scholarly journals Lifestyle Factors and Parkinson’s Disease Risk in a Rural New England Case-Control Study

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Angeline S. Andrew ◽  
Faith L. Anderson ◽  
Stephen L. Lee ◽  
Katharine M. Von Herrmann ◽  
Matthew C. Havrda

Introduction. Parkinson’s disease (PD) is an age-related neurodegenerative disease likely caused by complex interactions between genetic and environmental risk factors. Exposure to pesticides, toxic metals, solvents, and history of traumatic brain injury have been implicated as environmental risk factors for PD, underscoring the importance of identifying risk factors associated with PD across different communities. Methods. We conducted a questionnaire-based case-control study in a rural area on the New Hampshire/Vermont border, enrolling PD patients and age- and sex-matched controls from the general population between 2017 and 2020. We assessed frequent participation in a variety of recreational and occupational activities and surveyed potential chemical exposures. Results. Suffering from “head trauma or a concussion” prior to diagnosis was associated with a fourfold increased risk of PD. Adjustment for head trauma negated any risk of participation in “strenuous athletic activities.” We observed a 2.7-fold increased risk of PD associated with activities involving lead (adjusted p = 0.038 ). Conclusion. Implicating these factors in PD risk favors public health efforts in exposure mitigation while also motivating future work mechanisms and intervention opportunities.

1993 ◽  
Vol 12 (4) ◽  
pp. 209-218 ◽  
Author(s):  
Wen-zhi Wang ◽  
Xiang-hua Fang ◽  
Xue-ming Cheng ◽  
De-hua Jiang ◽  
Zhen-jian Lin

Neurology ◽  
1997 ◽  
Vol 48 (6) ◽  
pp. 1583-1588 ◽  
Author(s):  
H. H. Liou ◽  
M. C. Tsai ◽  
C. J. Chen ◽  
J. S. Jeng ◽  
Y. C. Chang ◽  
...  

Neurology ◽  
1986 ◽  
Vol 36 (2) ◽  
pp. 284-284 ◽  
Author(s):  
N. E. Bharucha ◽  
L. Stokes ◽  
B. S. Schoenberg ◽  
C. Ward ◽  
S. Ince ◽  
...  

1990 ◽  
Vol 17 (3) ◽  
pp. 349-355 ◽  
Author(s):  
Clyde Hertzman ◽  
Michele Wiens ◽  
David Bowering ◽  
Barry Snow ◽  
Donald Calne

2002 ◽  
Vol 18 (12) ◽  
pp. 1133-1142 ◽  
Author(s):  
Philippe Pals ◽  
Bart Van Everbroeck ◽  
Bart Grubben ◽  
Maria Kristina Viaene ◽  
René Dom ◽  
...  

2015 ◽  
Vol 40 (3) ◽  
pp. 113-117 ◽  
Author(s):  
A Jahan ◽  
SZR Rezina Parvin ◽  
D Bugum

This case-control study was done to identify the correlation between the familial, social and environmental risk factors and autism. This hospital and specialized centre based study done from January 2002 to November, 2004. Thirty two children from the autism group and 14 children from the control group were enrolled. Mean age were 3.75 yrs. and 2.83 yrs. respectively. Significant proportion of children were in the highest birth orders, 68.8% in autism and 78.6% in the control group. Full term children were 96.9% and 92.9% respectively. 53.1% children in the autism and 57.1% in the normal speech delay group were born by cesarean sections. Higher education of parents in autism group was statistically significant (p<0.05). Too much watching TV, inadequate opportunity to mix with peers and inadequate interactive relationship with the family members in the early childhood were significantly (p= 0.001) related to the development of autism.Bangladesh Med Res Counc Bull 2014; 40 (3): 113-117


2010 ◽  
Vol 104 (5) ◽  
pp. 757-764 ◽  
Author(s):  
Kentaro Murakami ◽  
Yoshihiro Miyake ◽  
Satoshi Sasaki ◽  
Keiko Tanaka ◽  
Wakaba Fukushima ◽  
...  

Increased homocysteine levels might accelerate dopaminergic cell death in Parkinson's disease (PD) through neurotoxic effects; thus, increasing intake of B vitamins involved in the regulation of homocysteine metabolism might decrease the risk of PD through decreasing plasma homocysteine. However, epidemiological evidence for the association of dietary B vitamins with PD is sparse, particularly in non-Western populations. We conducted a hospital-based case–control study in Japan to examine associations between dietary intake of folate, vitamin B6, vitamin B12 and riboflavin and the risk of PD. Patients with PD diagnosed using the UK PD Society Brain Bank criteria (n 249) and controls without neurodegenerative diseases (n 368) were recruited. Dietary intake during the preceding month was assessed at the time of study recruitment using a validated, self-administered, semi-quantitative, comprehensive diet history questionnaire. After adjustment for potential dietary and non-dietary confounding factors, intake of folate, vitamin B12 and riboflavin was not associated with the risk of PD (P for trend = 0·87, 0·70 and 0·11, respectively). However, low intake of vitamin B6 was associated with an increased risk of PD, independent of potential dietary and non-dietary confounders. Multivariate OR (95 % CI) for PD in the first, second, third and fourth quartiles of vitamin B6 were 1 (reference), 0·56 (0·33, 0·94), 0·69 (0·38, 1·25) and 0·48 (0·23, 0·99), respectively (P for trend = 0·10). In conclusion, in the present case–control study in Japan, low intake of vitamin B6, but not of folate, vitamin B12 or riboflavin, was independently associated with an increased risk of PD.


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