Al and Food is there a problem?
Over recent time there has been a considerable amount of concern over
the toxicity of
aluminium and aluminium compounds.
The original evidence seems to date back to a US army research project
by Kopeloff Barrera
and Kopeloff in 1942.
Since then there has been a considerable amount of evidence published
which relates to the
toxicity of aluminium compounds. Some of the examples are;
The brain damage to kidney dialysis patients caused by aluminium in
dialysis water.
Deaths of babys in the USA which were associated with the combined
effects of
aluminium contaminated milk formula and poor kidney function.
Desferrioxamine was found to retard the progression of alzhiemers
disease in
a 1991 study. It was suggested that desferrioxamine a chelating agent
was removing
or inactivating aluminium present in brain tissue.
Aluminium compounds have been used to induce brain lesions during
neural
pathway investigations in cats.
A group of miners suffered aluminium induced brain damage after the
administration
of aluminium compounds in an attempt to prevent silicosis.
Aluminium has been found in the brains of people who died from some
types of dementia.
There have been studies which have shown a statistical association of
aluminium
in the water supply with the incidence of Alzhiemers disease. Although
at least one
of these studies has been questioned.
Aluminium also interferes with the xtal structure of hydroxyapatite in
bones causing a
weakening and increased risk of bone fractures in elderly people.
There is little doubt that that there are toxic effects produced if
too much aluminium is taken
up in to the body by whatever means. As far as Alzhiemers disease is
concerned it seems
from the literature that there a number of causes which may separately
give rise to the set of
symptoms which we know as Alzhiemers disease. One of these is possibly
aluminium.
The chemical properties of aluminium compounds must be considered in
conjunction with
any discussion of the potential effects of aluminium in food.
Aluminium forms a large number of compounds in which the aluminium is
strongly
bound. The aluminium in these compounds is unlikely to be sufficiently
bioavailable to
cause problems. Much of the earths aluminium is strongly bound in the
form of
aluminosilicates. Aluminium also forms chelates and complex ions with
a number
of materials for example fluoride and citric acid. Much of the
aluminium found in food is in
the form of alumino-silicates. These are insoluble in dilute acids and
are unlikely to be a
significant source of bioavailable aluminium. Much has been made of
the levels of
aluminium in tea. Tea also contains significant amounts of fluoride.
The soluble aluminium
present in tea would almost certainly be bound to the fluoride and
would not be
bioavailable.
Some of the main commercial uses of aluminium compounds depends on the
ability
of aluminium to bind to negatively charged polymers crosslinking them.
eg. Flocculation and precipitation reactions in water treatment, in
the manufacture of
alginate fibres etc.
The precipitation and coagulation of glyco-proteins by alum is well
known.(the astringent
taste of alum for example ) Aluminium can also bind to a negative site
on a protein molecule
changing the charge at that point from a negative charge to a positive
charge. This would
change the antigenic properties of the protein molecule and may be the
reason aluminium is
used as an adjuvant in vaccine manufacture.
Taking into consideration the properties of aluminium it is possible
to speculate on a
probable pathway and fate for aluminium in the body.
The steps are;
(1) Acid soluble aluminium dissolves producing Aluminium ions.
In the absence of a chelating agent (such as citric acid ) the
aluminium binds to
glycoproteins and other negatively charged protein. Becoming
bound to and insolublising
a polymer the aluminium becomes non bioavailable and passes
through the intestine
unchanged.
(2) In the presence of citrate aluminium forms a chelate compound
probably of the type
Na3 (Al (cit)2). In this compound the aluminium is present as
negatively charged
complex ion without any of the properties normally associated
with aluminium ions.
(3) Because the citrato aluminium compound is not now able to bind to
proteins it is
able to be absorbed into the blood stream. Citrate is known to
increase the absorption
of aluminium.The citrato-aluminium ion is also similar in size
to sugar molecules and
can be transported throughout the body.
(4) In areas of high metabolic activity (for example brain tissue)
localised areas of citrate
depletion would be expected. When citrate becomes depleted the
Aluminium + citrate to
citrato-aluminium equilibrium is shifted to the left releasing
positively charged Aluminium
ions.
(5) These unprotected aluminium ions are then able to react with any
negatively charged
polymers in the immediate vicinity. For example;
(a) Crosslinking and precipitating glycoproteins. Amyloid is a
glycoprotein. Polymers
when crosslinked become more resistant to chemical
attack,hence any amyloid
clearing mechanism would be retarded.
(b) Change of point charges on proteins from negative charges
to positive charges.
This would change the antigenic properties of the protein
molecules with the result
that the immune system would fail to recognise the protein
as self.
The two latest theorys about Alzhiemers disease are ;
(1) It is an autoimmune disease in which the immune system fails to
recognise
some particular proteins as self. Remember aluminium is used as
an adjuvant in
vaccines to promote an immune reaction.
(2) It is a failure of the bodys clearance mechanism for amyloid. This
of course could be due
to either a faulty clearance mechanism or crosslinkage of the
amyloid.
In either case aluminium is potentially a contributor.
There are obviously good grounds for legal limits to be placed on the
levels of bioavailable
aluminium in foods. Unfortunately the current methods of analysis for
aluminium in foods are
based on either hot perchloric acid digestion or furnace Atomic
absorption. Both methods
determine all aluminium including the unavailable aluminium.
A dilute Hydrochloric acid digestion followed by Flame AA or ICP would
probably be a more
relevant procedure.
Any legal standard for aluminium in food would have to include both a
maximum limit and
a specified group of procedures. Not only this but the maximum legal
limit would have to
assume that any bioavailable aluminium present was in its most toxic
form, possibly citrate.
