Failed Replication of Oxytocin Effects on Trust: The Envelope Task Case.

The neurohormone Oxytocin (OT) has been one of the most studied peptides in behavioral sciences over the past two decades. Many studies have suggested that OT could increase trusting behaviors. A previous study, based on the "Envelope Task" paradigm, where trust is assessed by the degree of openness of an envelope containing participant's confidential information, showed that OT increases trusting behavior and reported one of the most powerful effects of OT on a behavioral variable. In this paper we present two failed replications of this effect, despite sufficient power to replicate the original large effect. The non-significant results of these two failed replications clearly exclude a large effect of OT on trust in this paradigm but are compatible with either a null effect of OT on trust, or a small effect, undetectable with small sample size (N = 95 and 61 in Study 1 and 2, respectively). Taken together, our results question the purported size of OT's effect on trust and emphasize the need for replications.

STR null alleles complicate parentage testing in South Africa.

BACKGROUND: Null alleles complicate parentage testing because they do not contribute positively to phenotypes.Objectives. To survey South African populations for null alleles at short tandem repeat (STR) loci used in parentage testing. METHODS: Paternity case data were scanned for apparent contradictions compared with Mendelian inheritance that could be due to null alleles. Estimates of null allele frequencies were obtained from tallies of apparent carriers. RESULTS: Three of 15 loci appeared to have null alleles at appreciable frequencies and five showed no evidence of null alleles. A null allele at the vWA locus reached a frequency of ~0.3% in the black population and approximately three times this frequency in the coloured population. No apparent vWA null carriers were detected in whites suggesting that the Khoisan were the major contributors of the null alleles to coloureds. The apparent genotypes of a sample of TPOX null carriers changed from homozygous to heterozygous when they were retyped using different polymerase chain reaction primers. The revealed allele was allele 6 in every case. A D13S317 null allele was detected at relatively low frequencies in the black and coloured samples but 2/145 Indian (Asian) parents appear to be carriers, suggesting that it could be common in Indians. CONCLUSION: Three of the 15 forensically relevant STR loci investigated had null alleles at significant frequencies in South African populations. Failure to allow for the presence of null alleles can have a large impact on the outcome of parentage tests.

Chitotriosidase deficiency: a mutation update in an african population.

Human plasma chitotriosidase activity is a commonly used diagnostic and therapeutic biomarker for non-neuronopathic Gaucher disease. Chitotriosidase deficiency is common in non-African populations and is primarily caused by a 24 bp duplication in the encoding gene (CHIT1). Allele frequencies for the 24 bp duplication range from 20-50 % outside Africa. The present study found chitotriosidase deficiency to be rare in the South African Black population (1.6 %) and the otherwise common 24 bp duplication is absent in this African population. Instead, chitotriosidase deficiency is caused by a 4 bp deletion across the exon/intron 10 boundary (E/I-10_delGAgt) of the CHIT1 gene. The exact position of this mutation was found to differ from the previously reported location. Allele frequencies for six coding variants of CHIT1 (p.G102S, p.G354R, 24 bp duplication, E/I-10_delGAgt, p.A442V/G) were determined and the 4 bp deletion was found to be in complete linkage disequilibrium (LD) with two of the coding variants (p.G354R and p.A442V). The in silico assessments of the two missense mutations in LD predict a protein-damaging nature and functional studies are needed to clarify if one or both abolish the enzyme's activity. Overall, the low frequency of chitotriosidase deficiency in South African Blacks makes chitotriosidase activity an excellent biomarker of choice in this population.

Oxytocin increases willingness to socially share one's emotions.

Oxytocin (OT) is a neuropeptide that is attracting growing attention from researchers interested in human emotional and social behavior. There is indeed increasing evidence that OT has a calming effect and that it facilitates pair-bonding and social interactions. Some of OT's effects are thought to be direct, but it has been suggested that OT also may have indirect effects, mediated by changes in behavior. One potentially relevant behavioral change is an increased propensity for "emotional sharing" as this behavior, like OT, is known to have both calming and bonding effects. In this study, 60 healthy young adult men were randomly assigned to receive either intranasal placebo (PL; n = 30) or oxytocin (OT; n = 30). Participants were then instructed to retrieve a painful memory. Subsequently, OT and placebo participants' willingness to disclose to another person event-related facts (factual sharing) vs. event-related emotions (emotional sharing) was evaluated. Whereas the two groups were equally willing to disclose event-related facts, oxytocin was found to specifically increase the willingness to share event-related emotions. This study provides the first evidence that OT increases people's willingness to share their emotions. Importantly, OT did not make people more talkative (word counts were comparable across the two groups) but instead increased the willingness to share the specific component that is responsible for the calming and bonding effects of social sharing: emotions. Findings suggest that OT may shape the form of social sharing so as to maximize its benefits. This might help explain the calming and bonding effects of OT.

Oxytocin not only increases trust when money is at stake, but also when confidential information is in the balance.

Past studies have suggested that the neuropeptide oxytocin (OT) could play a crucial role in human trusting behavior. Specifically, people on OT would be more willing to entrust someone with their money than would people on a placebo. Because alternative explanations-which do not involve trust-exist for these studies' findings, the present study aimed to rule out confounds and test how OT influences trust behavior in a totally different context. The variable at stake was not money but confidential information. Sixty participants were randomly assigned to receive either OT or a placebo. Results showed that oxytocin does increase trust, and that its effects extend beyond money. Specifically, participants on OT were 44 times more trusting that their privacy would not be violated than participants on placebo.

Glucocerebrosidase gene mutations in black South Africans with Gaucher disease.

Gaucher disease (GD) is caused by mutations in the glucocerebrocidase gene (GBA) and presents with variable severity. Type 1 is characterized by the lack of neurological symptoms in childhood, whereas types 2 and 3 are early onset neuronopathic forms and result in premature death. Only type 1 GD has been reported in black South Africans and the cases are clinically severe. In this study both GBA mutations were identified in 18/19 black GD patients. Two mutations accounted for 2/3 of all observed disease causing alleles: p.T36del (c.222-224delTAC) (17/38 alleles) and RecNcil (8/38 alleles). Three novel variants were identified and assessed as being likely pathogenic mutations: c.413delC, W357C and D405V. Haplotype analysis supported a single origin for the p.T36del mutation in black South Africans on a haplotype background that is rare in the present population. We hypothesise that the p.T36del results in intracellular mislocalisation of the protein, but confirmation of the altered function of this allele awaits functional studies. A diagnostic test for GD has been implemented for black South Africans.