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Low Vitamin D Levels Seen in Parkinson's Patients - full text of study below -
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"Active 1,25-dihydroxyvitamin D binds to VDRs and regulates approximately 200 genes involved in cell differentiation, proliferation, and apoptosis......optimal vitamin D status may be important for preventing or treating neurodegenerative disorders..... Vitamin D also regulates processes known to go awry in multiple sclerosis, Parkinson disease (PD), and other neurodegenerative disorders....Both 1{alpha}-OHase and vitamin D receptors (VDRs) are expressed in many extrarenal tissues, including muscle and brain"
"the finding of a high incidence of vitamin D deficiency in the PD and other cohorts highlights the importance of routinely checking the level of 25-(OH)D, particularly in elderly patients, since deficiency is strongly correlated with a higher incidence of osteoporosis, falls, and hip fractures and has been associated with a higher incidence of several forms of cancer and autoimmune disorders."
Study Suggests Possible Link Between Vitamin D and Parkinson's Disease
By Salynn Boyles
WebMD Health News
Reviewed by Laura J. Martin, MD
March 14, 2011 -- A study of newly diagnosed patients with Parkinson's disease found a high prevalence of vitamin D insufficiency, but vitamin D levels did not continue to decline as the disease progressed.
The research is one of several studies suggesting a link between low vitamin D levels and Parkinson's disease, a brain disorder that leads to tremors and problems with balance and coordination. Parkinson's affects as many as 1 million older Americans.
In a study from Finland published last summer, people with the lowest levels of vitamin D were significantly more likely to develop Parkinson's over almost three decades of follow-up, compared to people with the highest blood levels of the vitamin.
In the newly published study, almost 70% of patients with a recent diagnosis of Parkinson's disease had low blood levels of the vitamin.
But it is not yet clear if vitamin D insufficiency raises Parkinson's risk or if having high levels of the vitamin is protective, says study researcher Marian L. Evatt, MD, of Emory University School of Medicine and the Atlanta Veterans Affairs Medical Center.
"More research is needed to figure this out," she tells WebMD. "There is certainly an association, but we can't say if it is causal."
Does Vitamin D Protect the Brain?
Most people get the majority of their vitamin D from exposure to sunlight. Salmon, tuna, and fortified milk and other dairy products are the main food sources of the vitamin.
There are suggestions from animal and other studies that vitamin D protects the brain and central nervous system.
If this is the case, it would stand to reason that people with low vitamin D levels would have an increased risk for developing Parkinsons' and other neurodegenerative disorders like Alzheimer's disease as they age, Evatt says.
In earlier research, Evatt and colleagues found low vitamin D levels in 55% of Parkinson's patients they studied, compared to 41% of patients with Alzheimer's disease and 36% of healthy, elderly study participants.
In the newly published study, the researchers examined the prevalence of vitamin D insufficiency in untreated patients with early Parkinson's disease. They found that 69.4% of patients had vitamin D insufficiency and 26% had vitamin D deficiency.
The patients were followed for an average of 20 months.
"Contrary to our expectations that vitamin D levels might decrease over time because of disease related inactivity and reduced sun exposure, vitamin D levels increased over the study period," the researchers write.
They conclude that Parkinson's patients may have low vitamin D levels for many years before disease symptoms become evident.
Searching for Answers
Neurologist Andrew Feigin, MD, agrees more study is needed to better understand vitamin D's role, if any, in Parkinson's disease.
Feigin is an associate investigator with the Feinstein Institute for Medical Research in Manhasset, N.Y.
"The increase in vitamin D levels over the course of the study, during which there was a significant worsening in Parkinson's disease signs and symptoms, suggests that simply raising vitamin D levels may not result in improved Parkinson's symptoms," he says in a news release.
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Foods That Fight Alzheimer's Disease
Salad Dressing, Nuts, Fish, Poultry, and Some Fruits and Veggies May Lower Risk of Alzheimer's
By Jennifer Warner
WebMD Health News
Reviewed by Laura J. Martin, MD
Ginseng and Other Foods to Help You Focus
April 12, 2010 -- A low-fat diet with a lot of salad dressing, nuts, poultry, and certain fruits and vegetables may help prevent Alzheimer's disease, according to a new study.
