Effect of reproductive factors and postmenopausal hormone use on the risk of Parkinson disease

Popat, Rita A.; Eeden, Stephen K. Van Den; Tanner, Caroline M.; McGuire, V.; Bernstein, Allan L.; Bloch, D. A.; Leimpeter, Amethyst; Nelson, Lorene M.

doi:10.1212/01.wnl.0000171344.87802.94

Cited by 118 publications

(121 citation statements)

References 26 publications

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“…In addition to epidemiologic studies, 1 experimental study also showed preliminary evidence that estrogen may abolish neuroprotection by caffeine among ovariectomized female mice (23). Nevertheless, a potential role of estrogen in PD etiology has yet to be defined, and the evidence to date on estrogen and PD has been inconsistent in both human studies (24,25) and animal experiments (26,27). Further, recent research suggests that the health implications of hormone use among women may depend on composition of the hormone preparation, time of initiation, duration of use, and type of administration (28).…”

Section: Discussionmentioning

confidence: 99%

Caffeine Intake, Smoking, and Risk of Parkinson Disease in Men and Women

Guo

Park

et al. 2012

American Journal of Epidemiology

149

124

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The authors prospectively examined whether caffeine intake was associated with lower risk of Parkinson disease (PD) in both men and women among 304,980 participants in the National Institutes of Health-AARP Diet and Health Study and whether smoking affected this relation. Multivariate odds ratios and 95% confidence intervals were derived from logistic regression models. Higher caffeine intake as assessed in 1995-1996 was monotonically associated with lower PD risk (diagnosed in [2000][2001][2002][2003][2004][2005][2006] in both men and women. After adjustment for age, race, and physical activity, the odds ratio comparing the highest quintile of caffeine intake with the lowest was 0.75 (95% confidence interval: 0.60, 0.94; P trend ¼ 0.005) for men and 0.60 (95% confidence interval: 0.39, 0.91; P trend ¼ 0.005) for women. Further adjustment for duration of smoking and analyses carried out among never smokers showed similar results. A joint analysis with smoking suggested that smoking and caffeine may act independently in relation to PD risk. Finally, the authors conducted a metaanalysis of prospective studies and confirmed that caffeine intake was inversely associated with PD risk in both men and women. These findings suggest no gender difference in the relation between caffeine and PD. Lifestyle habits such as coffee drinking (1, 2) and cigarette smoking (1, 3, 4) have been repeatedly linked to a lower risk of Parkinson disease (PD) in many epidemiologic studies. The inverse association of coffee consumption and caffeine intake with PD has been shown in approximately 20 epidemiologic studies, including several prospective cohort studies (5-9). Further epidemiologic and experimental evidence suggests that caffeine may be the active component that underlies this relation (5,7,10). It has been hypothesized that caffeine and its major metabolites may protect dopaminergic neurons by antagonizing adenosine A 2A receptor (10).Some questions remain, however, concerning the epidemiologic evidence for a link between caffeine and PD. While the relation is fairly robust among men, it is inconsistent among women (5, 6). Further, in women, a potential interaction with postmenopausal hormone use has been observed (11,12). Adding complexity, coffee drinkers are more likely to smoke than nondrinkers (13,14). Previous studies might not have evaluated the potential influence of cigarette smoking on the caffeine-PD relation because of small sample sizes or inadequate data on smoking.Previously, using data from the National Institutes of Health (NIH)-AARP Diet and Health Study, we reported that smoking duration, rather than intensity, might underlie the strong inverse association between smoking and PD (4). In the current study, we evaluated caffeine intake in relation to PD, focusing on the relation in women and the potential influence of smoking on this relation.

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Section: Discussionmentioning

confidence: 99%

Caffeine Intake, Smoking, and Risk of Parkinson Disease in Men and Women

Guo

Park

et al. 2012

American Journal of Epidemiology

149

124

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“…40 However, other studies did or did not confirm these associations. 41,42 In the Mayo Clinic Cohort Study of Oophorectomy and Aging, women who underwent bilateral oophorectomy before the onset of menopause had an increased risk of parkinsonism compared with referent women (HR 1.80; 95% CI 1.00-3.26; P = 0.05), and the risk increased with younger age at oophorectomy (test for linear trend; P = 0.02). The findings were similar regardless of the indication for the oophorectomy (benign condition vs. prophylactic).…”

