Sutton's law and chronic illness
Remember Willie Sutton, the infamous bank robber of the early 20th century? When he was finally apprehended, a reporter asked him, "Willie, why do you rob banks?" His alleged response was quite simple: "Because that's where the money is."
Willy's retort (which he later denied saying) is often referred to as Sutton's law.
Today with all the concern about rapidly rising healthcare costs, there has been little public attention drawn to the fact that the majority of costs—some studies say up to 75%—are incurred by patients with one of a handful of so-called chronic illnesses: cancer, stroke, Alzheimer's, diabetes, arthritis, heart failure.
Sutton's law of healthcare says if you want to reduce healthcare costs, you have to find ways of reducing the economic impact of chronic illness, ideally by preventing or significantly delaying when affliction occurs, or finding better and more cost-effective ways of treating the illness.
At the Salk Institute, our scientists are engaged in understanding the processes by which important chronic diseases such as cancer, diseases of aging, autoimmune disease, diabetes, etc. damage the body. Often genetic mutations are associated with these diseases, so understanding the genome and how it functions is an underlying theme of many of the Salk investigators. A thorough understanding of the mechanisms by which diseases occur is the first step toward better therapy.
Perhaps you have heard the term disease markers. These are biological handles by which physicians and scientists can track the onset and progression of various diseases. An early biologic marker for diabetes, for example, was sugar in the urine; later, elevation of the fasting level of glucose in the blood was used. Today there are more sophisticated markers for diabetes— for example, a blood test called Hemoglobin A1c that allows an accurate assessment of how well insulin and dietary therapy are working.
Another test, the PSA, helps identify early the possibility of having prostate cancer. In the past decade, many genetic markers have been developed to indicate one's risk for a particular form of cancer, especially the risk for breast cancer.
It is axiomatic that unless one has good markers for susceptibility or to track the early onset and progress of a disease, one cannot readily find and evaluate new drugs or other treatment modalities. Alzheimer's disease is particularly challenging because the onset of the disease most likely occurs years and perhaps decades before clinical signs of dementia appear in the patient, at which point the brain damage may likely be too extensive to treat successfully.
Our desire for fast cures must be tempered by the understanding that much work needs to be done for many diseases at a very basic level before we have the knowledge to know what treatments have a good likelihood of success and which do not.
We need a good marker for the early detection of Alzheimer's disease, but right now one doesn't exist that could be used routinely. Part of the important work of scientists here at the Salk is to try to identify markers of diseases such as Alzheimer's and place them within the context of biological and genetic alterations that might characterize disease.