In the search for a magic bullet, orthodox medicine ignores preliminary evidence suggesting that some forms of dementia may be caused by metallic poisoning.
In the US around four million men and women suffer from Alzheimer’s disease (AD), and in the UK over 600,000, mostly over the age of 65 years. As the world elderly population increases, so too does the incidence of AD. The disease is ultimately fatal in every case, with an average seven years from onset to death.
Despite over 30 years of research, mainstream medicine has come up with neither a cause nor a cure for AD. In doing so, the establishment is ignoring startling new evidence that AD could be, to a large extent, an environmental disease. Although AD is an umbrella term, now used to characterize all sorts of dementias in the elderly, recent, preliminary evidence suggests that classic Alzheimer’s may have something to do with poisoning from toxic metals.
Aluminium an established neurotoxin has long been linked to AD; high levels of both metallic elements have been found in the brains of people with AD.
However, recent attention has focused on research published last year that claims there is no connection whatsoever between aluminium and AD (Nature, November 1994).
This study found no trace of aluminium in the brains of dead Alzheimer’s patients, and suggested that previous studies that had, did so as a result of laboratory contamination, possibly through dyes used to stain the tissue for analysis. This does not explain why aluminium was not found in the brain tissue taken from control groups, though.
It has also been suggested that the nuclear microscope the team used to examine brain tissue may not have been as sensitive to aluminium as the chemical method used in previous studies.
It is difficult to dismiss the many previous studies which have made a connection between aluminium and AD, the latest also published only last year, which concluded that their findings “are consistent with a role for aluminium in the development of AD-like pathology in patients subjected to prolonged aluminium exposure” (The Lancet, April 23, 1994).
This lends itself to the argument that, rather than being a cause of AD, aluminium may accumulate in the brain because of the disease processes. Dr John Growdon stated that aluminium may act as a neurotoxin in AD, or might just accumulate in dying nerve cells (New England Journal of Medicine, March 18, 1993), and a 1993 study concluded that aluminium and other metallic elements may gain increased access to the brain through alterations in the brain and other organs (Experimental Gerontology, July-Oct 1993).
An earlier study suggested that rather than being a cause of AD per se, high levels of aluminium in the brain may cause an AD-type dementia (Ciba Foundation Symposium, 1992; 169: 142-54). This is supported by high levels of aluminium having been found in the brains of people suffering from a brain disease known as dialysis dementia (The Lancet, March 21, 1992). High levels of aluminium have also been found in the brains of people with Down’s syndrome, which has similar neurochemical features to Alzheimer’s disease. People with Down’s also have a predisposition to AD (The Lancet, March 31, 1990).
As well as drinking water, in which aluminium levels vary from area to area, aluminium is found in foodstuffs, cosmetics, deodorants and pharmaceuticals, particularly some antacids. Aluminium utensils and drink cans have also been touted as a possible danger.
One study found that aluminium concentration was far higher in several commercially available brands of fresh and reconstituted orange juice, and concluded that drinking most brands of so called fresh and pure orange juice might result in far greater exposure to aluminium than drinking a similar volume of tap water (The Lancet, May 16, 1992).
Silicic acid and fluoride are said to protect against excess accumulation of aluminium, although increased accumulation in lung, bone and brain does occur with age (The Lancet, March 21, 1992).
But the most damning new research points the finger at mercury, a substance rated among the most toxic known to man, particularly that present in amalgam fillings.
A medical research team at the University of Kentucky in Lexington, Kentucky, who have been investigating the possible link between mercury and AD, found high levels of the element in the brain tissue of AD victims (Neurotoxicology, 1986; 7: 197-206; Biol Trace Element Res, 1987; 13: 19-23), and WR Markesbery and his team found that the highest trace element in the brains of 10 autopsied AD patients was mercury (Brain Research, 1990; 533: 125-31).
As with aluminium, however, the Markesbery study noted that whether mercury was a possible cause of AD, or simply a deposit on a degenerating brain, remained to be determined. They concluded: “This and our previous studies suggest that mercury toxicity could play a role in neuronal degeneration in AD.”
The link between mercury and AD was strengthened by Haley et al, who found that mercury fed rats developed a diminished tubulin level similar to people with AD. Tubulin is a protein needed for the healthy formation of nerve tissue in the brain, and a lack of tubulin will result in messages in the brain not connecting properly. When fed aluminium, the rats displayed no change in tubulin levels (Federation of American Societies for Experimental Biology, 75th Annual Meeting, 21-25 April 1991).
Markesbery and his team also found diminished levels of zinc and selenium in the 10 AD-affected brains they examined. This is significant in that zinc and selenium are known to have a protective role against heavy metal poisoning in tissue.
It has also been suggested that low levels of zinc, coupled with high levels of mercury, could make the brain more susceptible to aluminium deposits. Or that mercury and aluminium both contribute to AD.
