From the aDepartment of Public Health, Section of Social Medicine, University of Copenhagen, Copenhagen, Denmark; bDanish Cancer Society, Institute of Cancer Epidemiology, Copenhagen, Denmark; cSchool of Public Health, UCLA, Los Angeles, CA; dHarvard School of Public Health, Department of Epidemiology, Boston, MA; eDepartment of Neurology, Odense University Hospital, Odense, Denmark; and fThe Copenhagen Stress Research Center, Copenhagen, Denmark.
Caring for a chronically ill spouse is stressful, but the health effects of caregiving are not fully understood. We studied the effect on mortality of being married to a person with Parkinson disease.
All patients in Denmark with a first-time hospitalization for Parkinson disease between 1986 and 2009 were identified, and each case was matched to five population controls. We further identified all spouses of those with Parkinson disease (n = 8,515) and also the spouses of controls (n = 43,432). All spouses were followed in nationwide registries until 2011.
Among men, being married to a Parkinson disease patient was associated with a slightly higher risk of all-cause mortality (hazard ratio = 1.06 [95% confidence interval = 1.00-1.11]). Mortality was particularly high for death due to external causes (1.42 [1.09-1.84]) including suicide (1.89 [1.05-3.42]) and death from undefined symptoms/abnormal findings (1.25 [1.07-1.47]). Censoring at the time of death of the patient attenuated the findings for all-cause mortality in husbands (1.02 [0.95-1.09]), indicating that part of the association is with bereavement. Still, living with a person with Parkinson disease 5 years after first Parkinson hospitalization was associated with higher risk of all-cause mortality for both husbands (1.15 [1.07-1.23]) and wives (1.11 [1.04-1.17]).
Caring for a spouse with a serious chronic illness is associated with a slight but consistent elevation in mortality risk.
In earlier studies, we found high age-adjusted prevalences of Parkinson's disease (PD) in the Faroe Islands (209 per 100,000 inhabitants) and in Greenland (187.5 per 100,000 inhabitants) compared to the age-adjusted prevalence on the island of Als in the southern part of Denmark (98.3 per 100,000 inhabitants). We thoroughly examined patients with suspected parkinsonism using internationally accepted diagnostic criteria. In the present study, we found no significant clinical differences between patients with PD in the three areas, despite this high difference in prevalence. However, comparing the age at examination and age at treatment, the patients were younger in Greenland, a higher proportion of patients had cognitive decline, and they had a higher mean Hoehn and Yahr rating score, although they received a lower levodopa dose. A higher proportion of the patients in Greenland were newly diagnosed than in the other two areas.
Insulin contributes to normal brain function. Previous studies have suggested associations between midlife diabetes and neurodegenerative diseases, including Parkinson's disease. Using Danish population registers, we investigated whether a history of diabetes or the use of antidiabetes drugs was associated with Parkinson's disease.
From the nationwide Danish Hospital Register hospital records, we identified 1,931 patients with a first-time diagnosis of Parkinson's disease between 2001 and 2006. We randomly selected 9,651 population control subjects from the Central Population Registry and density matched them by birth year and sex. Pharmacy records comprising all antidiabetes and anti-Parkinson drug prescriptions in Denmark were available. Odds ratios (ORs) were estimated by logistic regression models.
Having diabetes, as defined by one or more hospitalizations and/or outpatient visits for the condition, was associated with a 36% increased risk of developing Parkinson's disease (OR 1.36 [95% CI 1.08-1.71]). Similarly, diabetes defined by the use of any antidiabetes medications was associated with a 35% increased Parkinson's disease risk (1.35 [1.10-1.65]). When diabetes was defined as the use of oral antidiabetes medications, effect estimates were stronger in women (2.92 [1.34-6.36]), whereas when diabetes was defined as any antidiabetes drug prescription, patients with early-onset Parkinson's disease were at highest risk (i.e., Parkinson's disease diagnosed before the age of 60 years; 3.07 [1.65-5.70]).
We found that a diagnosis of, or treatment received for, diabetes was significantly associated with an increased risk of developing Parkinson's disease, especially younger-onset Parkinson's disease. Our results suggest a common pathophysiologic pathway between the two diseases. Future studies should take age at Parkinson's disease onset into account.
A new educational training concept was introduced with the latest Danish national reform of specialist training of doctors in 2004. We performed a questionnaire survey, the aim of which was to explore the result of the implementation so far and to get ideas facilitating a sharper focus of our efforts to further develop the educational reform. The results showed high commitment within the system and also pointed to management support as an essential prerequisite for job satisfaction. The development and assessment of the specialist training, however, need further observation.
