Vitamin D and Sunlight Exposure in Newly-Diagnosed Parkinson’s Disease

Circulating vitamin D has previously been found to be lower in patients with Parkinson’s disease (PD), while the effects of sunlight exposure have not yet been fully investigated. Therefore, we evaluated the associations between serum vitamin D, vitamin D intake, sunlight exposure, and newly-diagnosed PD patients in a Chinese population. This case-control study measured serum 25-hydroxyvitamin D (25(OH)D) levels and sunlight exposure in 201 patients with newly-diagnosed PD and 199 controls without neurodegenerative diseases. Data on vitamin D intake and sunlight exposure were obtained using a self-report questionnaire. Multivariable logistic regressions were employed to evaluate the associations between serum 25(OH)D levels, sunlight exposure, and PD. Adjustments were made for sex, age, smoking, alcohol use, education, BMI, and vitamin D intake. There were significantly lower levels of serum 25(OH)D (20.6 ± 6.5 ng/mL), daily vitamin D intake (8.3 ± 3.7 g/day), and sunlight exposure (9.7 ± 4.1 h/week) in patients with PD compared to healthy controls (p < 0.05). Crude odds ratios (ORs) for PD in the quartiles of serum 25(OH)D were 1 (reference), 0.710 (0.401, 1.257), 0.631 (0.348, 1.209), and 0.483 (0.267, 0.874), respectively. Crude ORs for PD in quartiles of sunlight exposure were 1 (reference), 0.809 (0.454, 1.443), 0.623 (0.345, 1.124) and 0.533 (0.294, 0.966), respectively. A significant positive correlation between serum 25(OH)D and sunlight exposure was found, but serum 25(OH)D was not correlated with daily vitamin D intake. This study indicates that lower levels of serum 25(OH)D and sunlight exposure are significantly associated with an increased risk for PD.     

Associations between B Vitamins and Parkinson’s Disease

B vitamins may correlate with Parkinson’s disease (PD) through regulating homocysteine level. However, there is no comprehensive assessment on the associations between PD and B vitamins. The present study was designed to perform a meta-analytic assessment of the associations between folate, vitamin B6, and vitamin B12 and PD, including the status of B vitamins in PD patients compared with controls, and associations of dietary intakes of B vitamins and risk of PD. A literature search using Medline database obtained 10 eligible studies included in the meta-analyses. Stata 12.0 statistical software was used to perform the meta-analysis. Pooled data revealed that there was no obvious difference in folate level between PD patients and healthy controls, and PD patients had lower level of vitamin B12 than controls. Available data suggested that higher dietary intake of vitamin B6 was associated with a decreased risk of PD (odds ratio (OR) = 0.65, 95% confidence intervals (CI) = (0.30, 1.01)), while no significant association was observed for dietary intake of folate and vitamin B12 and risk of PD. PD patients had lower level of vitamin B12 and similar level of folate compared with controls. Dietary intake of vitamin B6 exhibited preventive effect of developing PD based on the available data. As the number of included studies is limited, more studies are needed to confirm the findings and elucidate the underpinning underlying these associations.     

Multiple Antioxidants in the Prevention and Treatment of Parkinson’s Disease

Parkinson’s disease (PD) is one of the major progressive neurological disorders for which no preventative or long-term effective treatment strategies are available. Epidemiologic studies have failed to identify specific environmental, dietary or lifestyle risk factors for PD except for toxic exposure to manganese, meperidine (Demerol®, the “designer drug” version of which often contains a toxic byproduct of the synthesis, 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine [MPTP]), and some herbicides and pesticides. The search for genetic risk factors such as mutation, overexpression or underexpression of nuclear genes in DA neurons in idiopathic PD has not been successful as yet. Polymorphism in certain genes appears to be a risk factor, but there is no direct evidence for the causal relationship between polymorphism and increased risk of PD. In familial PD, mutation in the α-synuclein gene is associated with the disease, but a direct role of this gene in degeneration of DA neurons remains to be established. Although mutations in the Parkin gene has been associated with autosomal recessive juvenile Parkinson’s disease, the role of this gene mutation in causing degeneration of DA neurons has not been defined. We have reported that in hereditary PD, a mutation in the α-synuclein gene may increase the sensitivity of DA neurons to neurotoxins. We hypothesize that, in idiopathic PD, epigenetic (mitochondria, membranes, protein modifications) rather than genetic events are primary targets which, when impaired, initiate degeneration in DA neurons, eventually leading to cell death. Although the nature of neurotoxins that cause degeneration in DA neurons in PD is not well understood, oxidative stress is one of the intermediary risk factors that could initiate and/or promote degeneration of DA neurons. Therefore, supplementation with antioxidants may prevent or reduce the rate of progression of this disease. Supplementation with multiple antioxidants at appropriate doses is essential because various types of free radicals are produced, antioxidants vary in their ability to quench different free radicals and cellular environments vary with respect to their lipid and aqueous phases. L-dihydroxyphenylalanine (L-dopa) is one of the agents used in the treatment of PD. Since L-dopa is known to produce free radicals during its normal metabolism, the combination of L-dopa with high levels of multiple antioxidants may improve the efficacy of L-dopa therapy.     

