Mineral Balancing

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Aluminium (Al)

John Bumpus

If our ancestors were considered to live in the Iron Age or Bronze Age, then for the last 125 years, we have been living in the Age of Aluminium. Aluminium was once thought to be inert in biological systems, but since we now live in a time where it is so rampant, and used in much of our technological society, aluminium has been under much investigation.  Exposure to aluminium levels that are naturally present in food, water and dirt, are not currently considered harmful (Centre for Disease Control, 2008). Since it is nearly impossible to avoid aluminium exposure in our modern environment, due primarily to manufactured goods, its biological implications must be investigated and discussed from such high exposures (Exley, 2013).

History of Aluminium

Aluminium (Al) gets its name from the Latin word alumen, which was used to describe potash alum. In the United States, it is often referred to as aluminum. Aluminium as the free metal know it in modern day, is not found in Nature. It is only found in combination with oxygen which forms a hard oxide called alumina. When contaminated with other elements alumina differentiates into gem stones, such as rubies and sapphires, which have been used in the art of Ayurvedic Medicine for thousands of years.

Pliny the Elder told a story about a first century craftsman who made a cup of an unknown metal that resembled silver, though it was too light to the Roman Emperor Tiberius.

In the early 1700’s, a clay that is particularly rich in aluminium was found in Las Baux, France that was named Bauxite. Aluminium is the third most abundant element in the Earth’s crust as well as the most abundant metallic element although it is not found in its metallic form in Nature.

Aluminium was named by Sir Humphry Davy in 1809. He theorised that aluminium could be produced from alumina (aluminium oxide) through electrolytic reduction. However, he was unable to prove this theory in practise.

In 1825, the Danish physicist Hans Christian Ørsted was successful in his experiments, though he only managed to create an alloy of aluminium by treating bauxite, with carbon and chlorine amalgams of potassium, resulting in a volatile mixture of mercury and aluminium. Once the mercury was separated as a vapor through the process of boiling, what remained was a powdery metal that resembled Tin in both colour and lustre. Ørsted’s work was continued by a German chemist named Friedrich Woehler, who, after 18 years of experimentation, was able to create small balls of solidified molten aluminium (globules) in the 1845 (Aluminium Leader).

Aluminium has since become one of the most widely used metals due to its versatility. It is lightweight and silver-white in colour. Aluminium in its pure state is quite soft, so it is typically used in an alloy with silicon and iron, making it quite strong. On the periodic table it is of the boron group.

Uses of Aluminium

Since aluminium occurs naturally in the soil, it can also be found in most plants and animals. Aluminium accumulates in Symplocos, Orites and Lycopodium. The accumulation of aluminium in Symplocos sp. is one of the reasons why traditional Indonesian weavers use the leaves and bark of this plant as a mordant in the dyeing process (Marco Schmitt, 2016).

Aluminium is often thought to be a toxic element. However, according to professor Gerhard Schrauzer, it should be listed as an essential mineral for all vertebrates including humans. The reason for this is that aluminium has a role in activating the enzymes, succinic dehydrogenase and alpha-ketoglutarate dehydrogenase (Zatta P, 2000). Succinic dehydrogenase has been shown to increase the survival rate of newborns, while alpha-ketoglutarate dehydrogenase is necessary in the Krebs cycle.  The necessity for aluminium in activating these two enzymes makes it an essential element for health. This means that, to a certain degree, aluminium is a nutrient. However, like all nutritional elements, when the mineral is in balance, it is fine, but in excess they can be just as detrimental as a deficiency (Britannica, 2019).

Eating large amounts of processed food that contain aluminium additives or regularly consuming acidic food in aluminium pots or pans may be a potential source for aluminium toxicity. Especially when compared to individuals who are not consuming very much processed foods or food which is cooked in stainless steel or glass pans. 

Even when aluminium is not an ingredient in fertilizer, the long-term use of artificial fertilisers increases soil acidity to such an extent that aluminium levels rise due to leaching. This is a result of the increased availability of aluminium in an acidic environment (Perl KJ, 1982). As much as 40% of the world's arable soil has elevated aluminium levels. Acid rain has affected fresh waters leading to extinction of some fish (Flaten TP, 1996).

Aluminium welders were found to have increased levels of aluminium in blood serum and urine, that affected their short-term memory, learning ability and concentration (Hänninen H, 1994).

