This study aims to determine if iron supplementation is associated with parkinsonism risk using comprehensive longitudinal data from UK Biobank.
In Parkinson’s disease (PD), dopaminergic neurons in the substantia nigra degenerate. A higher prevalence of Parkinson’s disease is among middle-aged and older individuals, characterized primarily by impaired motor functions, which can also progress to cognitive impairment.
A significant cause of Parkinson’s disease and parkinsonism is iron dysregulation. While iron plays a crucial role in dopamine production in the SN, excess iron can be found in patients with Parkinson’s and animal models.
A pathological Lewy body is also found in the SNs of parkinsonism patients, and iron is known to influence the synthesis, post-translation modifications, and aggregation of synuclein.
The use of iron in PD models has been proven to protect against motor dysfunction and degeneration. In contrast, using iron supplements in PD patients has led to a faster disease progression.
Researchers prospectively examined the risk of parkinsonism in subjects with or without symptoms (tremors, muscle rigidity, and slow movement).
They found that those taking iron supplements were more vulnerable and that intake was also associated with low hemoglobin (Hb) levels (associated with Parkinson’s disease).
Based on previous studies, the researchers explain that anemia, low Hb concentrations, and PD risk are related.
After accounting for potential confounders (such as age, gender, household income, education, employment status, deprivation level, body mass index, level of physical activity, blood pressure, and health status), researchers examined the association between iron supplement intake, hemoglobin levels, and all-cause parkinsonism risk.
What Did The Study Reveal?
A total of 22 assessment centers were used to collect data on subjects aged 40-69, including supplementation with vitamins and minerals.
1,329 participants with incident all-cause parkinsonism (exhibiting two or more symptoms) and 911 patients with all-cause parkinsonism (exhibiting the four main symptoms) were involved in the study. In addition, the UK Biobank of middle-aged adults provided socio-economic, educational, household income, and employment data.
The primary perspective analyses involved 385,898 subjects without incident parkinsonism and all-cause subjects. Hemoglobin concentrations, iron, vitamin C, and multivitamin intake were assessed using partial correlations and multiple logistic regressions.
The data also indicated significant incident parkinsonism among subjects without iron supplementation despite a significant negative correlation between hemoglobin concentrations and iron supplementation.
As a result, the association between low hemoglobin concentration and parkinsonism risk was stronger when overall health rating was excluded as a covariate, strongly associated with parkinsonism risk. According to these findings, the risk of parkinsonism may be influenced by many factors.
Furthermore, sensitivity analyses of iron supplementation combined with/without vitamin C and incident parkinsonism showed that iron supplementation was associated with a higher risk of parkinsonism.
Based on a large sample size, this relationship is statistically significant and was still significant after adjusting for various confounding factors and removing patients with cancers and other conditions.
It is proposed that subjects with PD risk or genetic predisposition have high hemoglobin concentrations and high PD risk. This may partly explain the link between low hemoglobin and higher PD risk.
A higher hemoglobin concentration was weakly and insignificantly associated with a lower risk of parkinsonism. There was no apparent relationship between multivitamins or vitamin C intake and disease risk.
According to the results, Parkinsonism risk may increase with excessive iron consumption. However, the researchers could not confirm or disprove the hypothesis that vitamin C intake reduces the risk of disease associated with iron supplements. Therefore, the researchers claim that interventional investigations are warranted to specify whether iron intake restriction benefits individuals without clinical iron deficiency.