Section: Parkinsonism and Parkinson's Diseasementioning

confidence: 99%

Prophylactic oophorectomy in premenopausal women and long-term health

Shuster¹,

Gostout²,

Grossardt³

et al. 2008

Menopause International

218

136

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Objective-To review the data on long-term outcomes in women who underwent prophylactic bilateral oophorectomy, a common surgical procedure that has more than doubled in frequency since the 1960s.Study design-Literature review of published data on consequences of prophylactic bilateral oophorectomy. Special emphasis was given to the Mayo Clinic Cohort Study of Oophorectomy and Aging.Main outcome measures-Overall mortality, cardiovascular disease, cognitive impairment and dementia, parkinsonism, osteoporosis, psychological well-being, and sexual function.Results-There is a growing body of evidence suggesting that the premature loss of ovarian function caused by bilateral oophorectomy performed before natural menopause is associated with several negative outcomes. In particular, studies have revealed an increased risk of premature death, cardiovascular disease, cognitive impairment or dementia, parkinsonism, osteoporosis and bone fractures, decline in psychological well-being, and decline in sexual function. The effects involve different organs (e.g., heart, bone, or brain), and different functions within organs (e.g., cognitive, motor, or emotional brain functions). Estrogen treatment may prevent some of these negative outcomes, but not all. Conclusion-The potential adverse effects of prophylactic bilateral oophorectomy on heart health, neurologic health, bone health, and quality of life should be carefully weighed against its potential benefits for cancer risk reduction in women at average risk of ovarian cancer.

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“…When estrogen was administered either immediately after or 1 week after MA treatment, no evidence for neuroprotection was present [10, 11]. This study may provide an understanding of the variations in results on the effects of estrogen upon the NSDA neurodegenerative disorder, Parkinson’s disease, where positive [30,31,32,33,34,35,36], negative [34, 37] and no [30, 38, 39] effects of estrogen have been reported. The current model now provides a means to both understand and study these apparently contradictory effects.…”

Section: Discussionmentioning

confidence: 98%

Effects of Estrogen and Related Agents upon Methamphetamine-Induced Neurotoxicity within an Impaired Nigrostriatal Dopaminergic System of Ovariectomized Mice

Liu

Dluzen²

2006

Neuroendocrinology

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Estrogen increases methamphetamine (MA)-induced neurotoxicity within the impaired nigrostriatal dopaminergic (NSDA) system of ovariectomized female mice, as defined by enhanced striatal dopamine (DA) depletion. In this study we compared the effects of a lower dose of estradiol benzoate (EB, 1 µg) with related agents – tamoxifen (TMX, 12.5 µg), testosterone (5 µg) and dehydroepiandrosterone (DHEA, 3 mg) in this paradigm. In experiment 1, ovariectomized mice received an initial treatment with MA. At 1 week after MA, mice were treated with EB, TMX, testosterone, DHEA or oil vehicle and 24 h later a second MA treatment. Striatal DA and 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations in the MA-treated groups were decreased compared to the non-MA-treated control. Neither EB nor any of the other agents tested showed enhanced neurodegenerative or neuroprotective effects against a second MA invasion. To verify that estrogen was capable of showing a neuroprotective effect under a condition of two administrations of MA, in experiment 2, EB was administered either once or twice prior to each of the two MA treatments. EB treatment prior to the first MA invasion or first and second MA protected the NSDA system against DA and DOPAC depletion. These results imply that a lower dose of EB, TMX, testosterone and DHEA cannot exert neurodegenerative or neuroprotective effects in the impaired NSDA model. However, EB administered prior to the introduction of neurotoxicity can protect the NSDA system. This study may provide an understanding of the variations in results on the effects of estrogen upon the NSDA neurodegenerative disorder, Parkinson’s disease.

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Effect of reproductive factors and postmenopausal hormone use on the risk of Parkinson disease

Abstract: Postmenopausal use of estrogen alone may increase the risk of Parkinson disease (PD) among women with a hysterectomy. Among women with natural menopause for whom the usual treatment is combined estrogen-progestin therapy, no increased risk of PD was observed.

Cited by 118 publications

References 26 publications

Caffeine Intake, Smoking, and Risk of Parkinson Disease in Men and Women

Caffeine Intake, Smoking, and Risk of Parkinson Disease in Men and Women

Prophylactic oophorectomy in premenopausal women and long-term health

Effects of Estrogen and Related Agents upon Methamphetamine-Induced Neurotoxicity within an Impaired Nigrostriatal Dopaminergic System of Ovariectomized Mice

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