There have been found associations of cigarette smoking with a decrease in the occurrence of Parkinson’s Disease (PD):
The abstract of this study is below in which smoking and coffee intake both currently decrease the risk of PD:
A reduced risk for Parkinson’s disease (PD) among cigarette smokers has been observed consistently during the past 30 years. Recent evidence suggests that caffeine may also be protective. Findings are presented regarding associations of PD with smoking, caffeine intake, and alcohol consumption from a case-control study conducted in western Washington State in 1992–2000. Incident PD cases (n = 210) and controls (n = 347), frequency matched on gender and age were identified from enrollees of the Group Health Cooperative health maintenance organization. Exposure data were obtained by in-person questionnaires. Ever having smoked cigarettes was associated with a reduced risk of PD (odds ratio (OR) = 0.5, 95% confidence interval (CI): 0.4, 0.8). A stronger relation was found among current smokers (OR = 0.3, 95% CI: 0.1, 0.7) than among ex-smokers (OR = 0.6, 95% CI: 0.4, 0.9), and there was an inverse gradient with pack-years smoked (trend p < 0.001). No associations were detected for coffee consumption or total caffeine intake or for alcohol consumption. However, reduced risks were observed for consumption of 2 cups/day or more of tea (OR = 0.4, 95% CI: 0.2, 0.9) and two or more cola drinks/day (OR = 0.6, 95% CI: 0.3, 1.4). The associations for tea and cola drinks were not confounded by smoking or coffee consumption. Am J Epidemiol 2002;155:732–8.
But cigarette smoking is bad for your lungs, increasing cancer risks and emphysema among other things, so why would anyone want to smoke just to decrease PD risk? Is there another way to decrease PD risk and why do cigarettes work for PD?
- The study at the top of the page (ANN NEUROL 2013;74:472–477) helps demonstrate the possibility that nicotine is neuro-protective among all the millions of compounds found in cigarette smoke.
- Nicotine is derived from nicotiana spp. of solanaceae species which includes capsicum and solanum species whose edible fruits and tubers include peppers, eggplants, potatoes, and tomatoes. All of these have nicotine in them. In peppers, there is approximately 102 micrograms/kg, while tomatoes have 43 mcg/kg of nicotine. A potato has ~19 mcg/kg of nicotine. Since we consume more tomatoes and potatoes than peppers, they make up most of the nicotine consumption in people.
- It is noted that nicotine stimulates alpha4beta2 (a4B2) receptors in the brain which protect dopaminergic neurons by binding the receptors. This may be how PD is prevented.
- In the study, 490 people with PD were assessed for vegetable intake, in particular peppers, tomatoes, and potatoes. It was found that PD frequency was inversely related to solanaceae intake but not other vegetables, in particular peppers. Weighted for those with the most nicotine intake, those with the highest nicotine consumption had the lowest frequency of PD. There were 644 controls in this study.
- After calculating risks, pepper consumption 2-4 times a week was associated with a 30% reduction in PD risk in people who did not smoke.
- The food impact was highest in non-smokers since the nicotine content in food is so much lower than the intake of nicotine in active smokers.