Systematic Review of the Prevalence and Incidence of Parkinson’s Disease in Asia

Background

Parkinson’s disease (PD) is a common neurodegenerative disorder in older people, and half of the world’s older population lives in Asia. However, the epidemiology of PD in Asian countries is poorly understood. This review assembles evidence on the prevalence and incidence of PD in Asian countries and identifies gaps in our present knowledge.

Methods

A systematic search of studies published from 1965 to October 2008 was conducted using MEDLINE and EMBASE. The selection criteria were defined a priori. Prevalence and incidence were standardized to the WHO World Standard Population 2000. Twenty-one original studies were selected for the review. Two studies that described the ethnic origin of participants and contained Asian populations were also included in the analysis.

Results

Excluding one study with questionably low prevalence and incidence, the remaining studies reported a standardized all-age prevalence of 51.3 to 176.9 per 100 000 in door-to-door surveys; prevalence in record-based studies ranged from 35.8 to 68.3 per 100 000. The standardized incidence rates were 8.7 per 100 000 person-years in door-to-door surveys and 6.7 to 8.3 per 100 000 person-years in record-based surveys.

Conclusions

The prevalence of PD in Asian countries was slightly lower than that in Western countries. However, comparison of incidence was difficult because of the small number of studies. Varying methodologies, diagnostic criteria, and case-finding strategies contributed to the considerable variation in the reported prevalence and incidence of PD.Key words: epidemiology, prevalence, incidence, Parkinson’s disease, Asia     

Manganese and Parkinson’s Disease: A Critical Review and New Findings

Background

Excess accumulation of manganese (Mn) in the brain results in a neurological syndrome with cognitive, psychiatric, and movement abnormalities. The highest concentrations of Mn in the brain are achieved in the basal ganglia, which may precipitate a form of parkinsonism with some clinical features that are similar and some that are different to those in Parkinson’s disease (PD). Recently, scientists have debated the possibility that Mn may have an etiological role in PD or that it may accelerate the expression of PD.

Objective

The goal of this review was to examine whether chronic Mn exposure produces dopamine neuron degeneration and PD or whether it has a distinct neuropathology and clinical presentation.

Data source

I reviewed available clinical, neuroimaging, and neuropathological studies in humans and nonhuman primates exposed to Mn or other human conditions that result in elevated brain Mn concentrations.

Data extraction

Human and nonhuman primate literature was examined to compare clinical, neuroimaging, and neuropathological changes associated with Mn-induced parkinsonism.

Data synthesis

Clinical, neuroimaging, and neuropathological evidence was used to examine whether Mn-induced parkinsonism involves degeneration of the nigrostriatal dopaminergic system as is the case in PD.

Conclusions

The overwhelming evidence shows that Mn-induced parkinsonism does not involve degeneration of midbrain dopamine neurons and that l-dopa is not an effective therapy. New evidence is presented on a putative mechanism by which Mn may produce movement abnormalities. Confirmation of this hypothesis in humans is essential to make rational decisions about treatment, devise effective therapeutic strategies, and set regulatory guidelines.     

