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Pancreatic cancer (PC) is a malignant tumor with high aggressiveness, easy metastasis and chemoresistance. Patients with PC have a very poor survival rate due to the difficulty of early diagnosis. It is estimated that 90% of PC cases are caused by environmental risk factors. About 50% of PC diseases are preventable from an unhealthy diet. Given this major feature of diet, many studies have evaluated the association between various dietary factors and PC. This article covers the ketogenic diet (KD), the Mediterranean diet (MD), and the low-carb diet. Their composition and mechanism of action are summarized and discussed. The associations between these three types of diet and PC were analyzed, and we aimed to provide more support and new insights for the prevention and treatment of PC.
Diet For Pancreatitis Patient
Pancreatic cancer (PC) is known for its insidious nature, rapid aggressiveness, and poor prognosis (1). Although radical resection is currently the primary treatment option, many patients miss the opportunity due to early clinical manifestations. Although great advances have been made in radiotherapy (RT), chemotherapy, and immunotherapy in recent years, the desired results have not yet been achieved (2). Avoiding high risk factors is the first and most critical step in changing its incidence. Current evidence suggests that one-third of cancers can be prevented by reducing risk factors, with unhealthy diet being one of the most important factors (3). Dietary composition can influence tumor growth and development, creating potential synergism or antagonism between new or existing drugs (4). Diet affects tumor growth through a variety of mechanisms that alter the metabolism of cancer cells (Figure 1). Dietary composition may even improve prognosis by influencing drug efficacy and resistance (5). Research on the relationship between dietary composition and cancer risk is becoming increasingly important. This review highlights several different typical diets and analyzes the effects of certain dietary components on PC therapy. The aim is to deepen knowledge about the role of diet in PC and the underlying mechanisms, which will provide evidence for further development of PC prevention strategies. Second, we hope that this research will fill in the gaps in computer therapy and improve treatment efficacy and patient survival. Finally, we aim to advance the field by promoting multidisciplinary research.
Pancreatic Enzyme Therapy (29.08.2011)
There is no clear definition of KD. Thus, many studies have defined it as any food that causes an increase in blood ketones (6), such as foods in which more than 50% of total calories come from fat (7). However, KDs are typically characterized by high fat, moderate protein, and very low carbohydrate intake. A classic KD consists of four parts fat, one part carbohydrate and one part protein (4:1:1) (8). It provides 90% of calories from fat, 8% from protein, and only 2% from carbohydrates. However, KDs used in clinical settings have ratios of fat to carbohydrate and fat to protein of at least 2:1 and 3:1 (9). KD’s development is pretty complete so far. All fluids and parenteral KD have been studied (10), so diet is often started in the outpatient setting (11).
KD is considered a widely used metabolic therapy in the treatment of epilepsy (12). Recent studies in the past decade have demonstrated the therapeutic potential of KD in many disease conditions, including diabetes, polycystic ovary syndrome, acne, neurodegenerative diseases, malignancies, and improving risk factors for respiratory and cardiovascular diseases (13, 14). A growing body of preliminary research suggests that KD as a dietary intervention is a potent cancer treatment (15).
Various investigators have used the term “therapeutic ketosis,” which refers to the achievement of plasma ketone body levels between 2 and 7 mmol/L, relative to concentrations maintained on various KDs. KD causes an increase in ketone bodies without restricting energy intake, which is an obvious advantage in the cancer setting (17). KD suppresses the Warburg effect by inducing tumor starvation, which is generally believed to be its anti-bacterial mechanism ( 18 ). The Warburg effect is mainly characterized by maintaining glycolysis as an energy source for tumor cell growth and biosynthesis in cancer (19). Glucose dependence and lactate production have been recognized as two important characteristics related to the invasiveness and invasive potential of cancer cells (20). Normal cells readily use ketones as an alternative energy source, and elevated ketone body levels cause a shift in the cellular energy supply from glucose to fatty acids and ketones (21). Cancer cells are unable to metabolize ketone bodies due to their metabolic inflexibility (22). As a result, ketone bodies cannot be consumed and tumor growth is inhibited (23). Many studies have shown that KD has positive effects on various cancers and can delay the development of gastric cancer, prostate cancer, and brain cancer in mouse models (24, 25). In addition, KD has been found to suppress tumor growth by inhibiting angiogenesis and reducing tumor volume in early trials (26). This function is associated with decreased glucose availability, insulin, and circulating insulin-like growth factor (IGF)-1 levels ( 27 , 28 ). Ketosis has been shown to be inversely related to serum insulin levels and associated with stable disease or partial remission (29).
Husain et al. . This suggests that multiple mechanisms may underlie the efficacy of KD in cancer therapy, far beyond the originally proposed inhibition of glucose/insulin signaling, including oxidative stress, mitochondrial metabolism, and inflammation. Increased oxidative stress and production of reactive oxygen species (ROS) lead to mitochondrial damage (32). In addition, chronic inflammation in persistent hypertension also represents an important source of intratumoral ROS production ( 33 ). Stafford et al. (34) reported that KD reduced tumor growth and prolonged survival by decreasing ROS production in cancer cells. Ketosis protects against oxidative stress in healthy tissues by simultaneously increasing antioxidant capacity and reducing ROS production. In addition, cancer cells are inefficient in metabolizing toxins (28). These factors selectively inhibited KD metabolism in cancer cells but not in normal cells.
Exocrine Pancreatic Insufficiency (epi)
Surgery is still the primary treatment for PC, and radical tumor resection can significantly reduce the risk of cancer recurrence and increase the 5-year survival rate (36). However, patients with pancreatic adenocarcinoma are prone to malnutrition and weight loss due to complications such as pancreatic insufficiency and delayed gastric emptying. KD has been shown to improve meal compliance, satiety, and energy intake in post-pancreatectomy patients without increasing gastrointestinal complications. It is a safe way to increase energy and nutrient intake in pancreatic cancer patients after surgery (38, 39). Unfortunately, only 20% to 30% of PC patients are candidates for surgical resection because most are diagnosed as locally advanced PC or metastatic PC (40). Consequently, chemotherapy must have a survival benefit in these patients. Recent guidelines recommend pearl metabolic therapy or pearl-based combination therapy. However, even the FOLFIRINOX (5-fluorooxide, folic acid [leucovorin], irinotecan, and oxaliplatin) regimen is considered an option for some patients (41, 42). RT, chemotherapy, and the current standard nonsurgical therapies for cancer treatment share a common mechanism, which is to kill cancer cells by increasing the production of ROS ( 43 ). Therefore, the use of KD during therapy selects the sensitivity of tumor cells to RT and chemotherapy by inducing oxidative stress.
Metabolic chemotherapy (MSCT) is a novel approach that targets dysregulated energy mechanisms of tumor cells and is commonly combined with KD, hypertensive treatment (HT), and hyperbaric oxygen therapy (HBOT) in advanced PC patients. A clinical trial investigated the effects of MSCT (administered concurrently with gambitabine-based or FOLFIRINOX-induced hypoglycemia) and the combination of KD, HT, and HBOT. A total of 25 patients with metastatic pancreatic ductal carcinoma (PDAC) were enrolled and previous data were compared. The results showed that the median survival was about 6.8 months for the patients who received the gemcitabine alone, and 11.1 months for the FOLFIRINOX group. Encouragingly, the combination of KD and MSCT resulted in a median survival of 15.8 months and progression-free survival of 12.9 months (Figure 2) (47). Talib et al. . In addition, there is evidence of increased survival in mice with high-grade glioma, lung, or PC cells when mice receive KD in combination with RT. ONE
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