NCBI
PubMed
A service of the
U.S. National Library of Medicine
and the
National Institutes of Health
My NCBI
[Sign In]
[Register]
All Databases
PubMed
Nucleotide
Protein
Genome
Structure
OMIM
PMC
Journals
Books
Search
Database name
PubMed
Protein
Nucleotide
GSS
EST
Structure
Genome
Books
CancerChromosomes
Conserved Domains
dbGaP
3D Domains
Gene
Genome Project
GENSAT
GEO Profiles
GEO DataSets
HomoloGene
Journals
MeSH
NCBI Web Site
NLM Catalog
OMIA
OMIM
PMC
PopSet
Probe
Protein Clusters
PubChem BioAssay
PubChem Compound
PubChem Substance
SNP
Taxonomy
ToolKit
UniGene
UniSTS
for
Search term
Go
Clear
Advanced Search
Limits
Preview/Index
History
Clipboard
Details
Your browser version may not work well with NCBI's Web applications. More information
here...
Display
Summary
Brief
Abstract
AbstractPlus
Citation
MEDLINE
XML
UI List
LinkOut
ASN.1
Related Articles
Cited in Books
CancerChrom Links
Domain Links
3D Domain Links
dbGaP Links
GEO DataSet Links
Gene Links
Gene (OMIM) Links
Gene (GeneRIF) Links
Genome Links
Project Links
GENSAT Links
GEO Profile Links
HomoloGene Links
Nucleotide Links
Nucleotide (RefSeq) Links
Nucleotide (Weighted) Links
EST Links
EST (RefSeq) Links
GSS Links
GSS (RefSeq) Links
OMIA Links
OMIM (calculated) Links
OMIM (cited) Links
BioAssay Links
Compound Links
Compound (MeSH Keyword)
Compound (Publisher) Links
Substance Links
Substance (MeSH Keyword)
Substance (Publisher) Links
PMC Links
Cited in PMC
PopSet Links
Probe Links
Protein Links
Protein (RefSeq) Links
Protein (Weighted) Links
Protein Cluster Links
Cited Articles
SNP Links
SNP (Cited)
Structure Links
Taxonomy via GenBank
UniGene Links
UniSTS Links
Show
5
10
20
50
100
200
500
Sort By
Pub Date
First Author
Last Author
Journal
Title
Send to
Text
File
Printer
Clipboard
Collections
E-mail
Order
All: 1
Review: 0
Click to change filter selection through MyNCBI.
1:
JAMA.
2002 Jun 26;287(24):3223-9.
Related Articles
,
Links
Comment in:
JAMA. 2002 Jun 26;287(24):3261-3.
JAMA. 2002 Nov 13;288(18):2265; author reply 2265-6.
JAMA. 2002 Nov 13;288(18):2265; author reply 2265-6.
Dietary intake of antioxidants and risk of Alzheimer disease.
Engelhart MJ
,
Geerlings MI
,
Ruitenberg A
,
van Swieten JC
,
Hofman A
,
Witteman JC
,
Breteler MM
.
Department of Epidemiology and Biostatistics, Erasmus Medical Center, 3000 DR Rotterdam, The Netherlands.
CONTEXT: Laboratory findings have suggested that oxidative stress may contribute to the pathogenesis of Alzheimer disease. Therefore, the risk of Alzheimer disease might be reduced by intake of antioxidants that counteract the detrimental effects of oxidative stress. OBJECTIVE: To determine whether dietary intake of antioxidants is related to risk of Alzheimer disease. DESIGN AND SETTING: The Rotterdam Study, a population-based, prospective cohort study conducted in the Netherlands. PARTICIPANTS: A total of 5395 participants who, at baseline (1990-1993), were aged at least 55 years, free of dementia, and noninstitutionalized and had reliable dietary assessment. Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for incident dementia. MAIN OUTCOME MEASURES: Incidence of Alzheimer disease, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R) criteria and National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer Disease and Related Disorders Association (NINCDS-ADRDA) criteria, associated with dietary intake of beta carotene, flavonoids, vitamin C, and vitamin E. RESULTS: After a mean follow-up of 6 years, 197 participants developed dementia, of whom 146 had Alzheimer disease. When adjustments were made for age, sex, baseline Mini-Mental State Examination score, alcohol intake, education, smoking habits, pack-years of smoking, body mass index, total energy intake, presence of carotid plaques, and use of antioxidative supplements, high intake of vitamin C and vitamin E was associated with lower risk of Alzheimer disease (rate ratios [RRs] per 1-SD increase in intake were 0.82 [95% confidence interval [CI], 0.68-0.99] and 0.82 [95% CI, 0.66-1.00], respectively). Among current smokers, this relationship was most pronounced (RRs, 0.65 [95% CI, 0.37-1.14] and 0.58 [95% CI, 0.30-1.12], respectively) and also was present for intake of beta carotene (RR, 0.49 [95% CI, 0.27-0.92]) and flavonoids (RR, 0.54 [95% CI, 0.31-0.96]). The associations did not vary by education or apolipoprotein E genotype. CONCLUSION: High dietary intake of vitamin C and vitamin E may lower the risk of Alzheimer disease.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 12076218 [PubMed - indexed for MEDLINE]
Display
Summary
Brief
Abstract
AbstractPlus
Citation
MEDLINE
XML
UI List
LinkOut
ASN.1
Related Articles
Cited in Books
CancerChrom Links
Domain Links
3D Domain Links
dbGaP Links
GEO DataSet Links
Gene Links
Gene (OMIM) Links
Gene (GeneRIF) Links
Genome Links
Project Links
GENSAT Links
GEO Profile Links
HomoloGene Links
Nucleotide Links
Nucleotide (RefSeq) Links
Nucleotide (Weighted) Links
EST Links
EST (RefSeq) Links
GSS Links
GSS (RefSeq) Links
OMIA Links
OMIM (calculated) Links
OMIM (cited) Links
BioAssay Links
Compound Links
Compound (MeSH Keyword)
Compound (Publisher) Links
Substance Links
Substance (MeSH Keyword)
Substance (Publisher) Links
PMC Links
Cited in PMC
PopSet Links
Probe Links
Protein Links
Protein (RefSeq) Links
Protein (Weighted) Links
Protein Cluster Links
Cited Articles
SNP Links
SNP (Cited)
Structure Links
Taxonomy via GenBank
UniGene Links
UniSTS Links
Show
5
10
20
50
100
200
500
Sort By
Pub Date
First Author
Last Author
Journal
Title
Send to
Text
File
Printer
Clipboard
Collections
E-mail
Order
About Entrez
Text Version
Entrez PubMed
Overview
Help
|
FAQ
Tutorials
New/Noteworthy
E-Utilities
PubMed Services
Journals Database
MeSH Database
Single Citation Matcher
Batch Citation Matcher
Clinical Queries
Special Queries
LinkOut
My NCBI
Related Resources
Order Documents
NLM Mobile
NLM Catalog
NLM Gateway
TOXNET
Consumer Health
Clinical Alerts
ClinicalTrials.gov
PubMed Central
Write to the Help Desk
NCBI
|
NLM
|
NIH
Department of Health & Human Services
Privacy Statement
|
Freedom of Information Act
|
Disclaimer