Researchers say evidence is mounting on which foods may prevent Alzheimer's disease. But because foods are not eaten in isolation and may work together to prevent disease, more information is needed on dietary patterns that reduce the risk of Alzheimer's disease.
In the study, published in the Archives of Neurology, researchers analyzed the dietary patterns of 2,148 people aged 65 and older living in New York. The participants gave information about their diets and were evaluated for signs of Alzheimer's disease and dementia every year and a half over a four-year period.
Researchers analyzed dietary intake for seven nutrients that have been shown in previous studies to be associated with dementia risk: saturated fatty acids, monounsaturated fatty acids, omega-3 fatty acids, omega-6 fatty acids, vitamin E, vitamin B12, and folate.
By the end of the study, 253 participants developed Alzheimer's disease. In particular, the study showed one particular dietary pattern was associated with a lower risk of Alzheimer's disease. The diet included low amounts of high-fat dairy products, red meat, organ meat, and butter. Foods in this diet that appeared to fight Alzheimer's disease were salad dressing, nuts, fish, poultry, tomatoes, fruits, and cruciferous and dark and green vegetables.
Researchers say the combination of nutrients and foods in this particular dietary pattern may fight Alzheimer's in a variety of ways.
"For example, vitamin B12 and folate are homocysteine-related vitamins that may have an impact on Alzheimer's disease via their ability of reducing circulating homocysteine levels, vitamin E might prevent Alzheimer's disease via its strong antioxidant effect, and fatty acids may be related to dementia and cognitive function through atherosclerosis, thrombosis, or inflammation via an effect on brain development and membrane functioning or via accumulation of beta-amyloid," write researcher Yian Gu, PhD, of Columbia University and colleagues.
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Prevalence of Vitamin D Insufficiency in Patients With Parkinson Disease and Alzheimer Disease
Marian L. Evatt, MD, MS; Mahlon R. DeLong, MD; Natasha Khazai, MD; Ami Rosen, MS; Shirley Triche, RN; Vin Tangpricha, MD, PhD
Arch Neurol. 2008;65(10):1348-1352.
ABSTRACT
Background - A role for vitamin D deficiency in Parkinson disease (PD) has recently been proposed.
Objective - To compare the prevalence of vitamin D deficiency in a research database cohort of patients with PD with the prevalence in age-matched healthy controls and patients with Alzheimer disease (AD).
Design - Survey study and blinded comparison of plasma 25-hydroxyvitamin D (25[OH]D) concentrations of stored samples in a clinical research database at Emory University School of Medicine.
Setting - Referral center (PD and AD patients), primary care clinics, and community setting (controls).
Participants - Participants were recruited into the study between May 1992 and March 2007. Every fifth consecutively enrolled PD patient was selected from the clinical research database. Unrelated AD (n = 97) and control (n = 99) participants were randomly selected from the database after matching for age, sex, race, APOE genotype, and geographic location.
Main Outcome Measures - Prevalence of suboptimal vitamin D and mean 25(OH)D concentrations.
Results - Significantly more patients with PD (55%) had insufficient vitamin D than did controls (36%) or patients with AD (41%; P = .02, {chi}2test). The mean (SD) 25(OH)D concentration in the PD cohort was significantly lower than in the AD and control cohorts (31.9 [13.6] ng/mL vs 34.8 [15.4] ng/mL and 37.0 [14.5] ng/mL, respectively; P = .03).
Conclusions This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD. These data support a possible role of vitamin D insufficiency in PD. Further studies are needed to determine the factors contributing to these differences and elucidate the potential role of vitamin D in pathogenesis and clinical course of PD.