Antacids are used in infancy to treat feeding troubles and reflux. This is concerning to me, since the antacids have been shown to increase blood plasma and urine levels of aluminium (Woodard-Knight L, 1992).

Toxic Effects of Aluminium

Aluminium has many implications in human health, such as respiratory effects (San LN, 1998), neurotoxicity (Savory J, 1996; Bolla KI, 1992), mental deterioration (Watts, 1995), osteomalacia, encephalopathy and anaemia, in severe instances of toxicity (Golub MS, 1996; Flaten TP, 1996). Toxic effects seem to occur where it accumulates most, the brain, which uptakes about 1mg in 36 years and may cause or contribute to many age-related diseases (Ganrot, 1986; Zatta P, 2000).

Various food acids such as malic, oxalic, tartaric, succinic, aspartic, and glutamic acids commonly found in foods can act upon aluminium in the digestive tract and increase its availability, particularly the breakdown and absorption of aluminium hydroxide which was found to be higher than aluminium phosphate.

The Lethal Dose of Aluminum sulfate, also called the LD50 is 6,207/mg/kg orally for a mouse. To consume this much aluminium, would be the equivalent of 500 grams for an 80 kg human per day.

Aluminium is neurotoxic. Higher Al levels have been associated with lower vocabulary scores and a decline in attention/concentration, frontal lobe functions (Bolla KI, 1992).

In animal studies, Aluminium blocks the action potential (electrical discharge) of neurons, reducing nervous system activity. It also blocks essential enzyme expression in the brain such as Na-K-ATPase and hexokinase. Aluminium may also inhibit uptake of important neurotransmitters such as dopamine, norepinephrine, and 5-hydroxytryptamine  (5-HTP) by nerve cells.

While Aluminium intake does indicate sensitivity to some individuals, resulting in contact dermatitis and digestive disturbances, however toxicology research has concluded that Aluminium is not as toxic as other elements such as mercury, cadmium, or arsenic. 

Aluminium pesticides, aluminium phosphide, is used as a fumigant grain perseverative and is known to be highly toxic to humans. It effects the lungs, heart, and blood vessels causing pulmonary edema, shock and arrhythmia (Mohan Gurjar, 2011). When an individual has been exposed to aluminium phosphide poisoning or exhibit aluminium toxicity, there may be increased requirements for superoxide dismutase (SOD). It seems the body ramps up production of SOD to protect from the toxicity (Chugh SN, 1996).

Some of the negative effects which have been attributed to aluminium is due to the creation of superoxide free radicals (O2-) perhaps also in association with other trace elements such as vanadium. Vitamin E and copper (II), substances with with SOD like activities seem to be helpful in toxicity of aluminium (Abou-Seif, 1997).

Increased aluminium intake from antacids during pregnancy may cause growth retardation, poor skeletal development, malformation and low maternal weight (Golub MS, 1996).

Detection of Aluminium in the body

All people have small amounts of aluminium present in their bodies (Exley, Burgess, Day, Jeffery, & Yokel, 1996). It can be measured by blood, bone, cerebrospinal fluid, faeces, urine and hair. In my experience it is rare to get a hair test and not detect aluminium.

  • Blood Tests. There is debate whether blood testing for aluminium has much value. Blood levels do not indicate total body load of aluminium. It can however indicate if you have been exposed to abnormal amounts of aluminium recently (Centre for Disease Control, 2008)

  • Bone. Measuring bone aluminium can indicate exposure to high amounts of aluminium. However, it requires a bone biopsy.

  • Hair Tissue Mineral Analysis. Aluminium levels appear to correlate well with bone levels of Aluminium. Several hair tests may be required before aluminium is revealed, however most often it is prevalent. Low Aluminium on an HTMA, may indicate that the element is tightly bound within body tissues, and may take several months on a nutritional balancing program to mobilise.