The relationship between Parkinson disease (PD) and smoking has been examined in several studies, but little is known about smoking in conjunction with other behaviors and a family history of PD. Using unconditional logistic regression analysis, we studied individual and joint associations of these factors with idiopathic PD among 1,808 Danish patients who were diagnosed in 1996-2009 and matched to 1,876 randomly selected population controls. Although there was a downward trend in duration of smoking, this was not observed for daily tobacco consumption. A moderate intake of caffeine (3.1-5 cups/day) was associated with a lower odds ratio for PD (0.45, 95% confidence interval: 0.34, 0.62), as was a moderate intake of alcohol (3.1-7 units/week) (odds ratio = 0.60, 95% confidence interval: 0.58, 0.84); a higher daily intake did not reduce the odds further. When these behaviors were studied in combination with smoking, the odds ratios were lower than those for each one alone. Compared with never smokers with no family history of PD, never smokers who did have a family history had an odds ratio of 2.81 (95% confidence interval: 1.91, 4.13); for smokers with a family history, the odds ratio was 1.60 (95% confidence interval: 1.15, 2.23). In conclusion, duration of smoking seems to be more important than intensity in the relationship between smoking and idiopathic PD. The finding of lower risk estimates for smoking in combination with caffeine or alcohol requires further confirmation.
Notes
Cites: Ann Neurol. 2001 Jul;50(1):56-6311456310
Cites: Ann Neurol. 2001 Dec;50(6):780-611761476
Cites: Drugs Aging. 2001;18(11):797-80611772120
Cites: Am J Epidemiol. 2002 Apr 15;155(8):732-811943691
Cites: Hum Mol Genet. 2003 Jan 1;12(1):79-8612490535
Cites: Neurology. 2003 Jul 8;61(1):11-712847149
Cites: Ann Neurol. 2003 Aug;54(2):170-512891669
Cites: Neurology. 2007 Mar 6;68(10):764-817339584
Cites: Alcohol Res Health. 2006;29(3):179-8517373406
Cites: Arch Neurol. 2007 Jul;64(7):990-717620489
Cites: Mov Disord. 2007 Nov 15;22(15):2242-817712848
Experimental evidence supports a preventative role for non-steroidal anti-inflammatory drugs (NSAIDs) in Parkinson's disease (PD).
We investigated associations between use of aspirin, nonaspirin NSAIDs, and acetaminophen and PD in a large population-based case-control study using Danish health and pharmacy registries. We identified 1,931 PD cases reported in hospital or outpatient clinic records who had received a primary diagnosis of PD between 2001 and 2006, and 9,651 age- and sex-matched controls from the Danish population register. Prescription medication use was documented in a pharmacy database covering all residents of Denmark since 1995.
Adjusting for age, sex, use of cardiovascular disease drugs, diagnosis of chronic pulmonary obstructive disorder, and Charlson comorbidity scores, and excluding prescriptions filled within 5 years before diagnosis, we found no evidence for an association between PD and either aspirin use (OR = 0.97; 95% CI 0.82, 1.14) or nonaspirin NSAID use (OR = 0.97; 95% CI 0.86, 1.09), regardless of intensity of use; further, there was no association between use of ibuprofen or acetaminophen and PD.
Our findings provide no evidence for a protective effect of nonaspirin and aspirin NSAID prescription drug use shortly before PD onset.
The objective of this study was to investigate whether statin (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor) use is associated with risk of Parkinson's disease (PD) in Denmark. We identified 1,931 patients with a first time diagnosis of PD reported in hospital or outpatient clinic records between 2001 and 2006. We density matched to these patients 9,651 population controls by birth year and sex relying on the Danish population register. For every participant, we identified pharmacy records of statin and anti-Parkinson drug prescriptions since 1995 and before index date from a prescription medication use database for all Danish residents. Whenever applicable, the index dates for cases and their corresponding controls were advanced to the date of first recorded prescription for anti-Parkinson drugs. In our primary analyses, we excluded all statin prescriptions 2-years before PD diagnosis. Employing logistic regression adjusting for age, sex, diagnosis of chronic obstructive pulmonary disease, and Charlson comorbidity, we observed none to slightly inverse associations between PD diagnosis and statin prescription drug use. Inverse associations with statin use were only observed for short-term (
