BackgroundIt has been suggested that the acidity of the diet may be related to increased risk of type 2 diabetes. To investigate this hypothesis, we tested if the acidity of the diet, measured as the Potential Renal Acid Load (PRAL) score, was associated with incident diabetes and diabetes-related intermediary traits.MethodsA total of 54,651 individuals from the Danish Diet, Cancer and Health (DCH) cohort were included in the prospective cox regression analyses of incident diabetes over a 15 years follow-up period. Moreover, 5724 Danish individuals with baseline data from the Inter99 cohort were included in the cross sectional, multivariate and logistic regression analyses of measures of insulin sensitivity, insulin release and glucose tolerance status derived from an oral glucose tolerance test (OGTT).ResultsIn the DCH cohort a trend analysis showed that quintiles of PRAL score were, after multifactorial adjustment, associated with a higher incidence of diabetes (ptrend = 6 × 10− 7). HR for incident diabetes was 1.24 (1.14; 1.35) (p = 7 × 10− 7) between first and fifth PRAL score quintile.In Inter99 higher PRAL score associated with insulin resistance as estimated by lower BIGTT-Si (an OGTT-derived index of insulin sensitivity) (p = 4 × 10− 7) and Matsuda index of insulin sensitivity (p = 2 × 10− 5) as well as higher HOMA-IR (p = 0.001). No association was observed for measures of insulin release, but higher PRAL score was associated with lower OGTT-based disposition index.ConclusionsA high dietary acidity load is associated with a higher risk of diabetes among middle-aged Danes. Although adjustment for BMI attenuated the effect sizes the association remained significant. The increased risk of diabetes may be related to our finding that a high dietary acidity load associates with impaired insulin sensitivity.Electronic supplementary materialThe online version of this article (10.1186/s12937-018-0395-1) contains supplementary material, which is available to authorized users.
Aims/hypothesisLong-term follow-up of the Steno-2 study demonstrated that intensified multifactorial intervention increased median lifespan by 7.9 years and delayed incident cardiovascular disease by a median of 8.1 years compared with conventional multifactorial intervention during 21.2 years of follow-up. In this post hoc analysis of data from the Steno-2 study, we aimed to study the difference in direct medical costs associated with conventional vs intensified treatment.MethodsIn 1993, 160 Danish individuals with type 2 diabetes and microalbuminuria were randomised to conventional or intensified multifactorial target-driven intervention for 7.8 years. Information on direct healthcare costs was retrieved from health registries, and the costs in the two groups of participants were compared by bootstrap t test analysis.ResultsOver 21.2 years of follow-up, there was no difference in total direct medical costs between the intensified treatment group, €12,126,900, and the conventional treatment group, €11,181,700 (p = 0.48). The mean cost per person-year during 1996–2014 was significantly lower in the intensified treatment group (€8725 in the intensive group and €10,091 in the conventional group, p = 0.045). The main driver of this difference was reduced costs associated with inpatient admissions related to cardiovascular disease (p = 0.0024).Conclusions/interpretationOver a follow-up period of 21.2 years, we found no difference in total costs and reduced cost per person-year associated with intensified multifactorial treatment for 7.8 years compared with conventional multifactorial treatment. Considering the substantial gain in life-years and health benefits achieved with intensified treatment, we conclude that intensified multifaceted intervention in high-risk individuals with type 2 diabetes seems to be highly feasible when balancing healthcare costs and treatment benefits in a Danish healthcare setting.Electronic supplementary materialThe online version of this article (10.1007/s00125-018-4739-3) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
Introduction: Follow-up at 21.2 years after the initiation of the Steno-2 study, demonstrated that intensified multifactorial intervention increases median life-span with 7.9 years and delays incident cardiovascular disease (CVD) with a median of 8.1 years compared to conventional multifactorial intervention. Here we aimed to analyse the direct medical costs in the two original treatment groups during 21.2 years of follow-up. Methods: In 1993, 160 Danish patients with type 2 diabetes and microalbuminuria were randomised to receive either conventional or intensified and target-driven multifactorial intervention for 7.8 years. Information on direct health costs was gathered from health registers and any difference of costs in the two groups was assessed by non-parametric bootstrap t-test analysis. Results: Intensified treatment was on average more expensive regarding drug prescriptions, but less expensive in primary health sector services (both p<0.0001) and in-patient admission costs (p=0.02), specifically related to CVD (p<0.0001) during the entire follow-up period. There was no significant difference in total costs between the intensified treatment group, $13.0M and the conventional treatment group, $12.3M (p=0.19). When further assessing the cost per patient year there was no significant difference between the intensified group, $9,648, and the conventional treatment group, $10,681 (p=0.13). Conclusion: Over an average follow-up of 21.2 years we found no significant increase in total costs or in costs per person year associated with intensified multipronged treatment for 7.8 years when compared to conventional multipronged treatment. Considering the substantial gain of years of life and health benefits achieved with intensified treatment we conclude that intensified multifaceted intervention in high-risk patients with type 2 diabetes is highly cost-effective in a Danish health care setting. Disclosure J. Gaede: None. J. Oellgaard: None. R. Ibsen: None. P. Gæde: None. E. Noertoft: Employee; Self; Novo Nordisk A/S. J. Kjellberg: None. O. Pedersen: None.
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