# Consequences of Glucose Enriched Diet on Oncologic Patients
## 2 Conclusions  
Life requires nutrients, and the availability of nutrients regulates cell death. The metabolic regulation of cell death probably happens on multiple levels, ranging from the control of BH3-only protein stability and stimulation to the control of caspase stimulation in the Death Inducing Signaling Complex. Utilizing the glucose requirement of tumor cells for diagnostic purposes, because tumor cells demand more glucose than normal cells, clinical studies were designed that have demonstrated that antipsychotics often induce cell death in tumor cells. Surprisingly little is known about the apoptotic pathways implicated in tumor cell death in response to fasting. The apoptotic role of BH3-specific proteins or caspase-8 has only been examined in non-transformed cells or in a few tumor cell lines in a number of previously cited studies. In addition to these few studies, the precise mechanisms by which glucose deprivation or antipsychotics destroy tumor cells remain unknown. Numerous tumor cells experience necrosis and perish in the absence of glucose, as proven by research. Molecules like RIPK1 are particularly effective in controlling some types of necrosis; understanding the probable molecules associated with tumor cell necrosis would help in its pharmaceutical regulation. In addition, it would be beneficial to discover the key chemicals involved in the sensitivity of tumor cells to chemotherapy and radiotherapy in order to build more effective combinations with antipsychotics. All of these studies raise the potential that brief hunger can enhance the efficacy of chemotherapy. Calorie restriction is known to increase the life span. To determine whether this would be true for cancer patients, numerous additional clinical trials and tests would be required. Alternative dietary interventions appear to be viable methods for assisting cancer patients, however, patients could not accept them due to their strictness. Patients who were able to maintain low-carbohydrate diets demonstrated slower growth, improved health, or decreased tumor mass. Fasting can sensitize cancer cells to chemotherapy and redirect energy to the maintenance and repair of healthy cells. Alternately, fasting can also increase autophagy regulation, and its process can have a bidirectional effect. Despite the fact that dietary alterations of several of the investigated metabolites have exhibited demonstrable benefit and some of them have shown promise in clinical studies, there are currently no definite guidelines or proposed dietary modification regimens for cancer patients. It is improbable that there is a single dietary composition or prescription for the treatment or prevention of cancer that applies to the complete diet. The dietary requirements, metabolic activity, and preferred energy source of various cancer forms differ. In addition, dietary modifications can affect the effectiveness of the drugs. Moreover, dietary modifications will not modify nutrient levels uniformly in all tumor microenvironments and tissues, therefore, the efficacy of dietary adjustments is highly dependent on the location of the tumor. This implies that, similar to new drug combinations, the combination of dietary modification and medicinal therapy must be clinically customized and studied for each kind, grade, and location of cancer. On the basis of recent promising preclinical and clinical discoveries, it has been determined that certain dietary interventions must be clinically evaluated to establish their therapeutic potential. These include lowering carbohydrate intake, which is expected to be beneficial for a substantial proportion of cancer patients since they are safe and simple dietary adjustments that can be easily examined clinically for their benefit in specific situations. It has not been established that sugar consumption directly increases cancer risk or progression. However, sugars and beverages that are significant sources of these sugars contribute a large number of calories to the diet, which can lead to weight gain.