In 2009, allegations that insulin causes cancer grabbed headlines. Experts from the American Diabetes Association and American Cancer Society evaluated this relationship but could neither confirm nor deny it. “Many patients with diabetes stopped taking their medications because of these unfounded allegations,” says Yehuda Handelsman, MD, FACP, FACE, FNLA. Recently, a task force from the American Association of Clinical Endocrinologists and American College of Endocrinology reviewed the roles of obesity and diabetes and their therapies in the context of the pathogenesis of cancer and published a consensus statement on the topic in Endocrine Practice.
Assessing the Link
It may generally take as long as 10 to 50 years for cancer to develop after a cell is exposed to a carcinogen. “Many of the allegations suggesting that diabetes medications may be responsible for the development of cancer were based on exposure of 6 to 24 months, making their role unlikely,” says Dr. Handelsman. Many of the publications implicating insulin in the increased long-term cancer risk were based on retrospective data on 3 to 5 years of insulin exposure.
The statement also notes that obese patients are at increased risk for cancer when compared with the general population, and patients with diabetes have a slightly higher risk of cancer than obese patients. As such, the task force recommends that patients with diabetes or obesity be screened early for cancer. It also recommends that young adults with cancer be screened for metabolic conditions.
With no direct relationships between diabetes medication and cancer development being proven, Dr. Handelsman says there is no reason for physicians to change how they manage diabetes, and patients should feel confident to continue with their current care. “The key, however, is to follow FDA recommendations to not use specific drugs, such as with pioglitazone in patients with bladder cancer and GLP-1 receptor agonists in patients with thyroid carcinoma.” He adds that there is no evidence of increased risk of pancreatic cancer in patients taking incretin-based therapy. “Chronic pancreatitis is required to develop pancreatic cancer,” Dr. Handelsman adds. “The incretin studies showed a minimal increase in acute pancreatitis, making the development of cancer via this method unlikely.”
Dr. Handelsman says collaboration between the fields of diabetes and cancer research is warranted. “Research on cellular changes in obesity is necessary and should go beyond single implications and single pathophysiological processes,” he says. “Studies involving medications should also focus on whether they increase or decrease cancer risk. Long-term population-based studies can also help since cancer development is a long-term process. This research will require many years and dollars, but it’s important considering how many Americans are affected by these diseases.”
Readings & Resources (click to view)
Handelsman Y, Leroith D, Bloomgarden Z, et al. Diabetes and cancer: an AACE/ACE consensus statement. Endocr Pract. 2013;19:675-693. Available at www.aace.com/files/position-statements/diabetes-and-cancer-consensus-statement.pdf.
Roberts D, Dive C, Renehan A. Biological mechanisms linking obesity and cancer risk: new perspectives. Annu Rev Med. 2010;61:301-316.
Druesne-Pecollo N, Touvier M, Barrandon E, et al. Excess body weight and second primary cancer risk after breast cancer: a systematic review and meta-analysis of prospective studies. Breast Cancer Res Treat. 2012;135:647-654.
Sinicrope F, Foster N, Sargent D, et al. Obesity is an independent prognostic variable in colon cancer survivors. Clin Cancer Res. 2010;16:1884-1893.
Waalkes S, Mersebruger A, Kramer M, et al. Obesity is associated with improved survival in patients with organ-confined clear-cell kidney cancer. Cancer Causes Control. 2010;21:1905-1910.