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Why Drinking Coffee Might Decrease Diabetes Risk

Studies have suggested a link between regular coffee consumption and a reduction in the risk of type 2 DM (T2DM). Investigators aimed to identify the role coffee might play in preventing diabetes in a study published in the December 28, 2011, issue of the Journal of Agricultural and Food Chemistry.

According to this study, a key indicator of T2DM is the presence of toxic amyloid fibrils in the pancreas. These arise from the misfolding of human islet amyloid polypeptide (hIAPP, or amylin). There is evidence that these toxic amyloids can cause the death of beta-cells that produce and release insulin.

This study investigated the properties of caffeine, caffeic acid (CA), and chlorogenic acid (CGA), the 3 major active components of coffee, and their effects on hIAPP folding. The effects of these compounds in preventing cytotoxicity from amyloids were also evaluated using cultured pancreatic cells.

The results of the study show that all 3 compounds inhibited amyloid formation to varying degrees. CA displayed the greatest potency in delaying conformational changes to hIAPP, CGA had intermediate potency, and caffeine had the least potent effect. CA also exhibited the highest protection to pancreatic cells, maintaining their viability at 96% by inhibiting amyloid formation. Caffeine and CGA were less effective.

It is important to note that these results were observed in a laboratory setting using cultured cells and not in humans or animals. Moreover, the studies that linked coffee consumption with a reduced risk of T2DM were epidemiologic in design, and no proven cause-and-effect link exists between drinking coffee and preventing T2DM.

Intensive Therapy for Type 1 Diabetes Associated with Better Kidney Outcomes

In a study published December 22, 2011, in The New England Journal of Medicine, researchers found that early intensive treatment in individuals with type 1 diabetes was associated with a lower risk of impaired glomerular filtration rate (GFR), which is associated with high rates of cardiovascular disease and progression to end-stage renal disease (ESRD) in diabetic patients.

A total of 1441 patients were randomized to receive either early intensive insulin therapy to achieve near-normal blood glucose levels, or to receive normal insulin therapy to prevent hyperglycemic symptoms. Participants were then followed in a long-term observational study. GFR was estimated from annual serum creatinine levels and patient data.

Intensive therapy was associated with smaller declines in GFR, compared with regular therapy. After 22 years of follow-up, 24 intensive therapy subjects and 46 conventional therapy subjects developed GFR impairment, representing a 50% risk reduction (95% confidence interval [CI], 18-69; P = .006). Eight patients undergoing intensive therapy progressed to ESRD, whereas twice as many did so in the conventional therapy group. Over the course of the 2 studies, the intensive therapy group saw an average decrease in GFR of 1.27 mL/min/1.73 m2 per year (95% CI, 1.20-1.35; P <.001) compared with 1.56 mL/min/1.73 m2 per year (95% CI, 1.48-1.63; P <.001) with conventional therapy.

The results mirror previous findings that intensive therapy decreased the rates of albuminuria, a marker of developing diabetic kidney failure. Limitations include the use of antihypertensive medications or inhibitors of the renin-angiotensinaldosterone system prescribed by physicians in a nonrandomized manner. The results remained significant after adjusting for the use of these medications.

Increased Risk of Diabetes Mellitus with Statin Use in Postmenopausal Women

A study published online in the Archives of Internal Medicine on January 9, 2012, reported that the use of statin drugs is associated with an increased risk of developing new-onset diabetes mellitus (DM) in postmenopausal women.

The study analyzed data from 153,840 women without DM who had been recruited for participation in the Women’s Health Initiative between 1993 and 1998. Statin use was reported at enrollment and after the third year.

Baseline statin use was associated with a significantly increased risk of DM (hazard ratio 1.71; 95% CI, 1.61-1.83). This result decreased but remained significant after adjustment for confounding factors such as age, ethnicity, body mass index (BMI), family history of DM, hormone therapy use, and cardiovascular disease (CVD). Additionally, statin use significantly increased DM risk among white, Hispanic, and Asian women, across all subgroups of BMI and also regardless of a history of CVD. Risks were similar regardless of whether the statin was of low (lovastatin, fluvastatin, and pravastatin) or high (simvastatin, atorvastatin) potency.

The study’s limitations include the unequal use of statin drugs. Only 7.04% of study participants used statins at baseline, and 14.5% used statins after 3 years of follow-up. Additionally, researchers lacked dosage information, could not rule out variations in patient care, and could not track medication use.

Still, the study results were similar to previously published studies, which found that the use of statins increased the risk of newonset DM. The authors conclude that these consequences require more study and current practice guidelines should not change.