The role of biofactors in the prevention and treatment of age‐related diseases

The present demographic changes toward an aging society caused a rise in the number of senior citizens and the incidence and burden of age‐related diseases (such as cardiovascular diseases [CVD], cancer, nonalcoholic fatty liver disease [NAFLD], diabetes mellitus, and dementia), of which nearly half is attributable to the population ≥60 years of age. Deficiencies in individual nutrients have been associated with increased risks for age‐related diseases and high intakes and/or blood concentrations with risk reduction. Nutrition in general and the dietary intake of essential and nonessential biofactors is a major determinant of human health, the risk to develop age‐related diseases, and ultimately of mortality in the older population. These biofactors can be a cost‐effective strategy to prevent or, in some cases, even treat age‐related diseases. Examples reviewed herein include omega‐3 fatty acids and dietary fiber for the prevention of CVD, α‐tocopherol (vitamin E) for the treatment of biopsy‐proven nonalcoholic steatohepatitis, vitamin D for the prevention of neurodegenerative diseases, thiamine and α‐lipoic acid for the treatment of diabetic neuropathy, and the role of folate in cancer epigenetics. This list of potentially helpful biofactors in the prevention and treatment of age‐related diseases, however, is not exhaustive and many more examples exist. Furthermore, since there is currently no generally accepted definition of the term biofactors , we here propose a definition that, when adopted by scientists, will enable a harmonization and consistent use of the term in the scientific literature

Vascular Effects of Dietary Advanced Glycation End Products

Evidence has accumulated lately demonstrating that advanced glycation end products (AGEs) play an important role in the development of diabetic and cardiovascular complications as well as the development of other chronic diseases. AGEs originating from diet have a significant contribution to the AGEs body pool and therefore dietary interventions aiming at reducing AGEs load are believed to exert health promoting effects. This review summarizes the evidence from clinical studies regarding effects of dietary AGEs on the vascular system, highlighting also the different aspects of vascular tests. It also advocates an extension of dietary recommendations towards the promotion of cooking methods that reduce dietary AGEs in consumed foods

Vascular Effects of Dietary Advanced Glycation End Products

Evidence has accumulated lately demonstrating that advanced glycation end products (AGEs) play an important role in the development of diabetic and cardiovascular complications as well as the development of other chronic diseases. AGEs originating from diet have a significant contribution to the AGEs body pool and therefore dietary interventions aiming at reducing AGEs load are believed to exert health promoting effects. This review summarizes the evidence from clinical studies regarding effects of dietary AGEs on the vascular system, highlighting also the different aspects of vascular tests. It also advocates an extension of dietary recommendations towards the promotion of cooking methods that reduce dietary AGEs in consumed foods

Benfotiamine Counteracts Smoking-Induced Vascular Dysfunction in Healthy Smokers

Background. Smoking induces endothelial dysfunction (ED) mainly by exacerbating oxidative stress (OS) and inflammation. Benfotiamine, a thiamine prodrug with high bioavailability, prevents nicotine-induced vascular dysfunction in rats. It remained unknown whether this effect also occurs in humans. Methods. Therefore, 20 healthy volunteers (mean age: 38 years) were investigated twice, 7–10 days apart in a randomized, cross-over, and investigator-blinded design. Vascular function was assessed by flow-mediated vasodilatation (FMD) of the brachial artery and by measurements of the soluble vascular cell adhesion molecule (sVCAM)-1. Investigations were performed after an overnight fast as well as 20 minutes after one cigarette smoking. On another day, the same procedure was applied following a 3-day oral therapy with benfotiamine (1050 mg/day). Ten patients were randomized to start with smoking alone, and ten started with benfotiamine. Results. Results are expressed as (mean ± SEM). Smoking acutely induced a decrease in FMD by 50% (∗∗P<0.001 versus baseline) an effect significantly reduced by benfotiamine treatment to 25%∗§ (∗P<0.05 versus baseline, §P<0.05 versus smoking alone). Smoking-induced elevation in sVCAM-1 was also prevented by benfotiamine. The endothelium-independent vasodilatation remained unaltered between days. Conclusion. In healthy volunteers, smoking blunts vascular function mirrored by a decrease in FMD and an increase in sVCAM-1. Short-term treatment with benfotiamine significantly reduces these effects, showing protective vascular properties

A randomised, active- and placebo-controlled, three-period crossover trial to investigate short-term effects of the dipeptidyl peptidase-4 inhibitor linagliptin on macro- and microvascular endothelial function in type 2 diabetes

Abstract Background Studies of dipeptidyl peptidase (DPP)-4 inhibitors report heterogeneous effects on endothelial function in patients with type 2 diabetes (T2D). This study assessed the effects of the DPP-4 inhibitor linagliptin versus the sulphonylurea glimepiride and placebo on measures of macro- and microvascular endothelial function in patients with T2D who represented a primary cardiovascular disease prevention population. Methods This crossover study randomised T2D patients (n\ua0=\ua042) with glycated haemoglobin (HbA1c) \u22647.5%, no diagnosed macro- or microvascular disease and on stable metformin background to linagliptin 5\ua0mg qd, glimepiride 1\u20134\ua0mg qd or placebo for 28\ua0days. Fasting and postprandial macrovascular endothelial function, measured using brachial flow-mediated vasodilation, and microvascular function, measured using laser-Doppler on the dorsal thenar site of the right hand, were analysed after 28\ua0days. Results Baseline mean (standard deviation) age, body mass index and HbA1c were 60.3 (6.0) years, 30.3 (3.0)\ua0kg/m 2 and 7.41 (0.61)%, respectively. After 28\ua0days, changes in fasting flow-mediated vasodilation were similar between the three study arms (treatment ratio, gMean [90% confidence interval]: linagliptin vs glimepiride, 0.884 [0.633\u20131.235]; linagliptin vs placebo, 0.884 [0.632\u20131.235]; glimepiride vs placebo, 1.000 [0.715\u20131.397]; P \ua0=\ua0not significant for all comparisons). Similarly, no differences were seen in postprandial flow-mediated vasodilation. However, under fasting conditions, linagliptin significantly improved microvascular function as shown by a 34% increase in hyperaemia area ( P \ua0=\ua00.045 vs glimepiride), a 34% increase in resting blow flow ( P \ua0=\ua00.011 vs glimepiride, P \ua0=\ua00.003 vs placebo), and a 25% increase in peak blood flow ( P \ua0=\ua00.009 vs glimepiride, P \ua0=\ua00.003 vs placebo). There were no significant differences between treatments in postprandial changes. Linagliptin had no effect on heart rate or blood pressure. Rates of overall adverse events with linagliptin, glimepiride and placebo were 27.5, 61.0 and 35.0%, respectively. Fewer hypoglycaemic events were seen with linagliptin (5.0%) and placebo ..