- There was an inverse association of PD in consumption of tomatoes (Fall PA, Fredrikson M, Axelson O, et al. Nutritional and occupational factors influencing the risk of Parkinson’s disease: a casecontrol study in southeastern Sweden. Mov Disord 1999;14:28–37) , potatoes ( Hellenbrand W, Seidler A, Boeing H, et al. Diet and Parkinson’s disease. I: A possible role for the past intake of specific foods and food groups. Results from a self-administered food-frequency questionnaire in a case-control study. (Neurology 1996;47: 636–643) and a Mediterranean Diet with tomatoes ( The Association between Mediterranean Diet Adherence and Parkinson’s Disease ) [ Abstract: The most consistent data support the association between higher consumption of dairy products and increased PD risk. More recently, a prospective analysis of two large cohorts, the Health Professionals Follow-Up Study (HPFS) and the Nurses’ Health Study (NHS), revealed an association between PD risk and dietary patterns as assessed by the Alternate Healthy Eating Index (AHEI) and the alternate Mediterranean Diet Score. The Mediterranean diet (MeDi) has received attention in recent years because of growing evidence associating MeDi with lower risk for AD, cardiovascular disease, several forms of cancer, and overall mortality.The MeDi is characterized by high intake of vegetables, legumes, fruits, and cereals; high intake of unsaturated fatty acids (mostly in the form of olive oil) compared to saturated fatty acids; a moderately high intake of fish; a low to-moderate intake of dairy products, meat and poultry; and a regular but moderate consumption of ethanol, primarily in the form of wine and generally during meals. This study suggests that lower adherence to MeDi is associated with PD status. The association persisted after adjustment for multiple potential confounders. The fact that among PD participants, lower adherence was associated with earlier PD age-at-onset further suggests a possible dose-response effect. The relation between MeDi adherence and PD status was not driven by any individual category of the diet but rather the whole pattern. Previous studies have indicated that environmental factors play a major role in PD; however, most nutritional studies in PD have shown conflicting results. Possible explanation for the conflicting data is that most studies have focused on single nutrients, e.g. vitamins C or E,7, rather than on dietary patterns. Indeed, the largest prospective study of dietary patterns identified a Mediterranean-like diet as protective of PD both in males (HPFS) and females (NHS). Assessing dietary patterns may be more informative than assessing specific nutrients separately. First, this approach is more consistent with individuals’ eating habits, and second, it takes into account interactions among nutrients. This approach has been successful in AD and in non-neurological diseases.The mechanism by which MeDi may be protective in neurodegenerative disorders is largely unknown. Mechanisms that have been hypothesized in the AD literature, include oxidative stress and inflammation. Indeed, oxidative stress has been implicated in the pathogenesis of PD. Complex phenols and other substances including vitamin C, vitamin E, and carotenoid may serve as antioxidants, and are found in high concentrations in the typical components of the MeDi. Inflammation has also been implicated in the pathogenesis of PD, and anti-inflammatory non-steroidal medications may be associated with a lower risk for PD. Adherence to the MeDi may attenuate inflammation. In addition, MeDi adherence may be protective because of lower consumption of compounds which are associated with higher PD risk. We and others have shown an association between animal fat consumption and PD, and the association between higher dairy intake and PD was previously reported.]
- There are still unknowns in this study – i.e relative to smoking, diet is a modest contributor of nicotine. Biological effects of Solanaceae nicotine has not been established but substantial a4B2 nicotine receptors are occupied without active smoking in patients who take in solanaceae products.As compared to smoking, smokers with just a puff get enough nicotine to occupy a third of the receptors for more than three hours. It is also unknown if french fries, salsa, sauces, or fried potatoes give a similar nicotine effect as the original vegetable.
