Statin use and pancreatic cancer risk in two prospective cohort studies

Background

Statins, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, are common lipid-lowering agents and may reduce the risk of several cancer types including pancreatic cancer. However, the association between statin use and pancreatic cancer risk has not been fully evaluated in prospective studies.

Methods

We studied the association between statin use and incident pancreatic cancer in 113,059 participants from the prospective Nurses’ Health Study and Health Professionals Follow-up Study. Statin use was self-reported via study questionnaires and updated biennially. Hazard ratios (HRs) and 95% confidence intervals (CIs) for incidence of pancreatic cancer were estimated using multivariable Cox proportional hazards models with adjustment for potential confounders.

Results

In total, 583 participants developed incident pancreatic cancer during 1.4 million person-years of follow-up. No difference was identified in pancreatic cancer risk for regular versus non-regular statin users (multivariable-adjusted HR 0.98; 95% CI 0.82–1.16). There was no significant heterogeneity in the association of statin use with pancreatic cancer risk between the cohorts. Similarly, longer duration of regular statin use was not associated with decreased risk of pancreatic cancer (P_trend = 0.65). The results remained similar when we examined statin use status at baseline or accounting for 4-year latency period. We observed no statistically significant effect modification for the association of statin use with pancreatic cancer risk by body mass index, smoking status, or diabetes mellitus status (all P_interaction > 0.21).

Conclusions

Regular statin use was not associated with pancreatic cancer risk in two large prospective cohort studies in the U.S.

     

Comparative effectiveness of once‐weekly glucagon‐like peptide‐1 receptor agonists with regard to 6‐month glycaemic control and weight outcomes in patients with type 2 diabetes

A retrospective cohort study was conducted in patients with type 2 diabetes in an electronic medical record database to compare real‐world, 6‐month glycated haemoglobin (HbA1c) and weight outcomes for exenatide once weekly with those for dulaglutide and albiglutide. The study included 2465 patients: exenatide once weekly, n = 2133; dulaglutide, n = 201; and albiglutide, n = 131. The overall mean (standard deviation [s.d.]) age was 60 (11) years and 54% were men; neither differed among the comparison groups. The mean (s.d.) baseline HbA1c was similar in the exenatide once‐weekly (8.3 [1.7]%) and dulaglutide groups (8.5 [1.5]%; P = .165), but higher in the albiglutide group (8.7 [1.7]%; P < .001). The overall mean (s.d.) HbA1c change was ?0.5 (1.5)% (P < .001) and this did not differ among the comparison groups in either adjusted or unadjusted analyses. The mean (s.d.) weight change was ?1.4 (4.7) kg for exenatide once weekly and ?1.6 (3.7) kg for albiglutide (P = .579), but was greater for dulaglutide, at ?2.7 (5.7) kg (P = .001). Outcomes were similar in subsets of insulin‐naive patients with baseline HbA1c ≥7.0% or ≥9.0%. All agents significantly reduced HbA1c at 6 months, with no significant differences among agents or according to baseline HbA1c in insulin‐naive subgroups.     

Mitochondrial genome of the critically endangered smalltooth sawfish <Emphasis Type="Italic">Pristis pectinata</Emphasis> from Veracruz,Mexico

Sawfishes, family Pristidae, occur in tropical and subtropical coastal marine, estuarine and freshwater ecosystems. The smalltooth sawfish (Pristis pectinata) has been wholly or nearly eliminated from large areas of its former range in the Atlantic Ocean by fishing pressure (trawl and inshore netting) and habitat modification. Here, we report the complete sequence of the mitochondrial genome of a specimen caught in Barra de Cazones by local fishermen, Veracruz, Mexico in 2015, where was thought to be almost extinct and compare it with the previously reported mitochondrial genome from an individual caught in Florida. The genome structure and composition of both specimens is almost identical, except for two nucleotide variations remarking the low variation between regions for this species. The mitochondrial genome has a total length of 16803 nucleotides; in average the base composition was A 32.1%, T 28.9%, C 26.0% and G 13.1%, containing 13 protein-coding genes, 2 rRNA genes; 22 tRNA genes.     

To Go or Not to Go: A Proof of Concept Study Testing Food‐Specific Inhibition Training for Women with Eating and Weight Disorders

Inefficient food‐specific inhibitory control is a potential mechanism that underlies binge eating in bulimia nervosa and binge eating disorder. Go/no‐go training tools have been developed to increase inhibitory control over eating impulses. Using a within‐subjects design, this study examined whether one session of food‐specific go/no‐go training, versus general inhibitory control training, modifies eating behaviour. The primary outcome measure was food consumption on a taste test following each training session. Women with bulimia nervosa and binge eating disorder had small non‐significant reductions in high‐calorie food consumption on the taste test following the food‐specific compared with the general training. There were no effects on eating disorder symptomatic behaviour (i.e. binge eating/purging) in the 24 h post‐training. The training task was found to be acceptable by the clinical groups. More research is needed with larger sample sizes to determine the effectiveness of this training approach for clinical populations. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.     

Sex differences in the phagocytic and migratory activity of microglia and their impairment by palmitic acid

Sex differences in the incidence, clinical manifestation, disease course, and prognosis of neurological diseases, such as autism spectrum disorders or Alzheimer's disease, have been reported. Obesity has been postulated as a risk factor for cognitive decline and Alzheimer's disease and, during pregnancy, increases the risk of autism spectrum disorders in the offspring. Obesity is associated with increased serum and brain levels of free fatty acids, such as palmitic acid, which activate microglial cells triggering a potent inflammatory cascade. In this study, we have determined the effect of palmitic acid in the inflammatory profile, motility, and phagocytosis of primary male and female microglia, both in basal conditions and in the presence of a pro‐inflammatory stimulus (interferon‐γ). Male microglia in vitro showed higher migration than female microglia under basal and stimulated conditions. In contrast, female microglia had higher basal and stimulated phagocytic activity than male microglia. Palmitic acid did not affect basal migration or phagocytosis, but abolished the migration and phagocytic activity of male and female microglia in response to interferon‐γ. These findings extend previous observations of sex differences in microglia and suggest that palmitic acid impairs the protective responses of these cells.