One Community’s Effort to Control Genetic Disease

In 1989, we established a small community health clinic to provide care for uninsured Amish and Mennonite children with genetic disorders. Over 20 years, we have used publicly available molecular data and sophisticated technologies to improve diagnostic efficiency, control laboratory costs, reduce hospitalizations, and prevent major neurological impairments within a rural underserved community. These actions allowed the clinic’s 2010 operating budget of $1.5 million to save local communities an estimated $20 to $25 million in aggregate medical costs. This exposes an unsettling fact: our failure to improve the lot of most people stricken with genetic disease is no longer a matter of scientific ignorance or prohibitive costs but of choices we make about how to implement existing knowledge and resources.KEY FINDINGS

• ▪ Successful integration of molecular technologies into primary care can improve diagnostic efficiency, control laboratory costs, reduce hospitalizations, and prevent catastrophic clinical outcomes.
• ▪ Population-specific genetic information is a strong foundation for regional preventative health services. New high-density, low-cost genotyping methods afford the opportunity to actuate this model of care in small underserved communities throughout the world.
• ▪Scaling molecular studies to small populations and even individual families is a reasonable scientific alternative to large scale genome wide association studies, and may help solve some intractable problems in human disease research and public health.

“I have no doubt that it is possible to give a new direction to technological development, a direction that shall lead it back to the real needs of man.”E. F. Schumacher, 19741“Stunning scientific and technological advances in genetics will mean little if they do not benefit people.”A. Guttmacher et al., 20012

     

Traffic-Related Air Pollution and Parkinson’s Disease in Denmark: A Case–Control Study

Background

Very little is currently known about air pollutants’ adverse effects on neurodegenerative diseases even though recent studies have linked particulate exposures to brain pathologies associated with Parkinson’s and Alzheimer’s disease.

Objective

In the present study, we investigated long-term exposure to traffic-related air pollution and Parkinson’s disease.

Methods

In a case–control study of 1,696 Parkinson’s disease (PD) patients identified from Danish hospital registries and diagnosed 1996–2009 and 1,800 population controls matched by sex and year of birth, we assessed long-term traffic-related air pollutant exposures (represented by nitrogen dioxide; NO₂) from a dispersion model, using residential addresses from 1971 to the date of diagnosis or first cardinal symptom for cases and the corresponding index date for their matched controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated with logistic regression, adjusting for matching factors and potential confounders.

Results

We found ambient air pollution from traffic sources to be associated with risk of PD, with a 9% higher risk (95% CI: 3, 16.0%) per interquartile range increase (2.97 μg/m³) in modeled NO₂. For participants living for ≥ 20 years in the capital city, ORs were larger (OR = 1.21; 95% CI: 1.11, 1.31) than in provincial towns (OR = 1.10; 95% CI: 0.97, 1.26), whereas there was no association among rural residents.

Conclusions

Our findings raise concerns about potential effects of air pollution from traffic and other sources on the risk of PD, particularly in populations with high or increasing exposures.

Citation

Ritz B, Lee PC, Hansen J, Funch Lassen C, Ketzel M, Sørensen M, Raaschou-Nielsen O. 2016. Traffic-related air pollution and Parkinson’s disease in Denmark: a case–control study. Environ Health Perspect 124:351–356; http://dx.doi.org/10.1289/ehp.1409313     

A Study of the Relationship between Health and Subjective Well-Being in Parkinson’s Disease Patients

ObjectivesGovernments are turning their attention to evidence on subjective measures of well-being to inform policy decisions. In the context of health, there is, therefore, growing interest in understanding how measures of health-related quality of life relate to subjective well-being and whether subjective well-being could provide a basis for resource allocation decisions in the future. This study investigates the relationship between health-related quality of life, as measured by the EuroQol five-dimensional (EQ-5D) questionnaire, and subjective well-being in Parkinson’s disease.MethodsA paper questionnaire including the EQ-5D questionnaire, four key subjective well-being questions taken from the Integrated Household Survey in England, and other demographic details was distributed to people with Parkinson’s disease in the United Kingdom. Responses were used to estimate multiple regression models explaining subjective well-being using the EQ-5D questionnaire index (UK weights), EQ-5D questionnaire dimensions and the visual analogue scale, and patients’ sociodemographic characteristics.ResultsA total of 199 responses were received. Combining visual analogue scale and EQ-5D questionnaire dimensions, especially anxiety/depression and, to a lesser extent, mobility, yielded the best-fitting models (adjusted R² range 0.36–0.53). Patients with Parkinson’s disease living in care homes report lower levels of subjective well-being than do those living alone. These effects are not captured by the health-related quality-of-life measures in the analysis.ConclusionsUsual health-related quality-of-life measures can partially explain different well-being dimensions, yet they fail to capture part of the broader impact of disease on subjective well-being. Further empirical research into the relationship between subjective well-being and the EQ-5D Parkinson’s disease longitudinally, and in different disease areas, is required, and further standardization of subjective well-being measures is recommended.     