- There may be other neuroprotective chemicals in these vegetables such as Anatabine, which is antiinflammatory and has less toxicity. Anatabine Ameliorates Experimental Autoimmune thyroiditis << Key components: Tobacco smoking has numerous detrimental effects on human health, but it has also been associated with a few apparent salutary actions, including the amelioration of autoimmune (Hashimoto) thyroiditis and ulcerative colitis. Smokers in the Third National Health and Nutrition Examination Survey were found to have lower prevalence of thyroperoxidase and/or thyroglobulin antibodies than nonsmokers (1). This protective effect of smoking was confirmed in two additional cross-sectional studies, one from the Amsterdam autoimmune thyroid disease cohort (2) and the other from the Danish population (3), as well as in a 5-yr prospective study also based on the Amsterdam autoimmune thyroid disease cohort (4). In the prospective study, cigarette smoking women who had one or more relative with documented thyroid autoimmunity but no thyroid dysfunction or autoantibodies at study entry showed lower odds of developing thyroperoxidase and/or thyroglobulin antibodies (4). Similarly in ulcerative colitis, smoking has been shown to decrease flares (5), hospitalizations (6), and a need for oral glucocorticoids (7) so that low-dose smoking resumption has been successfully used in ex-smokers with refractory disease (8). The mechanisms underlying this influence of tobacco smoking on some autoimmune diseases have been related to the effects of tobacco components on the immune system (9). There are numerous (4000) components in tobacco, including alkaloids (such as nicotine and anatabine), gases (e.g. carbon monoxide), and carcinogens (e.g. polycyclic aromatic hydrocarbons, aldehydes, free radicals, and solvents), and of them nicotine is known to possess antiinflammatory properties (10). Nicotine acts via binding to the nicotinic receptor, a pentameric ion channel (mainly for sodium and calcium) formed by the arrangement of 16 different subunits in hetero- or homomeric conformations (11). The receptor is classically expressed in the peripheral (all preganglionic fibers and neuromuscular synapses) and central nervous system, but more recently it has been described in cells of the immune system, including CD4 T lymphocytes, dendritic cells, and macrophages (12). Indeed, the 7-homopentameric nicotinic receptor has emerged as a novel therapeutic target for diseases with an inflammatory pathogenesis (13). Nicotine has been used successfully in mice with experimental autoimmune encephalomyelitis in which it reduced disease severity, shifting the autoimmune profile from pathogenic Th1 and Th17 responses to protective Th2 responses (14). Nicotine, however, cannot be used in humans because it is addictive and toxic and has a short 3-h plasma half-life. Consequently, we reasoned that other alkaloids of tobacco could share similar antiinflammatory properties but have a more favorable pharmacological profile. The minor tobacco alkaloid anatabine is nonaddictive and nontoxic at therapeutic doses and has a longer 8-hr half-life. Furthermore, anatabine has been recently shown to inhibit nuclear factor-B (NF-B) activation and reduce neuroinflammation in a mouse model of Alzheimer disease (15). In the present study, we therefore tested the antiinflammatory properties of anatabine in a mouse model of experimental autoimmune thyroiditis. Anatabine is an alkaloid with a structure similar to nicotine, found in tobacco and other solanaceous plantsas tomatoes, potatoes, green pepper, and eggplant. Its lack of addictive potential or any demonstrated toxicity. Given the structure similarity with nicotine, we postulated that anatabine initiates its effects by binding to the nicotine receptor and modulating the cholinergic control of inflammation (10, 24). The nicotinic receptor that has been clearly associated with antiinflammatory responses is the 7-homopentamer, classically found on neural cells but also on immune cells (12). Activation of the 7-nicotinic receptor present in lymphocytes, dendritic cells, and macrophages has been shown to suppress nuclear translocation of NF-B and transcription of high mobility group box 1, ultimately decreasing danger signals that initiate inflammation (25). Consistent with this mechanism, Paris and colleagues demonstrated that anatabine suppresses in a dose-dependent manner the transcription of NF-B induced by tumor necrosis factor- (15). However, anatabine suppressed the thyroidal expression of IL-18 and IL-1R2. IL-18, a member of the IL-1 family, is produced by activated macrophages and stimulates production of interferon- from T cells and natural killer cells (26), overall acting as a proinflammatory stimulus. IL-18 has been shown to increase during thyroid inflammation both in vitro (27) and in vivo (28) ]
- Capsinoids in peppers and capsaicinoids in spicy peppers may activat TRPV1 (Transient Receptor Potential Cation Channel subfamily vanilloid member 1) in the midbrain dopaminergic neurons. This seems to e protective. Transient Receptor Potential Vanilloid Subtype 1 Mediates Cell Death of Mesencephalic Dopaminergic Neurons In Vivo and In Vitro and Somatostatin prevents lipopolysaccharide‑induced neurodegenration
- Major nutritional issues in the management of Parkinson’s disease
Summary: To safely decrease your risk of Parkinson’s disease, increase your peppers, tomatoes, potatoes, and eggplant intake. They have nicotine that when consumed, is protective of dopaminergic receptors of your brain and seem to decrease the risk of PD.