Depression, Antidepressant Medication, and the Risk of Developing Type 2 Diabetes
Depression, Antidepressant Medication, and the Risk of Developing Type 2 Diabetes
US Endocrinology - Volume 4 - Issue II
Published: April 2009
Published: April 2009
People who have diabetes are 1.5 to two times more likely to be depressed than people in the general population,1 and depression in people with diabetes is associated with a range of poor outcomes, including higher blood glucose levels,2 an increased risk of complication3 and mortality rates,4 and higher healthcare costs.5
Could Depression Increase the Risk of Developing Diabetes?
In 1674, Thomas Willis, the famous British physician who identified glycosuria as a sign of diabetes, was the first to address the natural history of comorbid depression and diabetes when he wrote that diabetes was caused by “sadness or long sorrow and other depressions.”6 For almost 300 years no-one pursued Willis’ provocative hypothesis, and when some researchers finally did search for what they called the ‘diabetogenic personality’ in people with type 1 diabetes, the search proved fruitless.7,8 At that point researchers turned from looking for the emotional causes of diabetes to looking for its emotional consequences. However, just over a decade ago research interest in Willis’ original idea was renewed, with fascinating results.
In 1996 Eaton and his colleagues at Johns Hopkins published a study suggesting that Willis might have been right after all, at least when it comes to a person’s risk of developing type 2 diabetes.9 This study was followed several years later by one conducted in Japan by Kawakami and colleagues.10 This study also supported Willis’ hypothesis. In each of these studies, and in the many that followed in the next 10 years, the researchers identified a group of people who at the outset of the study did not have diabetes and divided the group into those who were depressed and those who were not depressed. The researchers then followed their subjects for a certain period of time (13 years in the Eaton study and eight years in the Kawakami study), and at the end of that period they compared the rates at which the originally depressed and ‘not depressed’ groups had developed diabetes.
Table 1 summarizes the studies designed to test Willis’ hypothesis.9–22 Not all of the studies fully supported the hypothesis, but most gave it at least some credence. Overall, these studies suggest that being depressed could increase a person’s risk of developing type 2 diabetes, although this effect could be limited to people in certain demographic groups (e.g. people under 50 years of age or those with less education), to people with high levels of depressive symptoms, or to people who are not already at a very high risk for developing diabetes. In the Diabetes Prevention Program (DPP), participants with elevated depression symptoms were not more likely to develop diabetes during the 3.2-year course of the study, perhaps because other diabetes risk factors might have overwhelmed the risk associated with depression.21
References:
- Egede LE, Zheng D, Diabetes Care, 2003;26:104–111.
- Lustman PJ, Anderson RJ, Freedland KE, et al., Diabetes Care, 2000;23:934–42.
- De Groot M, Anderson R, Freedland KE, et al., Psychosom Med, 2001;63:619–30.
- Katon WJ, Rutter C, Simon G, et al., Diabetes Care, 2005;28: 2668–72.
- Egede LE, Zheng D, Simpson K, Diabetes Care, 2002;25: 464–70.
- Willis T, A Medical Odyssey, New York, Tuckahoe, 1971.
- Menninger WC, J Nerv Ment Dis, 1935;81:1–13.
- Slawson DF, Flynn WR, Kollar EJ, JAMA, 1963;185:166–70.
- Eaton WE, Armenian H, Gallo J, et al., Diabetes Care, 1996;19: 1097–1102.
- Kawakami N, Takatsuka N, Shimizu H, Ishibashi H, Diabetes Care, 1999;22:1071–6.
- Golden SH, Williams JE, Ford DE, et al., Diabetes Care, 2004;27: 429–35.
- Carnethon MR, Kinder LS, Fair JM, et al., Am J Epidemiol, 2003;158:416–23.
- Brown LC, Majumdar SR, Newman SC, Johnson JA, Diabetes Care, 2005;28:1063–7.
- Everson-Rose SA, Meyer PM, Powell LH, et al., Diabetes Care, 2003;26:2856–62.
- Arroyo C, Hu FB, Ryan LM, et al., Diabetes Care, 2004;27:129–33.
- Kumari M, Head J, Marmot M, Arch Intern Med, 2004;164:1873–80.
- Palinkas LA, Lee PP, Barrett-Connor E, Diabet Med, 2004;11: 1185–91.
- Saydah SH, Brancatti FL, Golden SH, et al., Diabetes Metab Res Rev, 2003;19:202–8.
- Engum A, J Psychosom Res, 2007;62:31–8.
- Carnethon MR, Biggs ML, Barzilay JI, et al., Arch Intern Med, 2008;167:802–7.
- Rubin RR, Ma Y, Marrero DG, et al., Diabetes Care, 2008;31: 420–26.
- Golden SH, Lazo M, Carnethon M, et al., JAMA, 2008;299: 2751–9.
- Weinstein AR, Sesso HD, Lee IM, et al., JAMA, 2004;292: 1188–94.
- Pan XR, Li GW, Hu YH, et al., Diabetes Care, 1997;20:537–44.
- Tuomiletho J, Lindstorm J, Riksson JG, et al., N Engl J Med, 2001;344:1343–50.
- Knowler WC, Barrett-Connor E, Fowler SE, et al., N Engl J Med, 2002;346:393–403.
- Foy CG, Bell RA, Farmer DF, et al., Diabetes Care, 2005;28: 2501–7.
- Gottlieb DJ, Punjabi NM, Newman AB, et al., Arch Intern Med, 2005;165:863–7.
- Ayas NT, White DP, Al-Delaimy WK, et al., Diabetes Care, 2003;26: 380–84.
- Nilsson PM, Roost M, Engstrom G, et al., Diabetes Care, 2004;27: 2464–9.
- Perot M, Rubin RR, Diabetes Care, 1997;20:585–90.
- Rubin RR, Ciechanowski P, Egede LE, et al., Curr Diab Rep, 2004;4:119–25.
- Knol MJ, Twisk JWR, Beekman ATF, et al., Diabetologia, 2006;49: 837–45.
- Knol MJ, Geerlings MI, Egberts ACG, et al., Int Clin Psychopharmacol, 2007;22:382–6.
- Brown LC, Majumdar SR, Johnson JA, Diab Res Clin Pract, 2007.
- Sussman N, Ginsberg DL, Bikoff J, J Clin Psychiatry, 2001;62: 256–60.
- Maheux P, Ducros F, Bourque J, et al., Int J Obes Relat Metab Disord, 1997;21:97–102.
- The Diabetes Prevention Program Research Group, N Engl J Med, 2002;346:393–403.
- Lustman PJ, Griffith LS, Freedland KE, et al., Ann Intern Med, 1998;129:613–21.