INTRODUCTION
Vitamin D is important for maintaining many physiologic functions, and vitamin D deficiency is associated with increased risk of disease. Optimal balance, muscle strength, and innate immunity1-3 require adequate vitamin D levels; vitamin D deficiency is associated with increased risk for several types of cancer, as well as autoimmune and cardiovascular disorders.1, 3-7 Vitamin D also regulates processes known to go awry in multiple sclerosis, Parkinson disease (PD), and other neurodegenerative disorders, including neurotrophin, inducible nitric oxide synthase, glutathione and monoamine synthesis, and apoptosis.8-9 The enzyme 25-hydroxyvitamin D-1{alpha}-hydroxylase (1{alpha}-OHase) converts the storage 25-hydroxyvitamin D (25[OH]D) form to the biologically active vitamin D form, 1,25-dihydroxyvitamin D. Both 1{alpha}-OHase and vitamin D receptors (VDRs) are expressed in many extrarenal tissues, including muscle and brain. Given the high prevalence rates of vitamin D deficiency in such varied populations as elderly patients, chronically ill patients, and healthy young adults1 and the widespread distribution of the VDRs and 1{alpha}-OHase in brain and muscle,10-11 optimal vitamin D status may be important for preventing or treating neurodegenerative disorders.
Active 1,25-dihydroxyvitamin D binds to VDRs and regulates approximately 200 genes involved in cell differentiation, proliferation, and apoptosis.1 In the brain, VDRs localize in the nucleus, whereas 1{alpha}-OHase is distributed throughout the cytosol. In particular, hippocampal and substantia nigra cells demonstrate high concentrations of VDRs and 1{alpha}-OHase.10 Additional epidemiologic, animal, and human data support the concept that vitamin D deficiency may be involved in the pathogenesis, progression, and clinical manifestations of PD.12 Limited previous reports13-16 of vitamin D deficiency in PD focus on skeletal health associations in elderly (aged ³65 years) Asian populations, but these reports have not been confirmed in white populations. Furthermore, if vitamin D insufficiency is acquired as a result of chronic neurodegeneration, one would expect the prevalence of vitamin D to be similar in 2 populations with different neurodegenerative diseases. This report summarizes the prevalence of vitamin D deficiency in a research database cohort of patients with PD and 2 comparison cohorts-one of age-matched healthy controls and another of patients with Alzheimer disease (AD), also a slowly progressive neurodegenerative disease.
RESULTS
More than half of the PD participants (55%) had vitamin D insufficiency (25[OH]D, ²30 ng/mL) compared with approximately a third of the controls (Figure). Most participants in all 3 cohorts were white, reflecting the racial distribution of the PD population at our institution. All participants resided in southern latitudes (100% south of 39¡N and 90% south of 37¡N). The prevalence of vitamin D insufficiency was significantly higher in the PD cohort than in the AD and control cohorts (Table). Similarly, 23% of the PD cohort was vitamin D deficient (25[OH]D, <20 ng/mL) compared with 16% of the AD cohort and 10% of the control cohort (P = .01 for PD vs control participants and P = .18 for PD vs AD participants).
A significantly higher portion of the samples from the PD cohort were drawn in the summer to fall (when vitamin D levels are higher) than in samples from the control group. Although not statistically significant, the portion of samples from the PD group drawn in the summer to fall was also higher than in the AD cohort. Evaluation of the symptom duration in the AD and PD cohorts revealed a longer duration in the PD cohort but no significant correlation between duration of disease symptoms and 25(OH)D concentration (P = .35 and .11, Pearson test, for the AD and PD patients, respectively) (Table).
COMMENT
Vitamin D insufficiency is a common health problem in elderly individuals, who also have a high prevalence of neurodegenerative diseases. Vitamin D is primarily produced in the skin on exposure to UV-B radiation and is found in limited food sources1, 19; advancing age, obesity, avoidance of sun exposure, residence in northerly latitudes, and darker skin pigmentation are associated with increased risk of vitamin D deficiency. Patients with chronic neurodegenerative diseases frequently have many risk factors for vitamin D insufficiency. Consistent with our a priori hypothesis, we found the prevalence of vitamin D insufficiency in the PD cohort to be significantly higher than in the control group. Surprisingly, the prevalence of vitamin D insufficiency in the PD cohort was higher than in the comparison cohort with AD.