Association of Cumulative Lead Exposure with Parkinson’s Disease

Background

Research using reconstructed exposure histories has suggested an association between heavy metal exposures, including lead, and Parkinson’s disease (PD), but the only study that used bone lead, a biomarker of cumulative lead exposure, found a nonsignificant increase in risk of PD with increasing bone lead.

Objectives

We sought to assess the association between bone lead and PD.

Methods

Bone lead concentrations were measured using ¹⁰⁹Cd excited K-shell X-ray fluorescence from 330 PD patients (216 men, 114 women) and 308 controls (172 men, 136 women) recruited from four clinics for movement disorders and general-community cohorts. Adjusted odds ratios (ORs) for PD were calculated using logistic regression.

Results

The average age of cases and controls at bone lead measurement was 67 (SD = 10) and 69 (SD = 9) years of age, respectively. In primary analyses of cases and controls recruited from the same groups, compared with the lowest quartile of tibia lead, the OR for PD in the highest quartile was 3.21 [95% confidence interval (CI), 1.17–8.83]. Results were similar but slightly weaker in analyses restricted to cases and controls recruited from the movement disorders clinics only (fourth-quartile OR = 2.57; 95% CI, 1.11–5.93) or when we included controls recruited from sites that did not also contribute cases (fourth-quartile OR = 1.91; 95% CI, 1.01–3.60). We found no association with patella bone lead.

Conclusions

These findings, using an objective biological marker of cumulative lead exposure among typical PD patients seen in our movement disorders clinics, strengthen the evidence that cumulative exposure to lead increases the risk of PD.     

Vitamin D levels in Alzheimer’s and Parkinson’s diseases: A meta-analysis

ObjectiveRecent accumulating evidence shows that vitamin D deficiency is prevalent in individuals with AD and PD. The purpose of the present study is to perform a meta-analysis on the 25-hydroxyvitamin D (25(OH)D) status in this population of patients.MethodsWe searched all articles in English published up to March 2012 concerning the 25(OH)D level in AD and PD patients. For AD, six studies covering 319 patients and 573 controls were included in the meta-analysis. For PD, five studies discussing 434 patients and 3451 controls were included.ResultsIt was found that AD patients had lower levels of 25(OH)D than healthy controls (summary standardized mean difference [SMD], -1.39; 95% confidence interval [CI], -2.79 to 0.01). Similar results were found for PD patients versus healthy controls (summary SMD, -1.33; 95% CI, -2.44 to -0.21).ConclusionThe results indicate that despite the similar mean age between patients and healthy controls in each identified study, both AD and PD patients have lower levels of 25(OH)D than controls.     

Niacin metabolism and Parkinson’s disease

Epidemiological surveys suggest an important role for niacin in the causes of Parkinson’s disease, in that niacin deficiency, the nutritional condition that causes pellagra, appears to protect against Parkinson’s disease. Absorbed niacin is used in the synthesis of nicotinamide adenine dinucleotide (NAD) in the body, and in the metabolic process NAD releases nicotinamide by poly(ADP-ribosyl)ation, the activation of which has been reported to mediate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease. Recently nicotinamide N-methyltransferase (EC2.1.1.1) activity has been discovered in the human brain, and the released nicotinamide may be methylated to 1-methylnicotinamide (MNA), via this enzyme, in the brain. A deficiency in mitochondrial NADH: ubiquinone oxidoreductase (complex 1) activity is believed to be a critical factor in the development of Parkinson’s disease. MNA has been found to destroy several subunits of cerebral complex 1, leading to the suggestion that MNA is concerned in the pathogenesis of Parkinson’s disease. Based on these findings, it is hypothesized that niacin is a causal substance in the development of Parkinson’s disease through the following processes: NAD produced from niacin releases nicotinamide via poly(ADP-ribosyl)ation, activated by the hydroxyl radical. Released excess nicotinamide is methylated to MNA in the cytoplasm, and superoxides formed by MNA via complex I destroy complex 1 subunits directly, or indirectly via mitochondrial DNA damage. Hereditary or environmental factors may cause acceleration of this cycle, resulting in neuronal death.     

