Using prospective data from two population-based cohort studies in England and the USA, the current study shows for the first time that low religiosity in adulthood may be associated with an increased risk for developing PD, accounting for a wide range of potential confounders.
The findings of this longitudinal study are consistent with previous cross-sectional studies, which showed a robust association between PD and low religiosity (Boussac et al., 2021; Butler et al., 2010; Butler et al., 2011; Giaquinto et al., 2011; Kéri & Kelemen, 2016; McNamara et al., 2006; Pham et al., 2021), case-reports showing improvement of parkinsonism after intense religious experiences (Moreno & de Yebenes, 2009) and theoretical work, that has offered biologically plausible mechanisms by which religiosity could confer neuroprotection in PD (Yulug et al., 2015). The results are also in keeping with a recent neuroimaging study (Ferguson et al., 2022), which showed that brain lesions causing parkinsonism, intersect brain regions associated with religiosity.
It is noteworthy that participants who considered spirituality very important in their lives but not religion, had a higher risk for developing PD than participants who considered religion very important, and also participants who considered neither spirituality nor religion very important. This finding is consistent with an earlier study, which showed that individuals with PD, though less likely to have religious beliefs than matched controls, are on the other hand more likely than controls to have spiritual beliefs (Giaquinto et al., 2011). As such, this study corroborates previous research which suggests that individuals who have a spiritual understanding of life in the absence of a religious framework, may be more vulnerable to developing neuropsychiatric disorders (King et al., 2013; Vitorino et al., 2018).
These results are also in agreement with previous studies, which found higher religiosity to be associated with lower risk of developing a wide range of physical (Ahrenfeldt et al., 2017, 2019; Li et al., 2016), mental (Edlund et al., 2010; Miller et al., 2012; Opsahl et al., 2019) and cognitive disorders (Lin et al., 2015). However, the magnitude of the association found in this study is considerably higher than for any physical health condition previously reported, and therefore requires explanation. A recent study identified that individuals with high self-reported intrinsic religiosity may have significantly higher levels of brain-derived neurotrophic factor (BDNF) than individuals with low self-reported intrinsic religiosity (Mosqueiro et al., 2019). Given that BDNF has been shown to enhance the survival of dopaminergic neurons in animal models of PD (Palasz et al., 2020) and BDNF levels are significantly reduced in patients diagnosed with PD (Jiang et al., 2019), it is plausible that differences in BDNF levels among healthy adults with different levels of religiosity, could partially explain the dose–response relationship with PD risk observed in this study. In addition, there is accumulating evidence that dopaminergic pathways play a central role in mediating religious experience (Previc, 2006; van Elk & Aleman., 2017). A recent SPECT study found significant changes in dopamine transporter binding in the basal ganglia after attendance at a one-week Christian retreat (Newberg et al., 2018). Earlier studies showed increased dopamine release in the ventral striatum during certain forms of meditation (Kjaer, et al., 2002) and increased blood flow to the caudate nucleus during silent religious prayer (Schjødt et al., 2008). These studies suggest that habitual engagement in religious activities could modify dopamine levels in brain regions linked to PD pathology. Therefore, given strong preclinical evidence that enhancing dopamine neurotransmission with dopamine agonists confers neuroprotection in PD (Schapira & Olanow, 2003); it is plausible that individuals with higher religiosity, also have higher midbrain dopamine levels, and consequently have more protection against developing PD.
It is important to note however, that these results do not necessarily imply that religious participation should now be promoted by public health agencies as a preventative measure for PD; given that people’s religious beliefs and commitments are highly personal, and are not usually arrived at based on health concerns. Moreover, further studies are still required to confirm the exact biological mechanisms linking lower religiosity and PD.
Also, seemingly in contrast to the present findings, previous studies have repeatedly shown that clergy and religious workers—who are presumably high in religiosity—have a higher risk for developing PD compared to adults in the general population (Park et al., 2005; Schulte et al., 1996; Tanner et al., 2009). Although, this association is attenuated when the total number of years having worked in a religious occupation is adjusted for (Tanner et al., 2009). The most parsimonious explanation for this observation, would be that the increased risk for PD is confined to individuals with a religious occupation who subsequently experience a decline in religiosity. However, this suggestion is speculative and future studies will be required to confirm this hypothesis.
In addition, future studies are warranted to determine which aspects of religiosity are most associated with the risk of PD, especially given the striking change in the estimates when religious practices (particularly religious service attendance) were included as covariates in this analysis. On the surface, this would seem to imply that religious practices were harmful, i.e., participants with higher religiosity had a lower risk of developing PD despite engaging in more frequent religious practices. However, this would contradict the previously mentioned literature which seems to suggest that religious practices might be protective. Alternatively, it is possible that participants who engaged in more frequent religious practices, but considered religion relatively unimportant in their daily lives, may have exhibited low intrinsic religiosity—but high extrinsic religiosity. If so, it may be the case that having high extrinsic religiosity in the presence of low intrinsic religiosity, is an even stronger risk factor for developing PD than having consistently low religiosity (i.e., low intrinsic and extrinsic religiosity). Accordingly, adjusting for religious practices might have made the association more apparent—by isolating the effects of intrinsic religiosity on PD. Intriguingly, this theory may be in line with a recent cross-sectional study, which showed that newly diagnosed people with PD had lower intrinsic religiosity than age-and sex- matched healthy controls, despite the two groups being similar for frequency of religious practices (Kéri & Kelemen, 2016). Thus, if this theory is confirmed to be true, this might further explain why some clergy and religious workers are at higher risk of developing PD.