PIllness containers often include warnings about certain foods and drinks to avoid when taking certain medications. for example, grapefruit Juicing prevents the breakdown of statins in the intestines, causing the drugs to remain active in the body for a long time.1 Similarly, when consumed, alcohol Combining drugs is dangerous because it can alter the liver’s drug metabolism, causing additional or exaggerated side effects and possible liver damage by overtaxing the metabolic functions of the entire body. There may be cases.2
However, not all diet-drug interactions are bad. In recent research, davide ruggeroA cancer biologist at the University of California, San Francisco, he and his team have discovered that a high-fat, low-carbohydrate diet, known as a ketogenic or ketogenic diet, can remodel the translatome, or collection of molecules. I discovered something. Translation is active in fat-loving pancreatic cancer cells in mice. These modifications have enhanced the effectiveness of targeted cancer treatments to inhibit tumor growth. The survey results are naturelaid the foundation for researchers to study personalized drug and diet combinations as potential cancer treatments.3
“We live in an era where a variety of diets, such as intermittent fasting, ketogenic diets, and calorie restriction, are increasingly being used for metabolic diseases such as diabetes. When you think about it, there’s a lot of emphasis on using these diets,” Ruggiero said.
Previously, Ruggiero had discovered that mice on fasting or ketogenic diets Eukaryotic translation initiation factor (eIF4E)helped liver lipid metabolism.4 In their recent study, the team hoped to uncover the metabolic mechanisms underlying this beneficial effect and explore how the ketogenic pathway could be harnessed to promote cancer treatment.
First, the research team characterized the relationship between high fat and eIF4E by measuring high fat and eIF4E activity in the liver. Their experiments showed that a ketogenic diet increases fatty acids in the liver and initiates ketogenesis by activating a pathway that begins with phosphorylation of eIF4E. Increased phosphorylation of eIF4E altered translational control in hepatocytes and increased expression of genes involved in fat metabolism. This caused a metabolic change that burned fat for energy instead of the typical glucose. When fat is burned, ketone bodies are produced in the animal’s blood, which is a hallmark of a ketogenic diet.
Pancreatic cancer is one of the most deadly cancers. Ketone bodies serve as an energy sourceas a typical glucose replacement.3,5 So Ruggero and his team wondered if they could make pancreatic cancer cells dependent on this eIF4E-initiated energy pathway simply by changing the animals’ diets.
Ruggero’s team used a mouse model of pancreatic cancer to test the effects of a combination of tomibosertib, a drug that inhibits phosphorylated eIF4E, and a ketogenic diet. When the only food source was pharmacologically blocked, cancer cells were starved and tumor growth was stopped. However, the compound had no effect on mice fed a normal diet.
“It was a great result,” Ruggiero said. “Cancer is not made of cells from space or Mars or whatever, it’s actually a process that takes over something that was already happening.” [in our bodies] For other reasons. ”
“The buzzword now is ‘diet-drug interaction,'” he said. michael pollackan oncologist and researcher at McGill University, was not involved in the study. “If there was a diet that would cure cancer, that would definitely be my first choice,” Pollack said. Unfortunately, the scientific evidence shows otherwise, Pollack noted. “Although dietary modifications alone may not have a transformative effect, they may actually sensitize the tumor to certain drugs,” he explained.
Preclinical cancer studies in mice have shown some promise. keto diet.6 However, human experiments in this field It was difficult to interpretin part, There are many different methodsand the ideal combination of foods against different types of cancer is still unknown, so in this field draw a strong conclusion.7-9
Next, Ruggiero and his team want to investigate how and why different types of cancer respond more or less to different types of diets and therapies to help develop effective personalized medicine. I am. Mr. Ruggiero said: “We always think about personalized medicine from a pharmacological perspective. The great thing here is that if you can think about personalized medicine based on what you want to eat and what you can eat, patients…[to] We will self-guide treatments to increase the effectiveness of drugs. It’s great to think about personalized medicine based on food. ”
