Article
Fasting Blood Glucose and Pancreatic Cancer: Possible Link
Author(s):
The incidence and mortality of pancreatic adenocarcinoma, the fourth leading cause of cancer deaths in the United States, are both on the rise. Globally, the disease is responsible for 227,000 deaths annually. Researchers from the National Taiwan University College of Medicine recently published a meta-analysis that demonstrated a dose-response relationship between fasting blood glucose levels and pancreatic cancer risk. They also examined the link between prediabetes and pancreatic cancer risk.
The incidence and mortality of pancreatic adenocarcinoma, the fourth leading cause of cancer deaths in the United States, are both on the rise. Globally, the disease is responsible for 227,000 deaths annually. Researchers from the National Taiwan University College of Medicine recently published a meta-analysis that demonstrated a dose-response relationship between fasting blood glucose levels and pancreatic cancer risk. They also examined the link between prediabetes and pancreatic cancer risk. This study appears in the online issue of BMJ.
The connection between type 2 diabetes and cancer risk has been previously established, but studies exploring the connection between prediabetes and pancreatic cancer risk have yielded mixed results. The authors sought to clarify these results, and for the first time to examine linear and non-linear connections between fasting blood glucose and cancer risk.
Their meta-analysis incorporated 9 different studies for a total of 2408 pancreatic cancer-stricken patients. Due to the fact that pancreatic adenocarcinoma induces diabetes in approximately 40% of patients, the researchers eliminated retrospective studies to avoid reverse causality. After compiling appropriate studies for inclusion, they employed assorted statistical analyses to demonstrate the significance of their findings.
The researchers discovered that a 10 mg/dL increase in fasting blood glucose corresponds to a 14% increase in the rate of pancreatic cancer. They demonstrated that this dose-response relationship was linear and suggested that the underlying mechanism is pancreatic cancer cells’ increased glucose requirement for growth. The authors further observed that risk of developing pancreatic cancer increases in patients with type 2 diabetes and also in prediabetic patients.
The authors concluded that this finding, previously considered but unsubstantiated, highlighted the importance of the early detection of prediabetes. They consider prediabetes to be a modifiable risk factor for pancreatic cancer. They suggest that increased efforts to promote lifestyle changes in prediabetics could net reductions in cancer incidence and ultimately lead to long-term savings for health-care systems.
