The search for environmental risk factors for Alzheimer's
Disease has shown an increased level of aluminum in the brains of
Alzheimers's patients (1,2).   More recent studies utilizing laser
microprobe mass analyzers (which have concentration resolutions of 1-2
parts per million and a spatial resolution of 1 micrometer) have
demonstrated a specific and selective accumulation of aluminum within
neurofibrillary tangle (NFT) bearing neurons when compared with adjacent
NFT free neurons (3).
        Animal experiments (4) have shown that administration of
chelated aluminum compounds seriously worsened the learning ability of
rats and resulted in diminished cholinergic activity, a characteristic
of Alzheimer's Disease.   Insoluable aluminum compounds did not
influence learning ability.    Studies of miners exposed to "McIntyre
Powder" (finely ground aluminum and aluminum oxide) showed impaired
cognitive performance consistent with the putative neurotoxicity of
chronic aluminum exposure (5).    These experiments clearly implicate
aluminum as one of perhaps many environmental etiologic risk factors for
Alzheimer's disease.
        Because the form in which aluminum is ingested seems to
influence its ultimate concentration in the brain (4), then
environmental sources of aluminum which are highly soluable and which
would be readily incorporated into brain tissue should be scrutinized.
One potential source of brain aluminum stems from the consumption of
trans fatty acids (the primarily fat of hardened vegetable oils, ie.
margarines, shortenings etc).    In order to synthesize trans fatty
acids, hydrogen is bubbled through vegetable oil  in the presence of a
catalyst called "Raney Nickel".   Merck's Index reveals that Raney
Nickel is prepared by fusing 50 parts nickel with 50 parts aluminum.
The alloy is pulverized and most of the aluminum is dissolved out with
sodium hydroxide, however residual aluminum, amounting to several
percent, remains and appears to be necessary for proper catalytic
activity.    During the  hydrogenation process which forms trans fatty
acids, Raney Nickel (in the form of its oxide) is used in amounts of 0.5
to 1 per cent of the weight of the oils.   Although the metal is
filtered from the oil, an appreciable amount remains dissolved in the
oil, presumably in the form of a soap consisting of nickel, aluminum and
the mixture of lipids formed after the hydrogenation process.
         It is possible that these alumino-nickel soaps formed during
the synthesis of trans fatty acids provide a stable and highly soluable
vehicle for the biological uptake and transport of aluminum into the
membrane and storage lipids of body tissues, including brain.    To
date, I believe no radio tracer studies have either confirmed or denied
this hypothesis.
        How does this relate to paleonutrition.    Obviously, aluminum
exposure in the environment of pre-industrial man would have been
minimal.    The trans fatty acids produced via the hydrogenation of
vegetable oils have only been with us since shortly after the turn of
the century.    Meat from ruminants which humans have been consuming for
at least 2 million yrs or more, contain small amounts of trans fatty
acids, but these fatty acids (trans vacenic acid primarily) are
apparently benign (compared to the trans fat, elaidic acid produced
during hydrogenation) and do not contain either aluminum or nickel
because they are produced by bio-hydrogenation occuring in the rumen.

                                        Cordially,

                                        Loren Cordain, Ph.D.
                                        Professor, Colo State Univ

                                REFERENCES

1.      Crapper DR et al.  Brain aluminum distribution in Alzheimer's
disease and experimental neurofibrillary degeneration.  Science
1973;180:511-513.
2.      Crapper DR et al.  Aluminum, neurofibrillary degeneration and
Alzheimer's disease. Brain 1976;99:67-80.
3.      Good PF et al.  Selective accumulation of aluminum and iron in
the neurofibrillary tangles of Alzheimers Disease: A laser microprobe
(LAMMA) study. Ann Neurol 1992;31:286-92.
4.      Bilkei-Gorzo A.  Neurotoxic effect of enteral aluminium. Fd Chem
Toxic 1993;31:357-61.
5.      Rifat SL et al.  Effect of exposure of mineres to aluminum
powder. Lancet 1990;336:1162-65.