Advice Or Suggestions Regarding Alzheimer's

[GAF]

What aluminum in deodorant, etc? Avoid or ok?

 

[lollipop]

@GAF I would avoid if possible.

@Travis thanks for all the great research you are contributing on so many threads! Appreciated.

Looking at the list of foods in your article and in @David PS article once again reinforces why I only eat fresh foods and 99% of the time made by me. Processed foods might be one of the most disastrous experiments tried on humans.

 

[Travis]

I just got done reading about another pathway involved in Alzheimer's – lipid peroxidation.

Aluminum actually does this by displacing iron from tissues. It is unique in this respect, and can do this because it (Al³⁺) is trivalent like ferrous iron (Fe³⁺) is. Nearly all other physiological ions are either divalent (Mg²⁺, Ca²⁺) or monovalent (Na⁺, K⁺, Cl⁻, I⁻, OH⁻).

Lipid peroxidation can create reactive malondialdehyde and hydoxynonenal, two molecules which can crosslink proteins.

The other main causative factor besides iron and aluminum is homocysteine. This molecule can form a stable free·radical and cross the blood–brain barrier where it can initiate a free·radical chain reaction. A study published in 2002* reports a very high correlation coefficient (r=.924) between lipid peroxidation products and homocysteine in the cerebospinal fluid. This is a powerful statistical effect. You could almost be able to predict the lipid peroxidation concentration based on homocysteine levels.

The correlation between brain and plasma homocysteine was .850. This is still really high. A correlation coefficient of 1.00 is perfect and represents a perfectly-straight line with all data points connected.

Homocysteine is easy to control in most people. All you need is cobalamin (B₁₂), folate (B₉), and pyroxidal (B₆) – the B-vitamins in multiples-of-three (might as well add niacin for good measure). Vitamins B₁₂ and B₉ methylate (as an enzymatic cofactor) homocysteine back into methionine, but vitamin B₆ helps to transform it into the much preferred cysteine. Deficiencies in these vitamins have also been found associated with both high homocysteine levels and dementia.

Also important would be limiting methionine.

Low acetylcholine levels are commonly found as well, but this is most likely downstream of the lipid peroxidation – caused either by homocysteine, iron, or aluminum (by displacing iron).

And aluminum is also thought to act as a crosslinking agent directly, making it doubleplus bad.

* Selley, M. L., D. R. Close, and S. E. Stern. "The effect of increased concentrations of homocysteine on the concentration of (E)-4-hydroxy-2-nonenal in the plasma and cerebrospinal fluid of patients with Alzheimer’s disease." Neurobiology of aging 23.3 (2002): 383-388.

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Homocysteine is unique because it can form a stable free radical by virtue of it's longer "γ-tail." Cysteine has one carbon shorter, so the cysteine S-radical cannot transfer to the α-carbon through the amino group. Once it is on the α-carbon is has much greater long-range potential due to its stability. The longer γ-tail of homocysteine also makes it more lipid-soluble compared to cysteine, so you would expect to find it more around lipid membranes – the places most sensitive to lipid peroxidation.

 

[Amazoniac]

I just got done reading about another pathway involved in Alzheimer's – lipid peroxidation.

Aluminum actually does this by displacing iron from tissues. It is unique in this respect, and can do this because it (Al³⁺) is trivalent like ferrous iron (Fe³⁺) is. Nearly all other physiological ions are either divalent (Mg²⁺, Ca²⁺) or monovalent (Na⁺, K⁺, Cl⁻, I⁻, OH⁻).

Lipid peroxidation can create reactive malondialdehyde and hydoxynonenal, two molecules which can crosslink proteins.

The other main causative factor besides iron and aluminum is homocysteine. This molecule can form a stable free·radical and cross the blood–brain barrier where it can initiate a free·radical chain reaction. A study published in 2002* reports a very high correlation coefficient (r=.924) between lipid peroxidation products and homocysteine in the cerebospinal fluid. This is a powerful statistical effect. You could almost be able to predict the lipid peroxidation concentration based on homocysteine levels.

The correlation between brain and plasma homocysteine was .850. This is still really high. A correlation coefficient of 1.00 is perfect and represents a perfectly-straight line with all data points connected.

Homocysteine is easy to control in most people. All you need is cobalamin (B₁₂), folate (B₉), and pyroxidal (B₆) – the B-vitamins in multiples-of-three (might as well add niacin for good measure). Vitamins B₁₂ and B₉ methylate (as an enzymatic cofactor) homocysteine back into methionine, but vitamin B₆ helps to transform it into the much preferred cysteine. Deficiencies in these vitamins have also been found associated with both high homocysteine levels and dementia.

Also important would be limiting methionine.

Low acetylcholine levels are commonly found as well, but this is most likely downstream of the lipid peroxidation – caused either by homocysteine, iron, or aluminum (by displacing iron).

And aluminum is also thought to act as a crosslinking agent directly, making it doubleplus bad.

* Selley, M. L., D. R. Close, and S. E. Stern. "The effect of increased concentrations of homocysteine on the concentration of (E)-4-hydroxy-2-nonenal in the plasma and cerebrospinal fluid of patients with Alzheimer’s disease." Neurobiology of aging 23.3 (2002): 383-388.

―――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――――

Homocysteine is unique because it can form a stable free radical by virtue of it's longer "γ-tail." Cysteine has one carbon shorter, so the cysteine S-radical cannot transfer to the α-carbon through the amino group. Once it is on the α-carbon is has much greater long-range potential due to its stability. The longer γ-tail of homocysteine also makes it more lipid-soluble compared to cysteine, so you would expect to find it more around lipid membranes – the places most sensitive to lipid peroxidation.

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Always learning something from you! The pejorative connotation of heavy metals is sometimes bizarre, you can get intoxicated by light metals such as aluminium and titanium and you can improve your health with heavy metals such as zinc or copper.
Here's a related discussion:
https://www.iupac.org/publications/pac/2002/pdf/7405x0793.pdf

 

[Travis]

OMG. That looks like a 15-page β-slap from the International Union of Pure and Applied Chemistry.

Thus, the term “heavy metals” is both meaningless and misleading.

We all know that the word "heavy" is sometimes used too subjectively, but they even take issue with the use of the word "metal:"

Even the term “metal” is commonly misused in both toxicological literature and in legislation to mean the pure metal and all the chemical species in which it may exist.

This should be no surprise, as the IUPAC name for folic acid is N-(4-{[(2-amino-4-oxo-1,4-dihydropteridin-6-yl)methyl]amino}benzoyl)-L-glutamic acid.*

This, together with the absurdity of classifying magnesium as a “heavy metal”, when there has developed a conventional association of “heaviness” with toxicity...

I think William Taft could have had been partly responsible for that association.

Mining and industrial wastes and sewage sludge are potential sources of heavy metal pollution.

No mention of Def Leppard, at all. This is an great oversight by the IUPAC.

* These painfully-long names may seem pointless and pedandic to some. Well, they are – but they have utility. If you know what the pteridin ring looks like, then you can draw the entire molecule piecewise from the name itself. This seems pointless with the internet and modern computing, but there was a time when this was necessary. Not all books and journals had the typesetting, space, or inclination to draw-out the entire chemical formula way Back When.