The Failing Animal Research Paradigm for Human Diseases

“The history of cancer research has been a history of curing cancer in the mouse. We have cured mice of cancer for decades—and it simply didn’t work in humans.”

This statement was made by Richard Klausner, M.D., former director of the National Cancer Institute, to the Los Angeles Times(Cimons 1998). It is a statement that applies equally to many other common diseases. A decade ago, researchers reported on the existence of 195 published methods that prevented or delayed the development of type 2 diabetes in mice (Roep et al 2004). Yet none of these “breakthroughs” ever translated to human medicine.

What prevents successes in mice from becoming human cures and treatments? The reason is largely a simple one, as we showed when we recently analyzed the reputed contributions of mouse experiments to human type 2 diabetes research (Chandrasekera and Pippin 2013).

Type 2 diabetes (diabetes mellitus) is the fastest-growing disease in the United States, currently affecting approximately 26 million Americans, and estimated to quadruple in prevalence to affect one-third of Americans by 2050 (CDC 2011a). Type 2 diabetes is the seventh leading cause of death in the United States (CDC 2011b). It is a complex and multifactorial disease, characterized by many years (often decades) of sequential disruptions in glucose homeostasis. The pre-diabetes stage includes impairment of fasting glucose and glucose tolerance, often evolving into a specific metabolic syndrome that includes abdominal obesity, dyslipidemia, hypertension, and elevated fasting blood glucose. The eventual development of full-blown type 2 diabetes is signaled by overt hyperglycemia resulting from a combination of insulin resistance and dysfunction of insulin-producing pancreatic ß-cells. In other words, type 2 diabetes is a systemic disease occurring at several sites in the body.

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