Now we are six: lessons from New Zealand’s KiwiSaver

New Zealand’s KiwiSaver was introduced on 1 July 2007. New Zealand’s success with the ‘soft compulsion’ of automatic enrolment has been and is continuing to be an influence in the design of opt-out schemes in the UK and Ireland. While there have been numerous changes to KiwiSaver as outlined in this paper, six years on, the retirement saving scheme appears well accepted by the public and membership has exceeded most expectations. New Zealand’s experience suggests that auto-enrolment and large incentives to entice people to remain opted-in may ensure initial take-up is high. It also suggests the incentives may be reduced significantly ex post with little impact on membership. Core tax-funded KiwiSaver subsidies have been both substantially reduced and not indexed while membership has continued to grow strongly. Whether this auto-enrolment scheme, featuring generous provisions for withdrawals and contributions holidays, is sufficient to ensure that those who should be saving for their retirement are saving, and saving enough, is open to debate. If KiwiSaver is made compulsory, as some powerful lobbies propose, there are large complexities to resolve, including the future role of the universal state pension, New Zealand Superannuation. Lessons from KiwiSaver on what to avoid in the design of a national retirement saving scheme may include: opening it to children; offering housing subsidies; allowing too many providers and privileging some of these as ‘default providers’; ignoring the issue of decumulation; and obscure objectives. Advantages over previous work-based retirement saving schemes include the portability of KiwiSaver accounts facilitated by the IRD’s role as a clearing house. New Zealand has also limited regressivity in the design of its very modest tax incentives, but at a cost: many save just the minimum required to maximise the subsidies. The Working Paper surveys the first six years of KiwiSaver’s evolution to July 2013. In that time, the fundamental questions around its purpose and design have not been resolved. Is its purpose to enhance access to suitable wealth accumulation vehicles for those who have missed out on traditional work-based schemes? Or is it to reduce the pressures on the economy of an ageing population; or to solve the national saving problem? Will KiwiSavers in fact have more to spend during their retirement, or will they simply reduce other savings to compensate? In the long term, what are the implications for New Zealand’s overall pensions framework, and in particular the very successful universal state pension? As 2014 is an election year, political parties are positioning themselves on KiwiSaver policy. In the meantime there is strong international interest in New Zealand’s retirement saving scheme, with its unique features such as auto-enrolment. The Retirement Policy and Research Centre is pleased to publish KiwiSaver: Now we are six. It updates earlier working papers, including Working Paper 2010 KiwiSaver: lessons for Ireland. TheviewsinthisWorkingPaper’scommentaryarethoseoftheauthors

Concurrent Use of Cigarettes and Smokeless Tobacco in Minnesota

Cigarette smokers are being encouraged to use smokeless tobacco (SLT) in locations where smoking is banned. We examined state-wide data from Minnesota to measure changes over time in the use of SLT and concurrent use of cigarettes and SLT. The Minnesota Adult Tobacco Survey was conducted four times between 1999 and 2010 and has provided state-wide estimates of cigarette smoking, SLT use and concurrent use of SLT by smokers. The prevalence of SLT was essentially unchanged through 2007, then increased significantly between 2007 and 2010 (3.1% versus 4.3%, P < 0.05). Similarly, the prevalence of cigarette smokers who reported using SLT was stable then increased between 2007 and 2010 (4.4% versus 9.6%, P < 0.05). The finding of higher SLT use by smokers could indicate that smokers in Minnesota are in an experimental phase of testing alternative products as they adjust to recent public policies restricting smoking in public places. The findings are suggestive that some Minnesota smokers are switching to concurrent use of cigarettes and SLT. Future surveillance reports will be necessary to confirm the results

Direct radiocarbon dating of fish otoliths from mulloway (Argyrosomus japonicus) and black bream (Acanthopagrus butcheri) from Long Point, Coorong, South Australia

Accelerator Mass Spectrometry (AMS) radiocarbon dates (n=20) determined on fish otoliths from mulloway (Argyrosomus japonicus) and black bream (Acanthopagrus butcheri) are reported from five sites at Long Point, Coorong, South Australia. The dates range from 2938–2529 to 326–1 cal. BP, extending the known period of occupation of Long Point. Previous dating at the sites indicated intensive occupation of the area from 2455–2134 cal. BP. Results provide a detailed local chronology for the region, contributing to a more comprehensive understanding of Aboriginal use of Ngarrindjeri lands and waters. This study validates the use of fish otoliths for radiocarbon dating and reveals how dating different materials can result in different midden chronologies

Inhibition of Human Hepatic Bile Acid Transporters by Tolvaptan and Metabolites: Contributing Factors to Drug-Induced Liver Injury?

