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Commentary

Can Heart Rate Predict Risk of Diabetes?


January 13, 2016

The answer may be yes. Diabetes mellitus has reached panepidemic proportions across the world with approximately 382 million people diagnosed and is set to rise to 592 million by 2040.1 In 2013, half of all premature deaths in adults under the age of 60 were attributable to diabetes. Another 175 million are currently estimated to be under-diagnosed. A growing concern is that 80% of cases are progressing towards diabetes in low- and middle-income countries, which may result in global under-development.

Heart rate is a crude index of the balance between the sympathetic and parasympathetic systems.2 It correlates with sympathetic nerve activity and circulating norepinephrine levels.2 When sympathetic activity is heightened, vasoconstriction occurs resulting in decreased skeletal muscle flow and impaired glucose uptake into skeletal muscle.3 Higher sympathetic activity is also associated with reduced insulin sensitivity, higher blood pressure, obesity, and metabolic syndrome. 3-8 Although none of these mechanisms is directly related to development of diabetes mellitus, and there is a clear research need to understand the mechanistic link, they are clustered in the development of this devastating disease.

A recently published prospective study of 17,463  participants from Kailuan, China, sought to determine the relations between resting heart rate and the risk of developing impaired fasting glucose, diabetes or the conversion from impaired fasting glucose to diabetes.9 During four years of follow-up, for each 10/beat increase in heart rate there were 1.23 (95% CI: 1.19-1.27) incident diabetes, 1.11 (95% CI: 1.09-1.13) incident impaired fasting glucose, and 1.13 (95% CI: 1.08-1.17) conversions from impaired fasting glucose to diabetes. Importantly, the risk was higher in persons < 50 years of age compared to those > 50. 

Although not overwhelming hazard ratios, increasing fasting heart rate is associated with developing impaired fasting glucose and diabetes. So, can heart rate be used to identify individuals without other risk factors for the development of diabetes? Clinicians should be aware of higher heart rates, especially > 80 beats/min as a potential higher risk factor and prescribe therapy, including exercise, to reduce heart rate over time.

 

Mark A. Munger, PharmD, FCCP, FACC, is a Professor of Pharmacotherapy and Adjunct Professor of Internal Medicine, at the University of Utah, where he also serves as the Associate Dean, Academic Affairs for the College of Pharmacy.

 

References:

1. International Diabetes Federation. IDF Diabetes Atlas. www.idf.org. Accessed January 6, 2016.

2. Grassi G, Vailati S, Bertinieri G, et al. Heart rate as a marker of sympathetic activity. J Hypertens. 1998;16(11):1635-1639.

3. Julius S, Jamerson K. Sympathetics, insulin resistance and coronary risk in hypertension: the ‘chicken-and-egg’ question. J Hypertens. 1994;12(5):495-502.

4. Julius S, Gudbrandsson T, Jamerson K, Andersson O. The inter-connection between sympathetics, microcirculation, and insulin resistance in hypertension. Blood Press.1992;1(1):9-19.

5. Shigetoh Y, Adachi H, Yamagishi S, et al. Higher heart rate may predispose to obesity and diabetes mellitus: 20-year prospective study in a general population. Am J Hypertens. 2009;22(2):151-155.

6. Flanagan DE, Vaile JC, Petley GW, et al. The autonomic control of heart rate and the metabolic syndrome. J Hypertens. 2007;25:909-920.

7. Sajadieh A, Nielsen OW, Rasmussen V, Hein HO, Abedini S, Hansen JF. Increased heart rate and reduced heart-rate variability are associated with subclinical inflammation in middle-aged and elderly subjects with no apparent heart disease. Eur Heart J. 2004;25(5):363-370.

8. Shibao, C. Gamboa A, Diedrich A, et al. Autonomic contribution to blood pressure and metabolism in obesity. Hypertension 2007;49(1):27-33.

9. Wang L, Cui L, Wang Y, et al. Resting heart rate and the risk of developing impaired fasting glucose and diabetes: the Kailuan prospective study. Int J Epidemiol.2015;44(2)689-999.

 

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