Liver cancer, here's the right diet to help reduce its risk and slow its progression

Do you suffer from liver steatosis, with fat pervading the organ and slowing down the body's laboratory activity? If you are in this condition or otherwise have reduced liver function, be careful not to overdo it with protein. And do the same, always following your doctor's advice for specific dietary habits to reduce the risk of developing a liver tumour or to slow down its progression if the neoplasm is already present. Limiting protein intake, in fact, could prevent those alterations in the organ's metabolic 'waste' disposal processes that could somehow function as fuel for the pathological cells. The usefulness of a low-protein diet to protect the liver when it is not working well or has already developed a tumour is raised by research conducted in the laboratory, on animals only. But the resulting working hypothesis is nonetheless interesting. Because the study unveils a mechanism that could potentially explain how and to what extent excess protein could promote tumour development by directly feeding neoplastic cells.

The investigation, published in Science Advances, was conducted by experts at Rutgers University coordinated by Wei-Xing Zong. Basically, it sheds light on a pathway that, although demonstrated experimentally, seems to be able to occur in humans as well, given the right proportions. The key lies in the breakdown of dietary protein, which can naturally also be converted into ammonium, a toxic compound. While ammonium is converted into urea in the healthy liver and then eliminated in the urine, if it accumulates because the organ does not function due to a liver tumour, this mechanism is altered. The study aimed to answer this very question: is the impairment of liver function and thus the accumulation of ammonium only a consequence of the tumour or can it be the 'fuel' for neoplastic growth? The experts, starting from this question, first induced tumours in animals without altering the ammonium disposal systems, then using genetic editing techniques they deactivated the enzymes that process ammonium in some animals and not in others. Result: mice with deactivated enzymes and higher ammonium levels developed larger tumour loads and showed a much faster mortality rate than those with functioning systems. The reason? By tracing excess ammonium, it was seen to migrate into molecules that help tumour cells thrive, as ammonium itself is converted into amino acids and nucleotides, both of which tumour cells depend on for growth.

Once this mechanism was demonstrated, the scientists tried to intervene with a very simple dietary approach, i.e. reducing protein intake. In animals with tumours, a diet of low-protein foods was found to result in significantly slower tumour growth and longer life expectancy compared to other animals that were fed a diet of standard protein levels. In short. While those with a healthy liver need not worry, as their metabolism can handle even a high protein intake, in the presence of liver cancer, hepatic steatosis, viral hepatitis or other diseases it is always a good idea to talk to your doctor, remembering that any changes to the diet should be decided with a nutritionist. It should not be forgotten that standard dietary guidelines for cancer sufferers generally recommend a higher protein intake to help patients maintain muscle mass and strength, combating sarcopenia. Therefore, during treatment for cancer, the patient's health status and liver function should always be considered, always remembering that in the presence of high ammonium levels, a reduction in dietary protein may be indicated. 'If you suffer from a liver disease or damage that prevents proper liver function, you should seriously consider reducing your protein intake to reduce your risk of developing liver cancer,' is the advice offered by Wei-Xing Zong in a note from the American University.

'The study highlights, in animals, how in the presence of a liver tumour, the accumulation of ammonium linked to the degradation of proteins introduced in the diet is not only a consequence of the tumour, but can also be a fuel for neoplastic growth,' reports Giammarco Mocci, Medical Director SC Gastroenterology, ARNAS G. Brotzu of Cagliari. So much so that, by subjecting animals with liver cancer to a low-protein diet, the researchers observed much slower tumour growth than in animals that had been fed a diet with standard levels of protein'. In this sense, therefore, these observations, albeit only experimental, warn against excess protein in the diet, especially when the liver is not functioning properly. And they confirm how important it is to be careful with one's diet. 'For years, research has shown that a high-protein diet followed over time can fatigue the liver, which is responsible for protein metabolism,' says Mocci. This can lead to an increase in the deposition of triglycerides inside the liver cells, the hepatocytes, and in particular seems to produce a dramatic increase in a protein used as a marker of liver damage, as it is linked to hepatic steatosis and hepatocarcinoma. In the presence of even a 'fattened' liver with hepatic steatosis, therefore, it is better to favour fibre-rich foods, such as legumes and vegetables, lean protein sources, such as fish, and avoid foods rich in simple sugars and saturated fats. But above all, let's avoid DIY and rely on doctors, specialists in the field of nutrition'.

Hepatic steatosis, or MASLD (steatotic liver disease associated with metabolic dysfunction), is characterised by an accumulation of fat in the liver. It can progress to MASH (steatohepatitis associated with metabolic dysfunction), during which fibrosis and, eventually, cirrhosis and tumours can occur. Of concern in the latter case is the association of steatosis with inflammation, which progressively damages hepatocytes. These two mechanisms, especially if one consumes alcohol and has a diet particularly rich in lipids, especially those of animal origin, make it more difficult to dispose of or at least transform fatty lipids into energy, which then accumulate. Hence, liver cells burst with fat, break down and fatty tissue gradually replaces the active one. The proof of these cell 'explosions' comes from a parameter that is easily observed with a simple blood test. The 'transaminase' enzymes (those found in blood tests with the initials GOT and GPT) escape from the altered cells.