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Association between vitamin B12-containing supplement consumption and prevalence of biochemically defined B12 deficiency in adults in NHANES III (Third National Health and Nutrition Examination Survey)
- Marian L Evatt, Paul D Terry, Thomas R Ziegler, Godfrey P Oakley, Jr
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- Journal:
- Public Health Nutrition / Volume 13 / Issue 1 / January 2010
- Published online by Cambridge University Press:
- 11 June 2009, pp. 25-31
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- Article
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Objective
To explore the association between vitamin B12 (B12)-containing supplement use, low B12 concentrations and biochemically defined B12 deficiency in US adults.
DesignA cross-sectional study with adjustment for survey design. Prevalence ratios for two age groups (18–50 and >50 years) were estimated using unconditional logistic models. Outcome measures included prevalence of low serum B12 concentration (<148 pmol/l) and biochemical B12 deficiency (serum B12 < 148 pmol/l with concomitant homocysteine > 10 μmol/l).
SettingA population survey of health and nutritional measures.
SubjectsSubjects were non-institutionalized adults, aged 18 years and older, who participated in Phase 2 of NHANES III (Third National Health and Nutrition Examination Survey).
ResultsLow B12 concentrations were less prevalent among persons consuming B12-containing supplements (P = 0·001) with an adjusted prevalence ratio of 0·6 (95 % CI 0·3, 1·0). Biochemical B12 deficiency showed a similar trend (P = 0·0002), with an adjusted prevalence ratio of 0·3 (95 % CI 0·1, 0·8). Prevalence ratios were similar in adults >50 years of age, although the prevalence of low B12 and biochemical deficiency was proportionally higher.
ConclusionsConsumption of B12-containing supplements was associated with at least 50 % lower prevalence of both low serum B12 and biochemical B12 deficiency in a nationally representative sample of US adults, suggesting increased consumption of B12 from supplements or from fortified foods may reduce the prevalence of B12 deficiency. Additionally, the current Recommended Daily Allowance for B12 of 2·4 μg may be insufficient for those aged >50 years.
33 - Parkinson's disease
- from PART III - DISORDERS OF MOTOR CONTROL
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- By Marian L. Evatt, Department of Neurology, Emory University School of Medicine, Atlanta, Georgia, GA, USA, Mahlon R. DeLong, Department of Neurology, Emory University School of Medicine, Atlanta, Georgia, GA, USA, Jerrold L. Vitek, Department of Neurology, Emory University School of Medicine, Atlanta, Georgia, GA, USA
- Edited by Arthur K. Asbury, University of Pennsylvania School of Medicine, Guy M. McKhann, The Johns Hopkins University School of Medicine, W. Ian McDonald, University College London, Peter J. Goadsby, University College London, Justin C. McArthur, The Johns Hopkins University School of Medicine
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- Book:
- Diseases of the Nervous System
- Published online:
- 05 August 2016
- Print publication:
- 11 November 2002, pp 477-489
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Summary
Clinical neuroscience
Movement disorders may be classified as hyperkinetic, characterized by excessive, involuntary movement or hypokinetic, characterized by decreased and slowed movement. First described by James Parkinson in 1817, Parkinson's disease (PD) is the archetypal hypokinetic disorder and the second most common neurodegenerative disorder after Alzheimer's disease. Though incidence and prevalence increase with age, the total estimated incidence is 20/100000 and prevalence is 150/100000 (Schapira, 1999). In the United States, approximately one million patients have PD. The estimated societal cost tops $25 billion (Scheife et al., 2000) and is expected to rise as the population ages.
Parkinsonism: classification/clinical symptoms
‘Parkinsonism’ is a term describing syndromes combining bradykinesia, tremor, muscle rigidity, gait and balance disturbances. The term ‘idiopathic PD’ traditionally referred to patients exhibiting two or more of the cardinal signs (rest tremor, rigidity and bradykinesia) who responded to levodopa replacement therapy and did not show evidence of other neurologic disease. Given the discovery of inherited dopa-responsive PD, parkinsonian syndromes with good, sustained clinical response to dopaminergic therapy are best termed ‘primary PD’ (PPD). Infection, drugs, metabolic abnormalities, or other disease states may cause symptomatic parkinsonism. ‘Parkinson-plus’ (PD-plus) or atypical parkinsonism includes such syndromes as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), Lewy body disease (LBD), the tauopathies (corticobasalganglionic degeneration and frontotemporal dementias), as well as the amyloidopathies (Alzheimer's disease with parkinsonism). These conditions typically exhibit little or no response to levodopa therapy, prominent and early gait and balance disturbance, autonomic and cognitive symptoms (Table 33.1). Table 33.2 lists signs and symptoms occuring in PPD and parkinsonian syndromes. See Chapter 34 for further discussion of the atypical syndromes.
Diagnostic criteria and clinical features for primary Parkinson's disease (PPD)
Although James Parkinson published the first description of the ‘shaking palsy’ almost 200 years ago, we still have no standardized diagnostic test for PPD. Clinical criteria for PPD vary, but most movement disorders experts agree a patient must demonstrate at least two of the three cardinal signs and experience significant, long lasting (>5 years) improvement with dopaminergic therapy (Gelb et al., 1999). With these clinical criteria and experience, neurologists’ diagnostic accuracy can approach 92% (Jankovic et al., 2000).