The Markesbery team noted that “the source of brain mercury in AD is not known, although dental amalgams and environmental sources such as seafood are potential sources”. However, even the World Health Organization concedes that the public’s highest daily exposure to mercury comes from dental amalgam fillings. (For a more detailed analysis of the potential dangers associated with amalgam, see The WDDTY Dental Handbook).
To date, medicine has pooh-poohed the possible mercury connection, pouring all resources into the development of a magic bullet. Nevertheless, controversy rages over tacrine, the only drug licensed (in the US and France) for the treatment of AD. The drug is currently under consideration for licensing in other parts of Europe, including the UK.
Tacrine is a “cholinergic enhancer”. The cholinergic system is involved in cognitive functions, ie, learning process, memory, perception, reasoning, etc, which are all affected by AD. People with AD suffer a significant loss of cholinergic neurons.
The drug has been shown to benefit some patients with AD, in terms of reducing the decline in cognitive function, but only at very high doses, which few patients can tolerate. There is a high incidence of side effects, predominantly liver toxicity. Since a study in 1986 reported a dramatic improvement in 17 patients with apparent AD (New England Journal of Medicine, 1986; 315: 1241-5) further studies have been fairly equally divided on whether or not tacrine is an effective, and safe, treatment for AD.
The US Food and Drug Administration refused to approve tacrine for the treatment of AD four times before granting it limited use under its Treatment IND (Investigational New Drugs) programme in 1991. This allows people with life threatening conditions to be treated with experimental drugs. It stressed at the time that the favourable effects regarding its use were small and of uncertain real benefit, and that there was concern about liver toxicity.
Further research revealed little to refute or counteract this, and yet tacrine was eventually licensed in the US in September 1993.
In a six-week study in 1992, Davis et al, in conjunction with The Tacrine Collaborative Study Group, reported that they were unable to detect any clinical improvement in patients treated with tacrine, although it did reduce the decline in cognitive function. Most alarmingly, liver toxicity developed in 42 per cent of patients, and in the opinion of the Davis team, this could have been higher if the patients had continued to take the high doses of tacrine originally prescribed (The New England Journal of Medicine, October 29, 1992).
In the largest study, Watkins et al analyzed data from several randomized controlled trials to evaluate the risk of liver toxicity and attempted to identify risk factors. Of the 2446 people involved, 49 per cent developed liver toxicity, with women clearly more susceptible. Although it was noted that frequent monitoring appeared to identify those susceptible within the first 12 weeks of treatment, they also stated that “tacrine could produce life-threatening hepatotoxicity (liver toxicity) in some patients” (JAMA, April 6,1994).
Similar results regarding liver toxicity were found in a 30-week study by Knapp et al published in the same week. Patients were given up to 160mg of tacrine (the highest dose used in any trial to date). Less than half the patients completed the study and of the patients who made it through to the 160mg dosage group,72 per cent had to withdraw due to side effects. The study nevertheless came out in favour of administering high doses of tacrine to AD sufferers (JAMA, April 6, 1994).
But the study paper also noted that three liver biopsies performed on patients who developed liver toxicity following tacrine treatment in a trial in France revealed all three were suffering from hepatitis. Two were presumed linked to the tacrine treatment.
Liver toxicity, and the other common side effects such as nausea, vomiting, abdominal pain, diarrhea and increased sweating, have shown to be reversible in a matter of weeks once the patient stops taking tacrine (JAMA, April 6, 1994). Of the patients in the Watkins study who withdrew from tacrine treatment due to liver toxicity, 88 per cent were able to resume taking the drug with no evidence of liver toxicity. This finding suggested to Watkins et al that the liver may be able to adapt to the toxic effects of tacrine over time, and could also explain why liver toxicity rarely developed beyond the initial 12 weeks of treatment (JAMA April 6, 1994).
Nobody knows, however, who among those who have had an adverse reaction will be able to tolerate the drug on a second ground, and the long-term effects are not known.
Furthermore, trials to date have been carried out on patients with mild to moderate AD who were in moderately good health. Elderly demented patients with multiple medical illnesses may be more likely to develop side effects (JAMA, November 11, 1992). It has also been suggested that patients with more severe disease do not benefit from tacrine therapy (New England Journal of Medicine, 1986:315; 214-5).
But are the known risks involved in tacrine treatment worth it? Few can even agree about that. An editorial in the BMJ (April 2, 1994) reported that “modest” beneficial effects of tacrine treatment had been reported in between 3 per cent and 50 per cent of trial subjects, with only a very few patients improving greatly. Another study (JAMA, April 6, 1994) gave a one-in-three chance of improvement with tacrine.
Dr Margaret Winkler, a senior editor of JAMA, warned that even if a patient does respond positively to tacrine “the decline associated with AD continues, and since the drug’s action is temporary, if administration of the drug is stopped, the patient’s cognition will return to the level expected if the drug had never been administered” (JAMA, April 6, 1994).