Dietary antioxidants not a boon for Parkinson’s disease

There appears to be no benefit to taking dietary antioxidants, such as vitamins and carotenoids, in terms of reducing the risk of developing Parkinson’s disease (PD) in Asians, as shown in a Singapore study.

“At the cellular level, PD results from the dysfunction of dopaminergic neurons, and one of the main theories for the cause of this dysfunction, is oxidative stress… Thus, it is logical to hypothesize that reducing oxidative stress may be a potentially viable means of reducing PD risk,” according to the investigators.

“Indeed, preclinical studies of antioxidants in PD animal models have been promising, where rats injected with antioxidants were seen to exhibit reduced dopaminergic neuron death after induction of mitochondrial stress,” they added. [Mech Ageing Dev 2017;161:112-120; Iran Biomed J 2008;12:217-222]

The current study involved 63,257 men and women aged 45–74 years from the Singapore Chinese Health Study, of which 544 (mean age at diagnosis, 71.2 years) developed PD over a mean follow-up of 19.4 years. The incidence rate was 56.0 per 100,000 person‐years in men and 39.8 per 100,000 person‐years in women.

PD patients were significantly older at recruitment, more likely to be men, less likely to be smokers, and consumed less caffeine‐containing beverages and less dietary cholesterol as compared with the rest of the cohort.

Multivariable Cox proportional hazard regression models showed that dietary carotenoids (α-carotene, β-carotene, lycopene, β-cryptoxanthin, and lutein), individually or summed, had no effect on the risk of incident PD (highest vs lowest quartile of total carotenoids intake: hazard ratio, 0.98, 95 percent confidence interval, 0.76–1.28; p_trend=0.83). [Mov Disord 2020;doi:10.1002/mds.28173]

There were also no clear dose-dependent associations for dietary vitamins A, C, and E (p_trend≥0.10 for all). Sensitivity analyses with lag time and excluding supplement use did not considerably alter the risk estimates.

The investigators outlined potential biological explanations for their null results. First is that vitamin C may have attenuated its own antioxidant effects through its hypouricaemic effects, as urate has been shown to be another potent antioxidant protective against PD. Second, vitamin E has been previously reported to have no effect on the activity of nigrostriatal dopaminergic neurons and, hence, on the progression of PD. [Arthritis Rheum 2005;52:1843-1847; Medicine 2017;96:e8502; Arthritis Rheum 2008;59:1549-1554; Neurology 2016;86:520-526; Life Sci 2003;72:2641-2648]

Finally, in most preclinical studies reporting positive results, animals were either directly injected intraperitoneally with antioxidants or they were fed highly concentrated extracts, the investigators noted. [J Neurosci Res 2013;91:1609-1617; Proc Natl Acad Sci USA 2006;103:13520-13525; Iran Biomed J 2008;12:217-222]

“It is therefore possible that the dietary antioxidants we examined were not consumed in sufficient quantities in the Singaporean diet to have measurable effects in reducing PD risk in the population,” they added.

The present findings are in line with most other prospective studies conducted in other populations. [Mov Disord 2016;31:1909-1914; Neurology 1996;46:1270-1274; Neuroepidemiology 2001;20:118-124]

“As such, even though there is a strong biological plausibility underlying promising findings from experimental studies, more research in human studies is necessary to determine whether increasing the consumption of dietary antioxidants or the use of such supplements at midlife is a viable modification to reduce the risk of PD in ageing populations,” the investigators said.