Statins: risk of hyperglycaemia and diabetes

Statin use may be associated with a level of hyperglycaemia in some patients where formal diabetes care is appropriate.

Article date: January 2012

Statins are one of the most widely prescribed drug classes in Europe for lipid control and cardiovascular prophylaxis, and prescribing is continuing to grow. Between 2002 and 2008 in the UK, statin prevalence has doubled for those older than 40 year and quadrupled for those older than 80 years.  

In 2010, a clinical trial meta-analysis reported that statin therapy overall was associated with a slightly increased risk of new onset diabetes (NOD).[footnote 1] Although a small risk (odds ratio 1.09 [95% CI 1.02–1.17]), given the extent of prescribing even a relatively small increase in the risk of NOD could potentially result in a significant number of additional cases of diabetes per year. Treatment of 255 (95% CI 150–852) patients with statins for 4 years resulted in one extra case of diabetes.[footnote 1] However, the evidence suggests that risk depends markedly on individual risk factors.  

Comparison of studies across the statin class is limited by numerous factors including differences in patient populations, duration of study, and dose of statin used. Furthermore, the endpoint used to diagnose diabetes varied in terms of frequency and time of analysis, and whether fasting blood glucose or, more rarely, HbA1c levels were measured. Importantly, a recent study[footnote 2] of the association between atorvastatin and NOD suggests that stratification of patients by risk factors may yield different conclusions to those drawn when considering the patient population as a whole.  

There is sufficient evidence to support an association between statin use and NOD. However, the risk appears to be mainly in patients already at increased risk of developing diabetes. Raised fasting blood glucose at baseline is a key factor in determining this increased risk and may be sufficient to identify those at risk. Other risk factors include:  

  • history of hypertension
  • raised triglycerides
  • raised body mass index at baseline

There are limited data to support a further increased risk of diabetes with intensive high-dose atorvastatin or simvastatin therapy.[footnote 3] Given the important effect of patient characteristics on the risk of diabetes and the variability of the available studies, there are currently insufficient data to exclude any statin from the possibility of exacerbating the risk of NOD in a susceptible individual.  

Despite the increased risk of NOD in susceptible individuals, studies clearly show a benefit of statins in reducing major cardiovascular events.[footnote 3] [footnote 4]  [footnote 5] The overall benefits of statins strongly outweigh any risks, including in those at risk of diabetes and those with diabetes at baseline. However, steps should be taken to ascertain patients who are at risk, to identify the onset of NOD, and to manage the condition appropriately. Patients at risk should be monitored both clinically and biochemically according to national guidelines.  

Advice for healthcare professionals:  

  • there is sufficient evidence to support an association between statin use and NOD
  • the risk appears to be mainly in patients already at increased risk of developing diabetes
  • raised fasting blood glucose at baseline is a key risk factor. Other risk factors include:
    • a history of hypertension
    • raised triglycerides
    • raised body mass index at baseline
  • patients at risk should be monitored both clinically and biochemically according to national guidelines
  • the level of risk of NOD may vary between statins. However, there is insufficient evidence to confirm or exclude an increased risk for any member of the statin class
  • the reduced vascular risk from statin therapy outweighs the risk of diabetes, which is therefore not a reason for stopping statin treatment

Further information

BNF section 2.12 Lipid-regulating drugs

  1. Sattar N, et al. Lancet 2010; 375: 735–42.  2

  2. Waters DD, et al. J Am Coll Cardiol 2011; 57: 1535–45 

  3. Preiss D, et al. JAMA 2011; 305: 2556–64.  2

  4. The Cholesterol Treatment Trialists’ Collaborators. Lancet 2005; 366: 1267–78. 

  5. The Cholesterol Treatment Trialists’ Collaborators. Lancet 2008; 371: 117–25. 

Published 11 December 2014