Quality of life in Parkinson’s disease patients: validation of the Short-Form Eight-item Parkinson’s Disease Questionnaire (PDQ-8) in Taiwan

Purpose  

This study sought to evaluate the Chinese version of the eight-item Parkinson’s Disease Questionnaire (PDQ-8), through standard psychometric techniques.     

Nutritional status and dietary habits in Parkinson’s disease patients in Ghana

ObjectiveDietary treatment is important for the management of Parkinson’s disease (PD). Our objective was to describe the dietary habits and assess the nutritional status of Ghanaian patients with PD. This study is part of a larger project, for which Ghana has been selected as a pilot country.MethodsFifty-five Ghanaian patients with PD and 12 healthy Ghanaian controls were recruited. We assessed nutritional status, investigated dietary habits, and assessed the prevalence of the nutritional complications of PD (e.g., constipation and dysphagia).ResultsThe mean daily caloric intake was about 1200 kcal/d in patients with PD and in controls. The typical diet was based on semisolid foods, usually vegetable soups accompanied by cereal flour or root starch or sometimes chicken or fish. The intake of milk and its derivatives was low. The prevalences of constipation and dysphagia in patients with PD were 49% and 21%, respectively.ConclusionThis study has yielded information that could be useful for the study of the management of PD and for the assessment of response to therapy.     

A Cross-Sectional Study on Socioeconomic Systems Supporting Outpatients With Parkinson’s Disease in Japan

Objectives

We conducted a cross-sectional study to evaluate the socioeconomic systems supporting outpatients with Parkinson’s disease (PD) in Japan.

Methods

The study was performed in 2013 at two private hospitals and one clinic in Hokkaido Prefecture, Japan. A survey was conducted with 248 consecutive PD patients, and the data from 237 PD outpatients were analyzed after excluding 11 patients who did not meet inclusion criteria. Monthly medical and transportation payments as a PD outpatient were selected as outcome variables, and their association with various explanatory variables, such as utilization of support systems for PD outpatients, were evaluated using logistic regression model analysis.

Results

After controlling for potential confounding variables, the utilization of the system providing financial aid for treatment for patients with intractable disease was significantly inversely associated with monthly medical payment among PD outpatients (OR 0.46; 95% CI, 0.22–0.95). Experience of hospital admission for PD treatment was significantly positively associated with monthly transportation payment (OR 4.74; 95% CI, 2.18–10.32). Monthly medical payment was also significantly positively associated with monthly transportation payment (OR 4.01; 95% CI, 2.23–7.51).

Conclusions

Use of Japanese public financial support systems may be associated with reductions in medical payments for PD outpatients. However, those systems may not have supported transportation payments, and higher transportation payments may be associated with an increased risk of hospitalization.Key words: Parkinson’s disease, medical payment, cross-sectional study     

Environmental Exposure,Obesity, and Parkinson’s Disease: Lessons from Fat and Old Worms

Background

A common link has been exposed, namely, that metal exposure plays a role in obesity and in Parkinson’s disease (PD). This link may help to elucidate mechanisms of neurotoxicity.

Objective

We reviewed the utility of the nematode, Caenorhabditis elegans, as a model organism to study neurodegeneration in obesity and Parkinson’s disease (PD), with an emphasis on the neurotransmitter, dopamine (DA).

Data sources

A PubMed literature search was performed using the terms “obesity” and any of the following: “C. elegans,” “central nervous system,” “neurodegeneration,” “heavy metals,” “dopamine” or “Parkinson’s disease.” We reviewed the identified studies, including others cited therein, to summarize the current evidence of neurodegeneration in obesity and PD, with an emphasis on studies carried out in C. elegans and environmental toxins in the etiology of both diseases.

