Compensatory Control Theory (CCT) suggests that religious belief systems provide an external source of control that can substitute a perceived lack of personal control. In a seminal paper, Kay et al. (2008) experimentally demonstrated that a threat to personal control increases endorsement of the existence of a controlling God. In the current registered report, we conducted a high-powered (N = 829) direct replication of this effect, using samples from the Netherlands and the United States. Our results show moderate to strong evidence for the absence of an experimental effect across both countries: belief in a controlling God did not increase after a threat compared to an affirmation of personal control. In a complementary preregistered analysis, an inverse relation between general feelings of personal control and belief in a controlling God was found in the US, but not in the Netherlands. We discuss potential reasons for the replication failure of the experimental effect and cultural mechanisms explaining the cross-country difference in the correlational effect. Together, our findings suggest that experimental manipulations of control may be ineffective in shifting belief in God, but that individual differences in the experience of control may be related to religious beliefs in a way that is consistent with CCT.

Mycobacterium tuberculosis (Mtb) has co-evolved with humans for millennia and developed multiple mechanisms to evade host immunity. Restoring host immunity in order to shorten existing therapy and improve outcomes will require identifying the full complement by which host immunity is inhibited. Perturbing host DNA methylation is a mechanism induced by chronic infections such as HIV, HPV, LCMV and schistosomiasis to evade host immunity.Here, we evaluated the DNA methylation status of TB patients and their asymptomatic household contacts demonstrating that TB patients have DNA hyper-methylation of the IL-2-STAT5, TNF-NF-ϰB and IFN-γ signaling pathways. By MSRE-qPCR, multiple genes of the IL-12-IFN-γ signaling pathway (IL12B, IL12RB2, TYK2, IFNGR1, JAK1 and JAK2) were hypermethylated in TB patients. The DNA hyper-methylation of these pathways is associated with decreased immune responsiveness with decreased mitogen induced upregulation of IFN-γ, TNF, IL-6 and IL-1β production. The DNA hyper-methylation of the IL-12-IFN-γ pathway was associated with decreased IFN-γ induced gene expression and decreased IL-12 inducible upregulation of IFN-γ. This work demonstrates that immune cells from TB patients are characterized by DNA hyper-methylation of genes critical to mycobacterial immunity resulting in decreased mycobacteria-specific and non-specific immune responsiveness.

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