A 2018 meta-analysis found no favorable effect of DPP-4 inhibitors on all-cause mortality, cardiovascular mortality, myocardial infarction or stroke in patients with type 2 diabetes.[5]
A 2018 meta analysis showed that use of DPP-4 inhibitors was associated with a 58% increased risk of developing acute pancreatitis compared with placebo or no treatment.[22]
A 2018 observational study suggested an elevated risk of developing inflammatory bowel disease (specifically, ulcerative colitis), reaching a peak after three to four years of use and decreasing after more than four years of use.[23]
A 2020 Cochrane systematic review did not find enough evidence of reduction of all-cause mortality, serious adverse events, cardiovascular mortality, non-fatal myocardial infarction, non-fatal stroke or end-stage renal disease when comparing metformin monotherapy to dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes.[24]
FWIW EVEN FOR NON-LONGEVITY REASONS, it is sometimes nice to have an easy appetite-killing pill around just in case one gets explosively hungry at the wrong time (eg when all the local food is expensive or it’s after midnight or it makes you tempted to eat your roommate’s food).
[that said, emergency acarbose can sometimes be enough if the only options left are rice/bread. Rice is actually less “disgusting” than bread (it’s far less messy for one)]
ugh I really should try potassium salts. They taste nasty by themselves, but beans/rice are so delicious that they make them tolerable.
In conclusion, the present study, together with others, provides a strong rationale for the future evaluation of a gliptin in PD. In this regard, we propose that sitagliptin be considered as a candidate for clinical trials in PD. Although its brain uptake is low (CSF/plasma ratio 0.01), its induced DPP-4 inhibition was sufficient to significantly elevate CNS incretin levels in line with levels in rodent studies associated with sitagliptin-mediated efficacy in a 6-OHDA model of PD. To this end, a gliptin could be evaluated to augment the neurotrophic, neuroprotective, and anti-inflammatory actions of endogenous incretins either singularly, or in combination with an incretin mimetic. Although gliptins and incretin mimetics ultimately provide their pharmacological action through the same mechanism, the GLP-1/GIP receptors, their combination is not recommended in T2DM as it does not provide any clinically meaningful improvement in glycemic control over either agent singly. However, such additive or synergistic action might well be beneficial for a CNS-based disorder (in line with co-administration in Fig. 8). Importantly, sitagliptin is clinically approved, widely used, and well tolerated with weight neutral actions and no risk of hypoglycemia, which would allow rapid repurposing to human clinical trials for evaluation in PD and other age-associated neurodegenerative disorders. In this regard, early to moderate PD likely may represent the stages of disease most expected to respond to a gliptin, in the light of the demonstrated efficacy of the single GLP-1R incretin mimetics exenatide and lixisenatide in recent human clinical trials, and of exenatide in early-stage disease in a progressive PD preclinical model.