Mercury & Alzheimer’s Disease/Dementia
Mutter J, Naumann J, Sadaghiani C, Schneider R, Walach H. Alzheimer
disease: mercury as pathogenetic factor and apolipoprotein E as a moderator.
Neuro Endocrinol Lett. 2004
Oct;25(5):331-9.
The etiology of most cases of Alzheimer's disease (AD) is as yet unknown.
Epidemiological studies suggest that environmental factors may be involved
beside genetic risk factors. Some studies have shown higher mercury
concentrations in brains of deceased and in blood of living patients with
Alzheimer's disease. Experimental studies have found that even smallest
amounts of mercury but no other metals in low concentrations were able to
cause all nerve cell changes, which are typical for Alzheimer's disease. The
most importat genetic risk factor for sporadic Alzheimer's disease is the
presence of the apolipoprotein Ee4 allele whereas the apolipoprotein Ee2
allele reduces the risk of developing Alzheimer's disease. Some
investigators have suggested that apolipoprotein Ee4 has a reduced ability
to bind metals like mercury and therefore explain the higher risk for
Alzheimer's disease. Therapeutic approaches embrace pharmaceuticals which
bind metals in the brain of patients with Alzheimer's disease. In sum, both
the findings from epidemiological and demographical studies, the frequency
of amalgam application in industrialized countries, clinical studies,
experimental studies and the dental state of AD patients in comparison to
controls suggest a decisive role for inorganic mercury in the etiology of
AD
Kidd PM., Neurodegeneration from mitochondrial insufficiency:
nutrients, stem cells, growth factors, and prospects for brain rebuilding
using integrative management.
Altern Med Rev. 2005
Dec;10(4):268-293.
mitochondrial insufficiency contributes to the etiopathology of many disorders. Mercury exposure is a factor in such effects. Alzheimer's and other dementias, Down syndrome, stroke, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease, Friedreich's ataxia, aging are affected.
B vitamin group; vitamins E and K; and the antioxidant and energetic cofactors alpha-lipoic acid (ALA), ubiquinone (coenzyme Q10; CoQ10), and nicotinamide adenine dinucleotide, reduced (NADH) help. The trophic nutrients acetyl L-carnitine (ALCAR), glycerophosphocholine (GPC), and phosphatidylserine (PS) provide mitochondrial support and conserve growth factor receptors; all three improved cognition in double-blind trials. The omega-3 fatty acid docosahexaenoic acid (DHA) is enzymatically combined with GPC and PS to form membrane phospholipids for nerve cell expansion.
Schofield P, Dementia associated with toxic causes and autoimmune
disease.
Int Psychogeriatr. 2005;17 Suppl
1:S129-47.
Toxic causes of dementia include exposure to heavy metals such as lead, mercury and aluminum as well as to carbon monoxide and solvents. Such conditions can be prevented by avoiding toxic exposures.
Mutter J, Daschner F, et al, Amalgam risk assessment with coverage of
references up to 2005] , Gesundheitswesen. 2005 Mar;67(3):204-16.
[Article in German](Medline)
Abstract
Dental Amalgam contributes substantially to human mercury load. Mercury
accumulates in some organs, particularly in the brain, where it can bind to
protein more tightly than other heavy metals (e. g. lead, cadmium).
Therefore, the elimination half time is assumed to be up to 1 - 18 years in
the brain and bones. Mercury is assumed to be one of the most toxic
non-radioactive elements. There are pointers to show that mercury vapour is
more neurotoxic than methyl-mercury in fish. Review of recent literature
suggests that mercury from dental amalgam may lead to nephrotoxicity,
neurobehavioural changes, autoimmunity, oxidative stress, autism, skin and
mucosa alterations or non-specific symptoms and complaints. The development
of Alzheimer's disease or multiple sclerosis has also been
linked to low-dose mercury exposure. There may be ndividual genetical or
acquired susceptibilities for negative effects from dental amalgam. Mercury
levels in the blood, urine or other biomarkers do not reflect the mercury
load in critical organs. Some studies regarding dental amalgam reveal
substantial methodical flaws. Removal of dental amalgam leads to permanent
improvement of various chronic complaints in a relevant number of patients
in various trials. Summing up, available data suggests that dental amalgam
is an unsuitable material for medical, occupational and ecological reasons.