The prevalence of vitamin D deficiency (25[OH]D, <20 ng/mL) in our PD cohort (23%) was lower than that previously observed in a Japanese PD cohort13 (50 of 71 patients with PD [85%]). Both insufficiency (36%) and deficiency (10%) in our control cohort were also less prevalent than reported in controls from a study of prostate cancer risk20 (58% insufficient [<32 mg/mL] and 16% deficient [<20 ng/mL]). Because all our study participants resided in southern latitudes and were predominantly white and a greater proportion of our samples were collected in the summer to fall, a lower prevalence of hypovitaminosis D in all our cohorts is not unexpected. Also, the Japanese participants were drawn from a hospital population, whereas participants in this study were recruited from an outpatient clinic. Previous studies14, 21 indicate that hospitalized patients have lower mean vitamin D levels than age-matched participants recruited from the community. The higher prevalence of insufficiency in the PD cohorts compared with the control cohort is not unexpected given that PD may cause patients to have decreased activity levels and lower sunshine exposure.
However, the lower vitamin D levels in the PD vs AD cohort are intriguing. The typical course of AD is shorter than that of PD,22-23 and PD patients experience mobility problems more frequently than AD patients. Both factors could make a PD patient less likely to get sun exposure and account for the higher prevalence of vitamin D insufficiency. Supporting this notion, more severely affected PD patients with a longer mean (SD) disease duration (Hoehn and Yahr stages III-V, 7.1 [3.8] years) reportedly had a higher prevalence of 25(OH)D deficiency than less severely affected patients with shorter disease duration (Hoehn and Yahr stages I-II, 4.1 [2.3] years).13 In contrast, although the range and mean of symptom duration in our PD and AD cohorts were consistent with what one would expect to find in a neurology clinic, 25(OH)D insufficiency did not correlate with symptom duration in either cohort (AD or PD), suggesting that vitamin D insufficiency may be unique to PD. Alternatively, the possible correlation may be too weak to be detected with our current sample size.
Strengths of this analysis are that the sample size was relatively large (97-100 participants in each cohort) and that the cohorts were matched for sex (which, depending on cultural and social differences, could affect duration of sun exposure and degree of skin coverage or protection when in sunlight), age (known to affect susceptibility to vitamin D deficiency), and APOE genotyping (which has been postulated to be protective for vitamin D deficiency24). Age was not limited in our inclusion criteria, thus increasing the generalizability to PD and AD populations with younger and older patients. In addition, diagnoses were made by experienced subspecialty neurologists according to well-characterized criteria. Although this was a retrospective study, participants were identified and data were analyzed as if in a prospective cross-sectional study.
This analysis did not control for vitamin D intake, although in other populations vitamin D intake contributes little to 25(OH)D levels.25 In this cross-sectional study that lacks longitudinal data, we cannot address etiology for the clinical associations discussed. In addition, we do not have uniformly collected measures of PD severity (Hoehn and Yahr stage, Unified Parkinson Disease Rating Scale scores) or anthropomorphic and sun exposure data; therefore, we cannot assess what effect, if any, differences in body mass index and exposure to sunshine might have on these findings. Another weakness is that the portion of plasma samples drawn in the winter to spring and fall to summer were not matched across cohorts. Despite a significantly higher proportion of the samples from the PD cohort being drawn in the summer to fall, we still found higher rates of vitamin D insufficiency in the PD cohort compared with the AD and healthy control cohorts.
In summary, we found that PD patients have a higher prevalence of vitamin D insufficiency compared with patients with AD and healthy controls. These findings support the previously suggested need12 for further studies to assess what contribution a low 25(OH)D concentration adds to the risk of developing PD (vs other neurodegenerative disorders) and to determine whether correction of vitamin D insufficiency and deficiency will improve motor or nonmotor symptoms in PD. Finally, the finding of a high incidence of vitamin D deficiency in the PD and other cohorts highlights the importance of routinely checking the level of 25-(OH)D, particularly in elderly patients, since deficiency is strongly correlated with a higher incidence of osteoporosis, falls, and hip fractures and has been associated with a higher incidence of several forms of cancer and autoimmune disorders.
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