Are You Getting Too Much Aluminum In Your Diet?

More on Aluminum Toxicity

 

Are you getting too much aluminum in your diet?

The story begins in Guam, where a very high incidence of ALS has been reported consistently since 1954, at rates about 30 times higher than normal.

That is such an alarmingly high rate that it drew the attention of researchers from Japan, Europe, and America.

The cause was quickly found, denied, and suppressed…

…by using various unrealistic explanations to deflect attention from the obvious.

Most notable is the BMAA (beta-methylamino-L-alanine) hypothesis.

It’s an interesting hypothesis (more on that later), but it isn’t backed up by the facts.

It falls short when you look at the hard data gathered in the early days of ALS research.

The earliest indication that aluminum is the culprit was in 1982.

Japanese researcher Dr. Fumio Yoshimasu knew that injecting rabbits with aluminum causes nerve degeneration.

And he was intrigued by reports of the high aluminum content in Guam’s drinking water.

So he undertook to analyze the aluminum levels in people with ALS.

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Yoshimasu’s first subjects were Japanese: four people with ALS and three control subjects.

The ALS patients had twice the amount of aluminum in their brain tissue than the controls did.

He then turned his attention to Guam, and published two more studies on his findings.

“The volcanic soil on the southern part of the island where most cases occur contains a considerable amount of aluminum and manganese” —Yoshimasu

He found 749% more aluminum in the spinal cords of Parkinson’s patients compared to the controls.

That’s even more alarming when you realize that the control subjects were high in aluminum themselves, being from the same small island.

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By graphing aluminum and calcium concentrations across all parts of the nervous system, Yoshimasu found a clear picture.

The only difference between the ALS patients and the people without ALS was higher levels of aluminum and lower levels of calcium.

“A significantly high concentration of aluminum in the CNS tissue of the Guam ALS and PD cases was confirmed” —Yoshimasu

It appears from studies that calcium is antagonistic to aluminum.

Other studies on Alzheimer’s patients have found silica to be protective against aluminum from water.

The technique that Yoshimasu used for analysis, neutron activation, is very reliable.

His findings have been replicated in other studies using other techniques.

Also in 1982, Dr. Daniel Perl unveiled his findings in Science magazine, a high-profile publication.

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Like Yoshimasu, Perl measured aluminum levels in Guamanian ALS patients  but he used an even more accurate method, EDS (energy-dispersive spectroscopy).

He found, on average, 383% more aluminum in the ALS cases.

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These findings, as well as those from Japan, almost force one to conclude that aluminum causes ALS directly – by its mere presence.

“Intraneuronal accumulation of aluminum has been demonstrated in lumbar motor neurons in patients with ALS”  —Perl

Aluminum has also been imaged directly in ALS patients using wavelength dispersive spectrometry (Garruto, 1984), and solochrome azurine, an aluminum-specific stain (Picardo, 1988).

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Around this time, a new hypothesis was forming. The one involving an amino acid in cycad seeds, a native food of Guam.

This deflected attention from the undeniable role of aluminum.

The amino acid BMAA is not even toxic to rats, even in absurd doses – doses far higher than anything you’d get from eating cycad seeds (Perry, 1989).

The originator of the BMAA hypothesis viewed the amino acid as an excitotoxin, like MSG or aspartate.

Experiments proved otherwise.

McGeer & Lee – stunned that this BMAA charade had been going on for so long – published a scathing article on its 35th anniversary.

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They demonstrated that it can’t rightly be classed as a neurotoxin in any way.

“Beta-N-methylamino-L-alanine (BMAA) is routinely described in the literature as a neurotoxin … the validity of these hypotheses depends on whether BMAA is toxic toward human neurons. Because there are no data on this subject, we undertook an analysis of BMAA neurotoxicity against 3 human neuronal cell lines. We found the toxicity to be so low that it was comparable to the body-building nutritional supplement beta-alanine.”  —McGeer & Lee

The neurotoxicity of BMAA was so low as to be 300–400 times less toxic than glutamate, the body’s own neurotransmitter.

In 1991, Mark Duncan showed that BMAA barely crosses the blood–brain barrier. Only 0.08% of an injected dose is found there.

So the steady-state brain concentration, after continuous infusion of 400 mg/kg for two weeks, is only 10–30 μg/g.

This is far less than the concentration of the body’s own natural glutamate.

And no behavioral effects were noted in test rats in this study either.

He published a letter in The Lancet to explain how unlikely it is that BMAA could possibly cause ALS.

“We conclude that processed cycad flour as prepared by the Chamorros of Guam and Rota contains extremely low levels of BMAA, which are in the order of only 0.005% by weight. Thus, even when cycad flour is a dietary staple and eaten regularly, it seems unlikely that these low levels could cause the delayed and widespread neurofibrillary degeneration of nerve cells observed in ALS and the parkinsonism-dementia complex of Guam.”  —Duncan

But the BMAA cheerleaders wouldn’t let truth get in the way of their research funding…

So after killing about a million trees by printing plain B.S. bullshit, they decided to imagine an entirely different way for BMAA to be responsible for ALS.

Philosophers of science call this “saving the phenomena.”

They came up with the idea that BMAA incorporates directly into growing protein. As an amino acid, it could theoretically do this.

But this is more diversion, since massive doses in mice don’t lead to neurological changes.

The only thing that’s ever been proven to cause ALS in animals is aluminum.

Henry Sherp first demonstrated this in the ‘60s, on both rabbits and monkeys.

“The results show that 25% to 37% of the injected aluminum is retained in the central nervous system.”  —Sherp

Not much attention was given to such studies until Guam in the ‘80s. That’s when aluminum became synonymous with ALS.

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The scientists in this study decided to just prove in a straightforward manner that aluminum accumulates in the nervous system and causes ALS.

They fed the aluminum directly to the monkeys – no injections.

It was pressed into their food pellets. And they were given less calcium than usual.

One group of monkeys was fed cycad flour, the source of BMAA in Guam…

“Neurofibrillary pathology was most frequently seen in animals fed the low-calcium diet supplemented with aluminum and manganese.”  —Garruto

Just by feeding aluminum and restricting calcium they were able to replicate ALS in the monkeys.

Even the chemical mechanism has now been worked out.

Aluminum has a high affinity for phosphate.

The outer layer of the spinal cord is rich in phosphate. So are the Tau (τ) proteins, which are abundant in the nervous system.

“The magnitude and extent of lesions observed in these animals far exceeded that found in normal-aged monkeys.”  —Garruto

Also, feeding cycad “failed to accentuate the neuropathology.”

This is more confirmation that BMAA is basically harmless.

The scientists responsible for these studies – Garruto, Duncan, McGeer, Lee, and Perl – are quite certain that BMAA has nothing to do with ALS.

“BMAA should no longer be considered a neurotoxin and an environmental hazard.”  —McGeer & Lee

Aluminum is found in some packaged foods, so it’s a good habit to read labels.

Some municipal water supplies contain high levels of aluminum, just like the water in Guam.

The natural minerals calcium and silica are protective against aluminum toxicity, but it’s best to avoid aluminum altogether if you can.

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