Published September 24, 2013
Being overweight or obese is known to be associated with an array of health issues, such as cardiovascular disease and diabetes. But obesity and poor nutrition can also lead to another lesser known, yet very serious, health outcome: cancer.
According to the National Cancer Institute, obesity is associated with an increased risk of many types of cancers, but it is most strongly linked with cancers of the gastrointestinal tract, pancreatic cancer and post-menopausal breast cancer. One study estimated that if current trends continue, obesity will lead to approximately 500,000 additional cases of cancer by 2030.
Many theories exist as to why obesity directly increases the risk of cancer, and now, one NYU Steinhardt researcher may have pinpointed an underlying biological mechanism responsible for the obesity-cancer link. In a large population-based study, nutritional epidemiologist Niyati Parekh found that disturbances in body insulin and glucose levels were associated with obesity-related cancers – a finding that could lead to better treatments and management of these diseases.
“I knew there were a lot of underlying nutritional factors that could either prevent the recurrence of cancer or prevent cancer in general,” Parekh, an assistant professor within NYU Steinhardt’s department of nutrition, food studies and public health, told FoxNews.com. “Obesity is a very big problem in the United States...I wanted to know, what could the underlying mechanisms be in population studies?”
For her research, Parekh utilized data from the Framingham Heart Study, a 60-year research study funded by the National Institutes of Health that had initially been created to look for common factors or characteristics related to cardiovascular disease. Parekh was able to analyze a generation of approximately 4,600 participants, examining data in regards to their diets, medical issues, blood and physical history.
Through in-depth analysis of the study cohort, Parekh found an increased risk of obesity-related cancers among people with disturbances in their body insulin and glucose, conditions primarily associated with diabetes and pre-diabetes. The risk was even greater for individuals who had longer exposure to these disturbances prior to their cancers.
Parekh noted that her findings support what is known as the insulin-glucose hypothesis – one theory researchers use to explain the obesity-cancer association.
“Obese people are more likely to have (abnormal) insulin levels in their blood,” Parekh said. “Insulin is the gatekeeper for glucose entering the cells, so when insulin production is disrupted, (higher values of) glucose remain in the blood…And an increase of glucose in the blood creates an environment that is conducive for cancer cells to grow quickly.”
According to Parekh, glucose is the primary source of energy for many cells in the body, and cancer cells also use the sugar in order to replicate very quickly. Therefore, higher amounts of glucose in the blood stream may help provide a direct line of fuel for cancer cells to grow and spread.
Additionally, higher rates of insulin can also help to foster the spread of cancer, as insulin is a hormone known for encouraging cell growth.
“Insulin dictates many signaling pathways, and it has the ability to turn on and turn off genes,” Parekh said. “The pathways are stimulated to encourage cell growth, proliferation, and (metastasis)."
With the discovery of this underlying biological mechanism, Parekh hopes doctors and patients with obesity-related cancers will understand that treating weight issues is just as important as treating the cancer itself.
“It’s important for physicians or oncologists to consider comprehensive treatment,” Parekh said. “If a (patient) goes to the oncologist for cancer treatment, they may want to get rid of the tumor but not get rid of the diabetes. There needs to be recognition that they need to lose weight and also avoid diets that enhance glucose and insulin in the blood….They have to recognize this is an issue.”
The research was published in journal Cancer Epidemiology, Biomarkers, and Prevention and was funded by the National Cancer Society.