2010
DOI: 10.1001/archoto.2010.111
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The Bradford Hill Criteria and Zinc-Induced Anosmia

Abstract: The Bradford Hill criteria represent an important tool for scientifically determining cause between environmental exposure and disease. Increased Food and Drug Administration oversight of homeopathic medications is needed to monitor the safety of these popular remedies.

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Cited by 37 publications

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“…Olfactory ability declines in healthy humans from approximately 60 years of age 47 , 93 , and this may be related to the accumulation of zinc and lipofuscin in anterior olfactory nucleus cells, which are important in secondary olfactory processing 11 . Additionally, intranasal zinc causes hyposmia and anosmia in humans 24 26 and is commonly used to experimentally ablate olfaction in animal models 27 , lending support to this idea that olfactory bulb zinc causes olfactory dysfunction. This somatic free and loosely bound zinc may also make cells in the anterior olfactory nucleus more vulnerable to the aggregation of alpha-synuclein in early PD, especially within lipofuscin: alpha-synuclein-positive particles and small Lewy bodies have been detected within lipofuscin pigment in the PD brain stem 94 , although this has not been described in the olfactory bulb.…”
Section: Discussionmentioning
confidence: 82%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD). Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD. The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC). Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.
“…Olfactory ability declines in healthy humans from approximately 60 years of age 47 , 93 , and this may be related to the accumulation of zinc and lipofuscin in anterior olfactory nucleus cells, which are important in secondary olfactory processing 11 . Additionally, intranasal zinc causes hyposmia and anosmia in humans 24 26 and is commonly used to experimentally ablate olfaction in animal models 27 , lending support to this idea that olfactory bulb zinc causes olfactory dysfunction. This somatic free and loosely bound zinc may also make cells in the anterior olfactory nucleus more vulnerable to the aggregation of alpha-synuclein in early PD, especially within lipofuscin: alpha-synuclein-positive particles and small Lewy bodies have been detected within lipofuscin pigment in the PD brain stem 94 , although this has not been described in the olfactory bulb.…”
Section: Discussionmentioning
confidence: 82%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD). Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD. The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC). Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.
“…Interestingly, metals have a key role in olfaction [30], and prior literature suggests that metal ions are transported from the olfactory mucosa to the brain (review [31]). Studies in mice have demonstrated that intranasal administration of zinc sulfate results in transient anosmia [32], and the administration of inhalational forms of zinc in humans can cause hyposmia or anosmia [33]. It is believed that zinc can block the ion channels that facilitate signal transduction in the olfactory mucosa.…”
Section: Discussionmentioning
confidence: 99%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD). Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD. The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC). Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.
“…The association of DMSO and CRPS prevention has been proven to be causal. Pathogenesis of CRPS involves free radical formation which may be destroyed by vitamin C.(15,31,32)…”
Section: Methodsmentioning
confidence: 99%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD). Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD. The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC). Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.