Tolvaptan is a vasopressin

Hepatocellular Disposition and Transporter Interactions with Tolvaptan and Metabolites in Sandwich-Cultured Human Hepatocytes

Tolvaptan is a selective V2-receptor antagonist primarily metabolized by CYP 3A. The present study investigated the hepatocellular disposition of tolvaptan and the generated tolvaptan metabolites, DM-4103 and DM-4107, as well as the potential for drug-drug interactions (DDIs) with metabolic and transport proteins in sandwich-cultured human hepatocytes (SCHH). Tolvaptan was incubated with SCHH and quantified by liquid chromatography–tandem mass spectrometry. Pioglitazone, verapamil, MK-571, and elacridar were used as inhibitors to investigate mechanisms of transport and metabolism of tolvaptan and metabolites. Taurocholate (TCA), pravastatin, digoxin, and metformin were used as transporter probes to investigate which transport proteins were inhibited by tolvaptan and metabolites. Cellular accumulation of tolvaptan (0.15–50 μM), DM-4103, and DM-4107 in SCHH was concentration-dependent. Tolvaptan accumulation (15 μM) in SCHH was not altered markedly by 50 μM pioglitazone, verapamil, MK-571, or 10 μM elacridar. Coincubation of tolvaptan with pioglitazone, verapamil, MK-571, and elacridar reduced DM-4107 accumulation by 45.6, 79.8, 94.5, and 23.0%, respectively, relative to control. Coincubation with increasing tolvaptan concentrations (0.15–50 μM) decreased TCA (2.5 μM) cell+bile accumulation and the TCA biliary excretion index (BEI; from 76% to 51%), consistent with inhibition of the bile salt export pump (BSEP). Tolvaptan (15 μM) had no effect on the cellular accumulation of 2.5 μM pravastatin or metformin. Digoxin cellular accumulation increased, and the BEI of digoxin decreased from 23.9 to 8.1% in the presence of 15 μM tolvaptan, consistent with inhibition of P-glycoprotein. In summary, SCHH studies revealed potential metabolic- and transporter-mediated DDIs involving tolvaptan and metabolites

Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence

Peer behaviour plays an important role in the development of social adjustment, though little is known about its genetic architecture. We conducted a twin study combined with a genome-wide complex trait analysis (GCTA) and a genome-wide screen to characterise genetic influences on problematic peer behaviour during childhood and adolescence. This included a series of longitudinal measures (parent-reported Strengths-and-Difficulties Questionnaire) from a UK population-based birth-cohort (ALSPAC, 4–17 years), and a UK twin sample (TEDS, 4–11 years). Longitudinal twin analysis (TEDS; N ≤ 7,366 twin pairs) showed that peer problems in childhood are heritable (4–11 years, 0.60 < twin-h 2 ≤ 0.71) but genetically heterogeneous from age to age (4–11 years, twin-r g = 0.30). GCTA (ALSPAC: N ≤ 5,608, TEDS: N ≤ 2,691) provided furthermore little support for the contribution of measured common genetic variants during childhood (4–12 years, 0.02<GCTA−h2Meta ≤ 0.11) though these influences become stronger in adolescence (13–17 years, 0.14<GCTA−h2ALSPAC ≤ 0.27). A subsequent cross-sectional genome-wide screen in ALSPAC (N ≤ 6,000) focussed on peer problems with the highest GCTA-heritability (10, 13 and 17 years, 0.0002 < GCTA-P ≤ 0.03). Single variant signals (P ≤ 10−5) were followed up in TEDS (N ≤ 2835, 9 and 11 years) and, in search for autism quantitative trait loci, explored within two autism samples (AGRE: N Pedigrees = 793; ACC: N Cases = 1,453/N Controls = 7,070). There was, however, no evidence for association in TEDS and little evidence for an overlap with the autistic continuum. In summary, our findings suggest that problematic peer relationships are heritable but genetically complex and heterogeneous from age to age, with an increase in common measurable genetic variation during adolescence

Combination Lopinavir and Ritonavir Alter Exogenous and Endogenous Bile Acid Disposition in Sandwich-Cultured Rat Hepatocytes

Inhibition of the bile salt export pump (BSEP) can cause intracellular accumulation of bile acids and is a risk factor for drug-induced liver injury in humans. Antiretroviral protease inhibitors lopinavir (LPV) and ritonavir (RTV) are reported BSEP inhibitors. However, the consequences of LPV and RTV, alone and combined (LPV/r), on hepatocyte viability, bile acid transport, and endogenous bile acid disposition in rat hepatocytes have not been examined. The effect of LPV, RTV, and LPV/r on cellular viability and the disposition of [3H]taurocholic acid (TCA) and [14C]chenodeoxycholic acid (CDCA) was determined in sandwich-cultured rat hepatocytes (SCRH) and suspended rat hepatocytes. Lactate dehydrogenase and ATP assays revealed a concentration-dependent effect of LPV and RTV on cellular viability. LPV (5 µM), alone and combined with 5 µM RTV, significantly decreased [3H]TCA accumulation in cells + bile of SCRHs compared with control. LPV/r significantly increased [3H]TCA cellular accumulation (7.7 ± 0.1 pmol/mg of protein) compared with vehicle and 5 µM LPV alone (5.1 ± 0.7 and 5.0 ± 0.5 pmol/mg of protein). The [3H]TCA biliary clearance was reduced significantly by LPV and RTV and further reduced by LPV/r. LPV and RTV did not affect the initial uptake rates of [3H]TCA or [14C]CDCA in suspended rat hepatocytes. LPV (50 µM), RTV (5 µM), and LPV/r (5 and 50 µM/5 µM) significantly decreased the accumulation of total measured endogenous bile acids (TCA, glycocholic acid, taurochenodeoxycholic acid, glycochenodeoxycholic acid, and α/β-tauromuricholic acid) in SCRH. Quantification of endogenous bile acids in SCRH may reveal important adaptive responses associated with exposure to known BSEP inhibitors