Feb 07, 2026
3 min read
By reducing proteins, the potential "fuel" of neoplastic cells, "waste" is more easily eliminated.Animal studies show this.
Liver cancer, here's the right food to help lower your risk and slow progression
Animal studies have shown that by reducing the proteins that are the potential "fuel" of neoplastic cells, the "waste" is eliminated more easily.
Main points
Take 5'
Are you suffering from fatty liver disease, where fat spreads throughout the organ and the body's laboratory activity decreases?If you are in this condition or have decreased liver function, be careful not to overdo it with protein.And do the same, always follow the doctor's recommendations for specific indications regarding eating habits to reduce the risk of developing liver cancer or its progression if the neoplasm is already present.In fact, by limiting protein consumption, we can somehow prevent changes in the processes of excretion of metabolic "waste" in the organ, which could serve as fuel for pathological cells.The usefulness of a low-protein diet to protect the liver when the liver is not functioning well or a tumor has already developed has been highlighted by studies conducted exclusively on animals in the laboratory.However, the resulting working hypothesis is interesting.Because the study reveals a mechanism that could potentially explain how and to what extent excess proteins can promote tumor development by directly feeding neoplastic cells.
The key is ammonium
The research, published in Science Advances, was conducted by experts at Rutgers University under the coordination of Wei-Xing Zong.It shows a route that, although essentially experimentally proven, appears to be possible in humans if the necessary proportions are given.The key is breaking down dietary proteins, which can actually be converted into the toxic compound ammonium.In a healthy liver, ammonium is converted into urea and then excreted in the urine.This mechanism changes when it accumulates due to organ failure caused by a liver tumor.The aim of the study was to definitively answer this question: Are the liver dysfunctions and thus the accumulation of ammonium just a consequence of the tumor or can they be “fuel” for the neoplastic growth?Starting from this question, without altering the ammonium excretion systems in animals and then using genetic editing techniques, experts have disabled the enzymes that process ammonium in some animals but not others.The result: mice with deactivated enzymes and high ammonium levels developed significantly more tumor burdens and showed a much faster death rate than those with active systems.The reason?It turns out that ammonium itself is converted into amino acids and nucleotides, both elements that cancer cells rely on for growth.
Ordinary food
When this mechanism was demonstrated, researchers tried to intervene with a very simple dietary approach, namely by reducing protein intake.In tumor-bearing animals, a significantly slower tumor growth with extended lifespan was observed in the presence of a low-protein diet compared to other animals fed a standard level of protein instead.In short, but those with healthy livers do not need to worry, because their metabolism can cope with a high protein intake, even in the presence of liver cancer, fatty liver disease, viral hepatitis or other pathologies, it will always be advisable to talk to the doctor, remembering that it is important to decide on any change in the diet with those who deal with nutrition.It should not be forgotten that the standard dietary advice for people affected by cancer usually recommends an increased protein intake to help patients maintain muscle mass and strength.do, which fights sarcopenia.During cancer treatment, it is therefore always important to consider the patient's health and the state of liver function, always remembering that in the presence of high ammonium values, a reduction in dietary proteins may be indicated.In a memo from the American University Vice Zhongzong presented."
"The study highlights, in animals, as in the presence of liver tumors, that the accumulation of ammonium associated with the breakdown of proteins introduced into the diet is not only a consequence of the tumor, but can also be a fuel for the growth of neoplastics - reports Giammarco Mocci, medical director of SC Gastroenterology, ARNAS G. Brotzu, who is so exposed to Liver that the animal is exposed to Cagliari. diet with a low protein content, the researchers observed the growth of tumors that grow much slower than in animals fed standard levels of protein. In this sense, thisthe observations, although only experimental, therefore warn of excess protein in the diet, especially when the liver is not working well.And they confirm how important it is to pay attention to the diet."Research has shown for years that a high protein diet, which you follow over time, can tire the liver, which is responsible for the metabolism of proteins. This can lead to an increase in the deposition of triglycerides in the liver cells, and in particular, they seem to cause damage to the liver proteins.steatosis In the presence of only one "fatty" liver, with fatty liver disease, it is therefore better to give preference to foods rich in fiber, such as legumes and vegetables, lean sources of protein, such as fish, avoiding foods rich in simple sugars and saturated fats.
What is steatosis and steatohepatitis
Fatty liver disease or MASLD (metabolic dysfunction liver disease) is characterized by excess fat in the liver.This can progress to MASH (Metabolic Dysentery), leading to fibrosis and eventually cirrhosis and tumors.In the second case, which is worrying, cirrhosis is associated with inflammation, which gradually damages liver cells.These two mechanisms, especially if you drink alcohol and have food rich in fat, especially of animal origin, it will be difficult to process the fat in the fat or at least convert it into energy.Then the liver cells burst with fat and disintegrate, and the adipose tissue gradually replaces the active one.(those found in the test) come from the transformed cells.
