You cannot achieve what the paper is discussing through diet or supplements.
The paper is hypothesizing that if a drug could target the components of B. burgdorferi that regulate manganese then that would kill it.
You cannot deprive the cells of manganese or overwhelm them through supplementation or restrictive diet. You would damage your own body long before reaching levels that killed the Lyme infection.
I really hope the alternative medicine people don't start abusing this headline to push diets and supplements.
Deliberately inducing manganese deficiency (which I doubt you could pull off while still eating food) isn't "self care". It's a misunderstanding of what this article is saying.
Your body needs manganese and MnSOD (one of the target enzymes mentioned in the article) just as much as Lyme disease does.
You could theoretically kill the Lyme by killing the host body, like that classic XKCD about destroying anything in a petri dish if you don't care about collateral damage. The key to making a successful treatment is finding a way to kill the infection without killing the host.
Calling anything you're suggesting "self care" is dangerous and wrong.
Your guess would be wrong. Your body needs manganese for similar reasons that Lyme disease needs it. You also produce MnSOD.
If you starved your body of manganese sufficiently (which I doubt you could do without eating a completely synthetic diet for months) then you'd be killing yourself in parallel with the Lyme disease.
How long would it take you to die on a zero-manganese diet? If it's longer than it takes Borrelia, you still win!
Plenty of other treatments can remove manganese. But they all are biologically active in other unwanted ways.
I regularly find myself on a zero manganese diet for hours at a time, and I've yet to experience immediate death, screaming in agony.
Furthermore we have lots of data on how well humans can tolerate extended low manganese regimens. The standard treatment course for TB in the 1950s resulted in humans having low manganese for 1-2 years. This was unpleasant, but not lethal.
Any google search on PAS and manganese will show that it eliminates manganese from the body by chelating it, and is therefore used for treating manganese toxicity.
I don't have a specific reference for manganese levels in people undergoing the old TB treatment. But I'm sure that it should exist somewhere.
You've spread this claim throughout the comment section and called others "dead wrong", yet even you can't find a reference to support it?
The mechanism of PAS in TB is not manganese reduction: https://pmc.ncbi.nlm.nih.gov/articles/PMC5395024/
The mechanism of action of PAS against TB is in the Dihydrofolate Reductase pathway: https://pmc.ncbi.nlm.nih.gov/articles/PMC5395024/
I can only guess that this commenter saw that PAS can also be used for manganese chelation and jumped to conclusions?
That said, it is very unlikely that simply reducing manganese is preferable to existing antibiotics. But that doesn't rule out the potential effectiveness of a combination therapy.
Here is how we'd do that combination therapy. We'd mix a standard antibiotic with oral para-Aminosalicylic acid (PAS). Orally delivered PAS is the the standard treatment for treating excess manganese in humans. (Sorry, but you're dead wrong about needing a completely synthetic diet for months.) While PAS does harm a few kinds of stomach bacteria, it is far better than a broad spectrum antibiotic. And if the target disease is under stress already, then you need less antibiotic to finish them off.
Sure, a medicine that targets manganese in Lyme disease bacteria would be even better than this combination. But that medicine does not exist. And the combination in question is something that can be experimented with today, using drugs that have already been approved by the FDA.
Furthermore this is a combination that we already have a lot of experience with. Back in the 1950s, a variation on this, working on the same principles, was the standard treatment for tuberculosis. It was abandoned not because it was ineffective, but because we developed treatments with fewer side effects.
I responded to your comment above with this same claim. I cannot find any sources that say reducing manganese was the mechanism of PAS in TB.
A recent research paper on PAS in TB doesn't even mention manganese once. It identifies Dihydrofolate Reductase related actions as the mechanism against TB: https://pmc.ncbi.nlm.nih.gov/articles/PMC5395024/
> orally delivered PAS is the the standard treatment for treating excess manganese in humans.
EDTA has been the standard treatment. PAS has been explored and trialed. It can be used, but I don't know if I'd call it the "standard" treatment.
> (Sorry, but you're dead wrong about needing a completely synthetic diet for months.)
I was talking about a low-manganese diet, which the comment above me suggested. I don't know why you're so set on calling me "dead wrong" so much when you can't provide sources and aren't even reading what I'm writing.
> While PAS does harm a few kinds of stomach bacteria, it is far better than a broad spectrum antibiotic. And if the target disease is under stress already, then you need less antibiotic to finish them off.
You're really going to have to provide sources for PAS reducing manganese as a mechanism for fighting TB.
As I pointed out in my other comment, manganese is an essential cofactor for one of the other anti-TB drugs in the triple combination that was used in the past.
I wonder if a prolonged water fast would do the job.
> In its metallic state it appears to be inert when swallowed, unless it meets with much acidity in the alimentary canal, or is in a state of minute division ; its compounds are, however, all of them more or less poisonous.
> Mercury has been employed in one or other of its forms in almost all diseases ; but each of its numerous preparations is supposed to have some peculiarity of action of its own, combined with that common to all the compounds of this metal. The mercurials form, indeed, one of the most important classes of the materia medica.
He goes on to explain that mercuric acetate is the basis of Keyser's antivenereal pills (according to Robiquet), that mercuric chloride (which is probably what you meant by "mercuric chlorine") is "employed as an alterative, diaphoretic, and resolvent, in the chronic forms of secondary syphilis, rheumatism, scrofula, cancer, old dropsies, numerous skin diseases, &c." He also devotes a lot of space to emphasizing how important it is to be careful of it, describing the symptoms of poisoning with it, and explaining how to analyze "animal tissue" to detect mercury salts in it. He also discusses the use of mercuric nitrate in syphilis.
But never in all the pages he devotes to the uses of mercury and its compounds does he suggest that anyone ever used metallic mercury for syphilis.
I've also never seen a suggestion that mercuric chloride was ineffective against syphilis. Wikipedia says, "Once used as a first line treatment for syphilis, it has been replaced by the more effective and less toxic procaine penicillin since at least 1948."
[https://www.sciencemuseum.org.uk/objects-and-stories/history...]
Less academic of course. And mercuric chlorine was an autocorrect mistake from chloride.
If mercuric chloride was actually effective (without killing the patient) seems like total luck, and generally the first actual effective treatment was considered Salvarsan [https://en.wikipedia.org/wiki/Arsphenamine] - which was arsenic based yes?
Until antibiotics came around.
But people tried all sorts of things, including liquid mercury, as your source notes.
My source did not note that people tried liquid mercury.
Are you really saying that in that time, no one tried the most obvious form?
You’re right though that I was wrong it was the primary one - I’m truly horrified at the various things people tried. But I guess untreated syphilis is one of the worst possible ways to die, and I’d try pretty much anything too.
Unfortunately, this doesn't seem ubiquitous.