To prevent PD, attention must be paid to reducing individual risk factors. Behavioral risk factors
- Diet
- High intake of saturated fatty acids
- Micronutrient deficiency (vital substances) – see Prevention with micronutrients.
- Drug use
- Amphetamine-type stimulants (e.g., methamphetamine; colloquially, crystal meth, meth, or crystal) lead to a 2.8-fold risk of
- Physical activity
- Physical inactivity – subjects who spent ≥ 6 hours per week being physically active in the home and commuting to work had a 43% lower risk of developing PD than subjects who spent <2 hours per week on these activities
- Trauma-related – boxer’s encephalopathy.
Environmental exposure – intoxications (poisonings).
- Aluminum
- Lead
- Cobalt
- Disulfiram
- Insecticides
- Rotenone (pyranofurochromone derivative whose basic structure is derived from isoflavones).
- Air pollutants
- Particulate matter (PM2.5) – 13% increased risk of disease per 5 µg/m3 increase in particulate matter at residence (hazard ratio 1.13; 1.12 to 1.14); association was dose-dependent up to a PM2.5 concentration of 16 µg/m3.
- Carbon monoxide
- Carbon monoxide
- Manganese (manganese-containing fumes during welding) → development and progression of manganese parkinsonism.
- Methyl alcohol (methanol)
- MPTP (1-methyl-1-4-phenyl-1,2,3,6-tetrahydropyridine) [neurotoxin].
- Pesticides
- Organo-chlorine pesticides – e.g. beta-hexachlorocyclohexanes (beta-HCH) were more frequently detected in patients with PD (76%) compared to a control group (40%)
- Mercury amalgam (+58%).
- Cyanide
Prevention factors (protective factors)
- Gene variant that protects against Parkinson’s disease.
- Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
Coffee consumption: a group of researchers found that in the presence of the SNP rs4998386, in the allele constellation CT or TT, in the gene GRIN2A in combination with drinking coffee, the risk of developing Parkinson’s disease is reduced (no percentage data).
- Epidemiological studies have shown that smokers have a 60-70% reduced risk of PD compared to non-smokers. This was confirmed in another study, which demonstrated a low prevalence of current smokers in patients with PD compared with healthy controls. Thus, smoking may have neuroprotective effects. But it may be due, at least in part, to the increased prevalence (disease incidence) of former smokers among PD patients who quit smoking compared with healthy controls.
- Medications:
- Active users of glitazones among type 2 diabetics were 41% less likely to develop PD (IRR 0.59 (0.46-0.77).
- Patients with inflammatory bowel disease (IBD) virtually do not develop PD when treated with TNF inhibitors; both diseases share common pathomechanisms according to genomic analyses: variants in the gene for LRRK2, which increases the risk of PD, appear to have an important function as an immunomodulator, which is of importance in intestinal inflammation, as well as playing a role in inflammatory processes of neurodegenerative diseases.
- Surgeries: Appendectomy (appendectomy) in adolescence resulted in a cumulative risk reduction of approximately 20% – as much as 25% in people who lived in rural areas – for subsequent sporadic PD. In addition, patients had a higher age at the initial diagnosis of PD.Molecular studies in appendix samples from healthy people revealed evidence of pathogenic alpha-synuclein aggregates (presumed trigger before PD).
Secondary prevention
- Endurance training: up to four hours of exercise per week; after warming up, patients trained on a treadmill for 30 minutes to the limit of their performance (80 to 85 percent of their maximum heart rate): this initially slowed the progression of the disease in a randomized study (Unified Parkinson’s Disease Rating Scale (UPDRS): group with intensive training: minimal increase of 0.3 points; group with moderate training: increase 3.2 points).
