood lipids are not very high, the main way to adjust the blood lipids and prevent fatty liver is through diet and exercise to control weight and blood sugar; if the blood lipids are still high after 3 to 6 months of treatment, then lipid-lowering drugs can be used, but it is often necessary to reduce the dosage appropriately or combine with liver-protective drugs. Those who have a family history of hyperlipidemia and have a significant increase in lipids should be treated with lipid-lowering drugs, because at this time, lipid-lowering drugs can play a role in “treating both the symptoms and the root cause”.
Myth No. 5: Fatty liver with elevated transaminases need to take enzyme-lowering drugs
In the past, people often mistakenly believe that increased serum aminotransferase is hepatitis, while hepatitis is viral and contagious. As long as the aminotransferase is reduced to normal, then even viral hepatitis is not to be feared. For this reason, once elevated aminotransferases are found, people are often eager to apply drugs to bring them down to normal so that they can resume their “normal lives”. This is a self-deceptive approach that can lead to the deterioration of liver disease by concealing the disease and relaxing the implementation of basic treatment.
Epidemiological surveys have shown that the increased transaminases found in adults or children with fatty liver are mainly related to obesity and fatty liver, and that such increased transaminases are not contagious. It may seem unbelievable that a weight loss of 5-10% in 3-6 months can bring the increased serum transaminases of obese fatty liver patients to normal levels. There are reports that for every 1% reduction in body weight, transaminases drop by 8 or 3%; 10% reduction in body weight, the increased transaminases basically return to normal, with the enlarged liver shrinkage and fatty liver reversal; while those with high body weight often continue to increase transaminases, even if the application of liver protection and enzyme-lowering drugs are also difficult to work.
Myth No. 6: Fatty liver with elevated transaminases cannot be more active
Clinically, about 10% of patients with non-alcoholic fatty liver disease have elevated serum transaminases. Unlike acute viral hepatitis, non-alcoholic steatohepatitis does not require rest and nutrition, nor does it require disinfection and isolation measures. However, clinicians, family members and colleagues often ask patients to be less active and rest more, resulting in weight and waist circumference gain, serum aminotransferase abnormalities and persistence of fatty liver.
Epidemiological surveys have shown that obese fatty liver with elevated transaminases is closely related to a westernized diet and a sedentary lifestyle, and that moderate aerobic exercise for more than 150 minutes per week, along with a moderate diet, is the most effective treatment. Therefore, instead of taking more rest, patients with fatty liver with elevated transaminases need to increase their exercise. The best exercise for patients with fatty liver is to walk briskly, at least 3 km at a time, more than 5 times a week.
Myth No. 7: Chronic viral hepatitis combined with obesity fatty liver antiviral treatment is the most important
China is a large country with chronic hepatitis B virus infection, and in recent years the number of obese fatty liver patients has been increasing, the probability of the combined existence of the two diseases is increasingly high. For the treatment of patients with obesity, fatty liver and hepatitis B virus infection with elevated transaminases, antiviral drugs are usually thought of. In fact, not all liver damage in patients is caused by viral infection, and if it is not caused by viral infection, it is useless for you to use antivirals. In addition, even in hepatitis B, the presence of obesity and fatty liver can greatly reduce the probability of successful antiviral treatment. For this reason, in cases where chronic viral hepatitis coexists with obese fatty liver, weight loss treatment should be considered first. If the patient’s transaminases and fatty liver return to normal after weight loss, then the main conflict is obesity rather than viral infection, there is no need for antiviral therapy; if the patient’s transaminases continue to be abnormal after six months of weight loss treatment, then it is not too late for antiviral therapy, after all, it is easier to manage their weight, and the antiviral therapy is long, costly and has a low success rate.
Myth No. 8: Obese fatty liver patients have more fruit is good
Fresh fruit is rich in water, vitamins, fiber and minerals, and is undoubtedly beneficial to health when consumed regularly. However, the health effects of fruit are not the better. Because fruit contains certain sugars, long-term excessive consumption can lead to increased blood sugar and blood lipids, and even induce obesity, so obese, diabetic, hyperlipidemic and fatty liver patients should not eat more fruit.
At present, we should always consider the possible health hazards of excess dietary calories, and should use fruits with low sugar content such as apples and pears as far as possible, and the amount should not be too much, and if necessary, replace fruits with vegetables such as radishes, cucumbers and tomatoes; try to eat fruits before meals or between meals when hungry, in order to reduce the amount of meals eaten. Similarly, milk rich in protein and calcium is good for health in moderation, but a glass of milk before bedtime may not be suitable for obese fatty liver patients because it is easy to cause excess calories.
In short, for the masses after the solution of food and clothing, what is lacking is not “nutrition (calories)”, but exercise; what is urgently needed is not supplements and drugs, but a scientific lifestyle. At present, as long as we can “eat less, move more, drink less and use drugs carefully”, we will be able to effectively control the increasingly serious prevalence of fatty liver. Community intervention and guidance are particularly important. It is necessary to establish a long-term mechanism for community intervention.