The True Cost of Diabetes

Kenny Navarro // March 1, 2012

Diabetes is a serious and costly disease affecting approximately 8.3 percent of the United States population ( U.S. Department of Health and Human Services, 2011). By 2050, experts estimate that between one-fifth to one-third of all American citizens will have diabetes (Boyle, Thompson, Gregg, Barker, & Williamson, 2010).

Development of diabetes is closely linked to obesity. Since the mid 1970s, the proportion of the population classified as overweight or obese has steadily climbed (Flegal, Carroll, Ogden, & Curtin, 2010).

Due to the evolving American lifestyle, diabetes symptom onset is appearing earlier in life (Rowley & Bezold, 2012), potentially placing future generations at risk for debilitation during prime wage-earning years, thereby increasing health care costs for the entire country (Imperatore, Linder, & Pettitt, 2011).

The cost of diabetes to the 2007 US economy was $174 billion (American Diabetes Association, 2008); by 2025, experts project the total societal costs related to diabetes will increase to more than half a trillion dollars (Rowley & Bezold, 2012).

Diabetes mellitus is a chronic disease in which the body has trouble metabolizing glucose. Diabetes results from little or no insulin production in the body or may develop when the muscle, fat, or liver cells respond poorly to the available insulin.

Without insulin, the cells of the body cannot absorb glucose from the blood, regardless of how high the glucose levels rise. Without glucose, the cells begin to starve.

The starving cells force alpha cells within the pancreas to secrete glucagon, which stimulates the liver and muscles to break down stored glycogen and release glucose into the bloodstream.

However, since the cells cannot absorb glucose without insulin, the glucose levels in the blood rise even further.

From the cellular point of view, there does not seem to be any glucose available in the body. The brain responds by stimulating the hunger centers in hopes the patient will eat and deliver glucose. The lack of insulin stimulates the breakdown of fats in fat cells and proteins in muscle, leading to weight loss.

Despite the fact that diabetics eat more frequently, they often lose weight. The patient begins to feel tired and fatigues easily because the cells have nothing to burn for energy.

As the glucose-rich blood passes through the kidneys, some of the glucose spills over into the urine, resulting in an increase in urine production and frequent urination. This causes the patient to experience an increase in thirst as he or she tries to replace the lost fluid. Fluid transfer from the bloodstream to the urine results in more viscous blood.

Circulatory impairment results as the heart works harder to pump the thick blood through the blood vessels. The patient may complain of cold hands and feet. Circulatory changes within the capillaries of the eyes impacts vision, which, long term, results in blindness.

Poor circulation also causes numbness and pain or a burning sensation in the hands and feet, a condition called neuropathy. The extremities become prone to slow-healing wounds and frequent infections, which ultimately can lead to gangrene in the limbs with subsequent amputations.

Circulatory impairment worsens as the disease progresses, which leads to many cardiovascular problems, including high blood pressure, heart attack, and stroke. Kidney failure is also a frequent long-term complication in diabetes.

The effectiveness of drug therapy at preventing the progression of prediabetes to diabetes is still unclear (Knowler et al.,1995), perhaps reflecting more on our fragmented health care system rather than the ineffectiveness of pharmacologic therapy (Rowley & Bezold, 2012).

One strategy for reducing the human and economic impact of diabetes calls for changes in physical activity and diet. Data from the Diabetes Prevention Program Research Group (Diabetes Prevention Program Research Group, 2002) suggests that these changes can reduce body weight by 5 percent – 10 percent, thereby preventing the progression of prediabetes by 58 percent.

Substituting artificial sweeteners for sugar is a common strategy for weight loss and decreasing the risk of developing diabetes (Fowler et al., 2008). Data from the United States Department of Agriculture Economic Research Service indicates that per capita diet soft drink consumption increased by almost 8 gallons per capita since the mid-1970s (United States Department of Agriculture Economic Research Service, 2011).

However, artificial sweeteners may interfere with the body’s natural ability to anticipate caloric intake, thereby resulting in increased food consumption (Davidson & Swithers, 2004).

A longitudinal study in Texas demonstrated an association between diet drink consumption and long-term weight gain (Fowler et al., 2008). Daily diet soft drink consumption is associated with an increased risk for vascular events, defined as stroke, MI, or vascular death (Gardener et al., 2012) and components of metabolic syndrome (Lutsey, Steffen, & Stevens, 2008).


1. Metabolic syndrome is a cluster of risk factors associated with insulin dependant diabetes (Resnick et al., 2003; Sattar et al., 2003).

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3. Boyle, J. P., Thompson, T. J., Gregg, E. W., Barker, L. E., & Williamson, D. F. (2010). Projection of the year 2050 burden of diabetes in the US adult population: Dynamic modeling of incidence, mortality, and prediabetes prevalence. Population Health Metrics, 8, 29.

4. Davidson, T. L., & Swithers, S. E. (2004). A Pavlovian approach to the problem of obesity. International Journal of Obesity, 28, 933–935. doi:10.1038/sj.ijo.0802660

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6. Flegal, K. M., Carroll, M. D., Ogden, C. L., & Curtin, L. R. (2010). Prevalence and trends in obesity among US sdults, 1999-2008. Journal of the American Medical Association, 303(3), 235-241. doi:10.1001/jama.2009.2014

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9. Imperatore, G., Linder, B., & Pettitt, D. J. (2011). Diabetes in the young (pp. 631-633). In: Narayan, K. M., Williams, D., Gregg, E. W., & Cowie, C. C. Diabetes public health: From data to policy. New York, NY: Oxford University Press.

10.Knowler, W. C., Narayan, K. M. V., Hanson, R. L., Nelson, R. G., Bennett, P. H., Tuomilehto, J., Schersten, B., & Pettitt, D. J. (1995). Preventing non-insulin-dependent diabetes. Diabetes, 44(5), 483-488. doi:10.2337/diabetes.44.5.483

11. Lutsey, P. L., Steffen, L. M., & Stevens, J. (2008). Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation, 117, 754–761. doi:10.1161/ CIRCULATIONAHA.107.716159

12. Resnick, H. E., Jones, K., Ruotolo ,G., Jain, A. K., Henderson, J., Lu, W., & Howard, B. V. (2003). Insulin resistance, the metabolic syndrome, and risk of incident cardiovascular disease in nondiabetic American Indians: The Strong Heart Study. (2003). Diabetes Care, 26(3), 861–867. doi: 10.2337/diacare.26.3.861

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15. United States Department of Agriculture Economic Research Service (2011). Food availability. Retrieved by

16. U.S. Department of Health and Human Services. (2011). National Diabetes Information Clearinghouse (NDIC). Retrieved from


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