Hair Tissue Mineral Analysis

Hair has been extensively used to detect aluminium levels in humans (Zerbino DD, 1994; Shrestha KP, 1989; Paschal DC, 1989; Yokel, 1982). The ideal value of aluminium in the hair is 0.2 - 0.4 mg%. Since it is so abundant in the Earth and in modern day applications, it should be expected to see aluminium in the hair within this range. A level above 0.2mg% is an indication that toxic forms of iron and manganese may also be present whether identified on the hair analysis or not. A level above 0.4mg% indicates elevated levels of aluminium in the body. If the level is below 0.2mg%, it is called a poor eliminator pattern. This is an indication that the metal is accumulating due to detoxification and elimination weaknesses. A level below 0.1mg% indicates very poor elimination, and possibly serious accumulation in the body.

Aluminium is more readily absorbed in individuals with hyperparathyroidism (Burnatowska-Hledin MA, 1983) and is very common in individuals with high hair calcium levels (Watts, 1995). This is likely due to low thyroid gland activity and thus high parathyroid gland activity. Thus, high aluminium is more likely to occur in slow oxidisers. This does not mean however, that fast oxidisers cannot also have high aluminium levels.

Hair aluminium levels appear to correlate well with bone levels of aluminium. Sequential hair tests and committing oneself to a Mineral Balancing nutrition program, along with daily saunas may be required to mobilize the aluminium as it is often be tightly bound within body tissues. I have found that using vitamins E, C and sometimes D can also enhance the elimination of aluminium into the hair, thus raising hair aluminium levels. This should be perceived as an elimination of aluminium. Minerals that also can do this include; calcium, zinc, copper, iron, magnesium, silver, boron, phosphorus, lithium and silica. Boron and Lithium have proven effective for the detoxification of aluminium from the body, including the brain (Bumpus, 2019).

Possible Conditions Associated with Aluminium

Aluminium is known to compete for absorption with Calcium and phosphorus. Thus, increased amounts of dietary intake can decrease skeletal mineralisation, leading to osteopenia. 

Early symptoms of aluminium toxicity include flatulence, headaches, colic, dryness of skin and mucous membranes, a tendency for colds, burning pain in head relieved by food, heartburn and an aversion to meat.

Later symptoms include paralytic muscular conditions, loss of memory and mental confusion.

Kidney disease seems to correlate with people storing more aluminium in their bodies. This is because the kidney is one of the primarily routes for aluminium detoxification (Centre for Disease Control, 2008). Haemodialysis patients are susceptible to aluminium toxicity and have reduced visual memory function when high levels of aluminium are present (Bolla KI, 1992).

Animal studies of aluminium toxicity show that the nervous system is a sensitive target. According to the CDC (2008) there were no obvious signs of toxicity at high oral doses, but they did note that animals did not perform as well on tests that measured the strength of their grip or how much they moved around.

Brain and bone disease caused by aluminium have been observed in children with kidney disease. This could also be due to the medications they were taking. Bone damage is caused by aluminium blocking the intestinal absorption of phosphate (Centre for Disease Control, 2008).

Aluminium does not appear to cause birth defects in people, but they have not been seen in animals. When their mothers were exposed to large amounts of aluminium during pregnancy and nursing, very young animals appeared weaker and less active in their cages, with less coordinated movement. Aluminium also impacted the animal’s memory negatively, similar to the effects that have been observed in adults. Children and adult animals are both sensitive to aluminium (Centre for Disease Control, 2008).

Sources Of Aluminum Toxicity (Centre for Disease Control, 2008)

  • Baking powders (sodium aluminium phosphate) (Melvyn R, 1998)

  • Buffered Asprin may contain 10-20 mg per tablet

  • Some bottled water (FDA limit of 0.2mg/L)

  • Cookware

  • Colouring agents (Lake)

  • Cosmetics

  • Anticaking agents

  • Aluminium cans (soda pop and beer)

  • Food cooked in aluminium cookware

  • Aluminium-containing antacids

  • Antiperspirants and deodorants (aluminium chlorhydrate) (check “crystal deodorants for form of aluminium)

  • Antacids (aluminium hydroxide)

  • Water (Aluminum sulphate is frequently added to municipal water)

  • Fluoridated water increases leaching of aluminium from aluminium pots and pans.

  • As a drying agent in salt and other products.

  • Processed cheese

  • Bleached flour

  • Medications (aluminium phosphate) (Melvyn R, 1998)

  • Pesticides (Aluminium phosphide)

  • Vaccines (no greater than 0.85mg/dose)

  • Today children are often born with elevated aluminium, that is passed from mother to foetus through the placenta

References

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