Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease
In our previous study, higher serum 25-hydroxyvitamin D [25(OH)D] concentrations and the vitamin D receptor (VDR) FokI CC genotype were associated with milder Parkinson disease (PD). We evaluated whether vitamin D3 supplementation inhibits the progression of PD on the basis of patient VDR subgroups....
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| Veröffentlicht in: | The American journal of clinical nutrition 2013-05, Vol.97 (5), p.1004-1013 |
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| creator | SUZUKI, Masahiko YOSHIOKA, Masayuki HASHIMOTO, Masaya MURAKAMI, Maiko NOYA, Miki TAKAHASHI, Daisuke URASHIMA, Mitsuyoshi |
| description | In our previous study, higher serum 25-hydroxyvitamin D [25(OH)D] concentrations and the vitamin D receptor (VDR) FokI CC genotype were associated with milder Parkinson disease (PD).
We evaluated whether vitamin D3 supplementation inhibits the progression of PD on the basis of patient VDR subgroups.
Patients with PD (n = 114) were randomly assigned to receive vitamin D3 supplements (n = 56; 1200 IU/d) or a placebo (n = 58) for 12 mo in a double-blind setting. Outcomes were clinical changes from baseline and the percentage of patients who showed no worsening of the modified Hoehn and Yahr (HY) stage and Unified Parkinson's Disease Rating Scale (UPDRS).
Compared with the placebo, vitamin D3 significantly prevented the deterioration of the HY stage in patients [difference between groups: P = 0.005; mean ± SD change within vitamin D3 group: +0.02 ± 0.62 (P = 0.79); change within placebo group: +0.33 ± 0.70 (P = 0.0006)]. Interaction analyses showed that VDR FokI genotypes modified the effect of vitamin D3 on changes in the HY stage (P-interaction = 0.045), UPDRS total (P-interaction = 0.039), and UPDRS part II (P-interaction = 0.021). Compared with the placebo, vitamin D3 significantly prevented deterioration of the HY stage in patients with FokI TT [difference between groups: P = 0.009; change within vitamin D3 group: -0.38 ± 0.48 (P = 0.91); change within placebo group, +0.63 ± 0.77 (P = 0.009)] and FokI CT [difference between groups: P = 0.020; change within vitamin D3 group: ±0.00 ± 0.60 (P = 0.78); change within placebo group: +0.37 ± 0.74 (P = 0.014)] but not FokI CC. Similar trends were observed in UPDRS total and part II.
Vitamin D3 supplementation may stabilize PD for a short period in patients with FokI TT or CT genotypes without triggering hypercalcemia, although this effect may be nonspecific for PD. This trial was registered at UMIN Clinical Trials Registry as UMIN000001841. |
| doi_str_mv | 10.3945/ajcn.112.051664 |
| format | Article |
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We evaluated whether vitamin D3 supplementation inhibits the progression of PD on the basis of patient VDR subgroups.
Patients with PD (n = 114) were randomly assigned to receive vitamin D3 supplements (n = 56; 1200 IU/d) or a placebo (n = 58) for 12 mo in a double-blind setting. Outcomes were clinical changes from baseline and the percentage of patients who showed no worsening of the modified Hoehn and Yahr (HY) stage and Unified Parkinson's Disease Rating Scale (UPDRS).
Compared with the placebo, vitamin D3 significantly prevented the deterioration of the HY stage in patients [difference between groups: P = 0.005; mean ± SD change within vitamin D3 group: +0.02 ± 0.62 (P = 0.79); change within placebo group: +0.33 ± 0.70 (P = 0.0006)]. Interaction analyses showed that VDR FokI genotypes modified the effect of vitamin D3 on changes in the HY stage (P-interaction = 0.045), UPDRS total (P-interaction = 0.039), and UPDRS part II (P-interaction = 0.021). Compared with the placebo, vitamin D3 significantly prevented deterioration of the HY stage in patients with FokI TT [difference between groups: P = 0.009; change within vitamin D3 group: -0.38 ± 0.48 (P = 0.91); change within placebo group, +0.63 ± 0.77 (P = 0.009)] and FokI CT [difference between groups: P = 0.020; change within vitamin D3 group: ±0.00 ± 0.60 (P = 0.78); change within placebo group: +0.37 ± 0.74 (P = 0.014)] but not FokI CC. Similar trends were observed in UPDRS total and part II.