Data extraction and data synthesis

Heavy metals and DA have both been linked to diet-induced obesity, which has led to the notion that the mechanism of environmentally induced neurodegeneration in PD may also apply to obesity. C. elegans has been instrumental in expanding our mechanism-based knowledge of PD, and this species is emerging as a good model of obesity. With well-established toxicity and neurogenetic assays, it is now feasible to explore the putative link between metal-and chemical-induced neurodegeneration.

Conclusions

One side effect of an aging population is an increase in the prevalence of obesity, metabolic disorders, and neurodegenerative orders, diseases that are likely to co-occur. Environmental toxins, especially heavy metals, may prove to be a previously neglected part of the puzzle.     

Cardiometabolic factors and disease duration in patients with Parkinson’s disease

ObjectivePrevious studies have reported that patients with Parkinson’s disease (PD) have a favorable cardiometabolic risk profile. The aim of this study was to investigate the relationship between cardiometabolic risk factors and the duration of disease.MethodsOne hundred and fifty patients with PD (56.7% men) were studied, measuring body mass index (BMI), waist circumference (WC), body fat percentage (BF%) by impedance, fasting glucose, serum lipids, and transaminases.ResultsIn sex- and age-adjusted correlation models, duration of PD was inversely related to BMI (r = ?0.20; P < 0.05) and BF% (r = ?0.29; P < 0.005). Using multivariable regression models (adjustments: age, gender, smoking status, levodopa dose and, alternatively, BMI, WC, or BF%), high-density lipoprotein (HDL) levels were positively correlated with disease duration (P < 0.01 for all). In models adjusted for WC and BF%, total HDL-cholesterol ratio was also inversely associated with duration of PD (P < 0.05 for both). No other association between biochemical variables and the duration of PD was found. Moreover, no dose–response effect of levodopa on metabolic risk factors was observed.ConclusionsHDL levels and total HDL-cholesterol ratio were favorably associated with duration of PD. This factor may contribute to cardiometabolic protection in PD. The mechanisms underlying this association deserve further investigation.     

Alzheimer’s Disease Dietary Supplements in Websites

Consumer demand for health information and health services has rapidly evolved to capture and even propel the movement to online health information seeking. Seventeen percent (52 million) of health information internet users will look for information about memory loss, dementia and Alzheimer’s disease (AD) (Fox Pew Internet & American life project: Online health search. Report. Pew Research Center. http://pewinternet.org/Reports/2006/Online-Health-Search-2006.aspx 2006, Pew Research Center. http://pewinternet.org/Reports/2011/HealthTopics.aspx 2011). We examined the content of the 25 most frequently retrieved websites marketing AD dietary supplements. We found that the majority of websites and their products claimed AD-related benefits, including improvement and enhancement of function, treatment for AD, prevention of AD, maintenance of function, delayed progression of AD, and decreased symptoms. Supplements were described as effective, natural, powerful or strong, dependable and pure or of high quality. Peer reviewed references to proper scientific studies were infrequent on websites. Statements highlighting the risks of dietary supplements were as common as statements mitigating or minimizing these risks. Different strategies were used to promote supplements such as popular appeals and testimonials. Further enforcement of relevant policy is needed and preparation of clinicians to deal with requests of patients and caregivers is indicated.     

Employment Resources for People with Parkinson’s Disease: A Resource Review and Needs Assessment

Journal of Occupational Rehabilitation - Purpose People with Parkinson’s disease (PwP) exit the workforce on average 5&nbsp;years earlier than people without Parkinson’s due to...     

Consumption of fish and Alzheimer’s Disease

Alzheimer’s Disease (AD) has been described as ‘one of the most disabling and burdensome health conditions worldwide’ and is responsible for approximately 70% of dementia in the elderly. Based on the current prevalence of AD, an aging world population and the associated projected health care requirements, it is estimated that by 2050, the prevalence of AD will reach 104 million with around 43% requiring ongoing health care. If the onset of AD can be reduced by as little as one year, the prevalence could be reduced by 10%. There is substantial commonality in research findings to date around the positive influence of seafood consumption in reducing the risk of dementia and AD. Emerging concern about the sustainability of global fisheries supports the recommendation of selective consumption of sustainable wild caught and increased emphasis on production of farmed fish supplies to meet consumption needs.