The major tissue sites of aluminium toxicity are the nervous system, immune system, bone, liver, and red blood cells. Aluminum may also interfere with heme (porphyrin) synthesis.
Aluminum is used to produce things, such as:
- beverage cans
- cooking pots
- siding
- roofing
- aluminum foil
- airplanes
Further, it is found in:
- antacids
- buffered aspirin
- food additives (especially in grains and cheeses)
- astringents
- vaccinations
- cat litter
- antiperspirants
- infant formula
- baking soda
Aluminum has been detected in calcium, magnesium, and phosphate salts used in parenteral solutions, and it has been found high in lung tissue as a result of tobacco and cannabis smoke inhalation. When aluminum is used in water treatment facilities, concentration in community water supplies can reach 93 µmol/L (2,500 µg/L).
Aluminum and Alzheimer’s disease:
Though not proven as a causative agent, it is striking that the neurofibrillary tangles of neurons that characterize the brains of Alzheimer’s patients (as well as in patients with amyotrophic lateral sclerosis and Parkinson’s and Huntington’s diseases) accumulate aluminum. A study group with aluminum exposure had higher vanilmandelic and homovanillic acids in urine and were significantly different from controls on neurobehavioral tests. As yet no study or group of studies has been able to confirm that aluminium is involved in the development of Alzheimer’s disease.
Aluminum in the body:
Aluminum replaces calcium in bone, disrupting normal osteoid formation and mineralization. Iron deficiency predisposes laboratory animals to higher aluminum absorption and, conversely, aluminum decreases absorption and uptake of iron. Aluminum concentration was found high in the liver and kidney and distribution of essential minerals, in tissues such as bone, brain, liver, and kidney, were altered in aluminum-treated rats.
Copper, zinc, and iron status:
Assessing copper, zinc, and iron status helps to determine vulnerability to the toxic effects of aluminum, and appropriate elemental treatments may help to overcome aluminum toxicity. Testing for anemia is indicated in patients with high RBC, plasma, or serum aluminum. Higher plasma aluminum is seen in infants fed soy formula compared with breast-fed infants.
Serum, erythrocyte, and plasma Aluminum:
Serum, erythrocyte, and plasma aluminum levels appear to correlate. Serum aluminum levels above 5 μmol/L (135 μg/L) are predictive of aluminum toxicity. Testing for anemia is indicated in patients with high blood levels of aluminum.
Hair Aluminum:
High hair aluminum has been shown in aluminum toxicity and therefore, a high value in hair likely reflects a regular source of exposure and should be eliminated.
Urinary Aluminum:
Urinary aluminum can provide information about aluminum intake and has been used to monitor humans exposed to dangerous amounts of aluminum. Because aluminum is ubiquitous in the environment, contamination of a patient’s specimen with aluminum is possible when collection containers are opened in living and work environments.
Desferrioxamine (DFO):
Desferrioxamine (DFO) is a chelator of aluminum and iron that has been used to treat acute aluminum toxicity. In fact, cases of aluminum toxicity are managed similarly to iron toxicity. DFO decreased RBC and plasma aluminum and improved hemoglobin, hematocrit, and mean cell volume in 13 patients. Chelation treatment with desferrioxamine should be handled conservatively due to the risk of inadvertently mobilizing large amounts of aluminum to the brain, which may enhance encephalopathy or a chemical interaction.
DMHP:
The chelator, L1 (1,2-dimethyl-1,3-hydroxypyrid-4-one deferiprone or DMHP) has also been used to lower aluminum total-body burden.
Others:
Ascorbate combined with DFO has been used to remove aluminum from human brain cells. Glycine has been used to help mobilize aluminum.
It is important to assure adequate status of essential elements (calcium, iron, copper, zinc).
Silicon is an antagonist of aluminum.
Further testing:
Further testing of an aluminum-toxicity might involve measurement of bone resorption, urinary catecholamines, oxidative stress, and even vitamin D.
References:
-https://www.alzheimers.org.uk/about-dementia/risk-factors-and-prevention/metals-and-dementia
-https://www.ncbi.nlm.nih.gov/pubmed/8943470
-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782734/
-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144270/
-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4691126/
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Consequences of aluminum toxicity are encephalopathy and abnormal speech, myoclonic jerks, convulsions, and a predisposition to osteomalacic fractures. Exposure to aluminum is ubiquitous via food, water, air and soil.
Associated Symptoms and Diseases:
Abnormal speech, myoclonic jerks, osteomalacia, progressive encephalopathy, Alzheimer’s disease, Parkinson’s disease.
Sources:
Aluminum cookware, antacids, drinking water, tobacco, and cannabis smoke.
Protective Measures:
Adequate iron (check ferritin), glycine, calcium, phosphorus (lowers intestinal absorption)
Chelating Agents:
Desferoxamine, DMHP
Possible treatment:
Identify and avoid exposure to the toxic element:
Increase elimination by improving GI, liver, and kidney function:
Protect against damage:
Consider oral or intravenous chelation if warranted by clinical symptoms and test data.
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