Vitamin D3 supplementation may stabilize PD for a short period in patients with FokI TT or CT genotypes without triggering hypercalcemia, although this effect may be nonspecific for PD. This trial was registered at UMIN Clinical Trials Registry as UMIN000001841.</description><identifier>ISSN: 0002-9165</identifier><identifier>EISSN: 1938-3207</identifier><identifier>DOI: 10.3945/ajcn.112.051664</identifier><identifier>PMID: 23485413</identifier><identifier>CODEN: AJCNAC</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Nutrition</publisher><subject>Aged ; Biological and medical sciences ; Blood Pressure ; Body Mass Index ; Calcium, Dietary - blood ; Cholecalciferol - administration & dosage ; Cholecalciferol - blood ; Clinical trials ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dietary Supplements ; Disease Progression ; Double-Blind Method ; Endpoint Determination ; Feeding. Feeding behavior ; Female ; Follow-Up Studies ; Fundamental and applied biological sciences. Psychology ; Genotype ; Humans ; Male ; Medical sciences ; Middle Aged ; Nervous system (semeiology, syndromes) ; Nervous system as a whole ; Neurology ; Nutrition ; Parathyroid Hormone - blood ; Parkinson Disease - drug therapy ; Parkinson Disease - genetics ; Parkinson's disease ; Receptors, Calcitriol - genetics ; Receptors, Calcitriol - metabolism ; Surveys and Questionnaires ; Vertebrates: anatomy and physiology, studies on body, several organs or systems ; Vitamin D</subject><ispartof>The American journal of clinical nutrition, 2013-05, Vol.97 (5), p.1004-1013</ispartof><rights>2014 INIST-CNRS</rights><rights>Copyright American Society for Clinical Nutrition, Inc. May 1, 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-c4edbdeb445e0d8424e3994a7db1e85afa350b4b9a879d0a768f4de6295025d83</citedby><cites>FETCH-LOGICAL-c396t-c4edbdeb445e0d8424e3994a7db1e85afa350b4b9a879d0a768f4de6295025d83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27247267$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23485413$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SUZUKI, Masahiko</creatorcontrib><creatorcontrib>YOSHIOKA, Masayuki</creatorcontrib><creatorcontrib>HASHIMOTO, Masaya</creatorcontrib><creatorcontrib>MURAKAMI, Maiko</creatorcontrib><creatorcontrib>NOYA, Miki</creatorcontrib><creatorcontrib>TAKAHASHI, Daisuke</creatorcontrib><creatorcontrib>URASHIMA, Mitsuyoshi</creatorcontrib><title>Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease</title><title>The American journal of clinical nutrition</title><addtitle>Am J Clin Nutr</addtitle><description>In our previous study, higher serum 25-hydroxyvitamin D [25(OH)D] concentrations and the vitamin D receptor (VDR) FokI CC genotype were associated with milder Parkinson disease (PD).
We evaluated whether vitamin D3 supplementation inhibits the progression of PD on the basis of patient VDR subgroups.
Patients with PD (n = 114) were randomly assigned to receive vitamin D3 supplements (n = 56; 1200 IU/d) or a placebo (n = 58) for 12 mo in a double-blind setting. Outcomes were clinical changes from baseline and the percentage of patients who showed no worsening of the modified Hoehn and Yahr (HY) stage and Unified Parkinson's Disease Rating Scale (UPDRS).
Compared with the placebo, vitamin D3 significantly prevented the deterioration of the HY stage in patients [difference between groups: P = 0.005; mean ± SD change within vitamin D3 group: +0.02 ± 0.62 (P = 0.79); change within placebo group: +0.33 ± 0.70 (P = 0.0006)]. Interaction analyses showed that VDR FokI genotypes modified the effect of vitamin D3 on changes in the HY stage (P-interaction = 0.045), UPDRS total (P-interaction = 0.039), and UPDRS part II (P-interaction = 0.021). Compared with the placebo, vitamin D3 significantly prevented deterioration of the HY stage in patients with FokI TT [difference between groups: P = 0.009; change within vitamin D3 group: -0.38 ± 0.48 (P = 0.91); change within placebo group, +0.63 ± 0.77 (P = 0.009)] and FokI CT [difference between groups: P = 0.020; change within vitamin D3 group: ±0.00 ± 0.60 (P = 0.78); change within placebo group: +0.37 ± 0.74 (P = 0.014)] but not FokI CC. Similar trends were observed in UPDRS total and part II.
Vitamin D3 supplementation may stabilize PD for a short period in patients with FokI TT or CT genotypes without triggering hypercalcemia, although this effect may be nonspecific for PD. This trial was registered at UMIN Clinical Trials Registry as UMIN000001841.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Body Mass Index</subject><subject>Calcium, Dietary - blood</subject><subject>Cholecalciferol - administration & dosage</subject><subject>Cholecalciferol - blood</subject><subject>Clinical trials</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dietary Supplements</subject><subject>Disease Progression</subject><subject>Double-Blind Method</subject><subject>Endpoint Determination</subject><subject>Feeding. Feeding behavior</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Fundamental and applied biological sciences. 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Leukodystrophies. Prion diseases</topic><topic>Dietary Supplements</topic><topic>Disease Progression</topic><topic>Double-Blind Method</topic><topic>Endpoint Determination</topic><topic>Feeding. Feeding behavior</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Fundamental and applied biological sciences. 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We evaluated whether vitamin D3 supplementation inhibits the progression of PD on the basis of patient VDR subgroups.
Patients with PD (n = 114) were randomly assigned to receive vitamin D3 supplements (n = 56; 1200 IU/d) or a placebo (n = 58) for 12 mo in a double-blind setting. Outcomes were clinical changes from baseline and the percentage of patients who showed no worsening of the modified Hoehn and Yahr (HY) stage and Unified Parkinson's Disease Rating Scale (UPDRS).
Compared with the placebo, vitamin D3 significantly prevented the deterioration of the HY stage in patients [difference between groups: P = 0.005; mean ± SD change within vitamin D3 group: +0.02 ± 0.62 (P = 0.79); change within placebo group: +0.33 ± 0.70 (P = 0.0006)]. Interaction analyses showed that VDR FokI genotypes modified the effect of vitamin D3 on changes in the HY stage (P-interaction = 0.045), UPDRS total (P-interaction = 0.039), and UPDRS part II (P-interaction = 0.021). Compared with the placebo, vitamin D3 significantly prevented deterioration of the HY stage in patients with FokI TT [difference between groups: P = 0.009; change within vitamin D3 group: -0.38 ± 0.48 (P = 0.91); change within placebo group, +0.63 ± 0.77 (P = 0.009)] and FokI CT [difference between groups: P = 0.020; change within vitamin D3 group: ±0.00 ± 0.60 (P = 0.78); change within placebo group: +0.37 ± 0.74 (P = 0.014)] but not FokI CC. Similar trends were observed in UPDRS total and part II.
Vitamin D3 supplementation may stabilize PD for a short period in patients with FokI TT or CT genotypes without triggering hypercalcemia, although this effect may be nonspecific for PD. This trial was registered at UMIN Clinical Trials Registry as UMIN000001841.</abstract><cop>Bethesda, MD</cop><pub>American Society for Nutrition</pub><pmid>23485413</pmid><doi>10.3945/ajcn.112.051664</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The American journal of clinical nutrition, 2013-05, Vol.97 (5), p.1004-1013 |
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| subjects | Aged Biological and medical sciences Blood Pressure Body Mass Index Calcium, Dietary - blood Cholecalciferol - administration & dosage Cholecalciferol - blood Clinical trials Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dietary Supplements Disease Progression Double-Blind Method Endpoint Determination Feeding. Feeding behavior Female Follow-Up Studies Fundamental and applied biological sciences. Psychology Genotype Humans Male Medical sciences Middle Aged Nervous system (semeiology, syndromes) Nervous system as a whole Neurology Nutrition Parathyroid Hormone - blood Parkinson Disease - drug therapy Parkinson Disease - genetics Parkinson's disease Receptors, Calcitriol - genetics Receptors, Calcitriol - metabolism Surveys and Questionnaires Vertebrates: anatomy and physiology, studies on body, several organs or systems Vitamin D |
| title | Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease |
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