You're the smart one.. Unfortunately I didn't find the tick on time and have been sick with persistent Lyme for over 10 years. Hoping for some kind of solution soon.
I have a brain disease driven by an infection that gets better with long term antibiotics.
One of my main symptoms was MCI. Interesting that after long term treatment not only the MCI improved or subsided but also my very long standing ADHD (present for as long as I can remember) got dramatically better, makes you wonder.
For someone who has been forced to try countless substances / diet regimens / health strategies due to a pervasive chronic disease, I beg to differ. There's so many things that you can personally do that will alter your cognitive abilities, sometimes to an incredible extent. The tricky bit is that there is indeed no silver bullet, and what works for someone might do nothing or create harm for another. So in my opinion, understanding that there are alternatives to resignation is really the critical component.
Hearing very interesting (yet unpublished) results coming out of Dayan Goodenowe's trials of supplementing Plasmalogen precursors on Alzheimer patients. A lot of folks over at APoE4.info have been on the precursors for many months.
Seems it wasn’t just “possession of an oil filter silencer”:
> Candelario sold and manufactured AR-15 style assault rifles in Maryland without a license. The ATF caught Candelario by using an anonymous man to purchase the firearms in a gas station parking lot. This agent purchased six rifles, as well as two fuel filter silencers.
With respect to Dayan Goodenowe and his Plasmalogen theory, I think the Rush study should be reproduced by other groups. I am no qualified to judge it either, but thinking critically, unless some glaring statistical mistakes were made, or error measuring the levels, or simply that plasmalogen deficiency is a biomarker more than causative (he goes at length as to why he considers it to be the latter), we are talking about natural compounds (Plasmalogen precursors, or IV plasmalogens) that do not require FDA approval, so it should be fairly straightforward to fund, develop and test.
“The clinical implications of this study are obvious. This is the first reported evidence of a metabolic phenotype with the same clinical characteristics as the APOE ε2ε3 genotype. The probability of dementia in participants with either a high PBV or an APOE ε2ε3 genotype was indistinguishable”
I recommend to take a look at this interview by the very Bredesen, to a scientist called Dayan Goodenowe, working also on the Alzheimer problem. He has a very interesting book called "Breaking Alzheimer" that postulates that DHA Plasmalogen deficiency is causative for Alzheimer. Very interesting stuff:
"Organophosphate poisoning is highly lethal as organophosphates, which are commonly found in insecticides and nerve agents, cause irreversible phosphorylation and inactivation of acetylcholinesterase (AChE), leading to neuromuscular disorders via accumulation of acetylcholine in the body."
Depends on the antibiotic. I believe their molecular mass has to be lower than around 500 Da for them to reliably cross the blood brain barrier. It also depend whether meningeal inflammation is present or not
"Ticks love to be in moist, low grass, so a lot of games, whether it's football, baseball, tend to happen in the morning. There may be dew on the grass and that's where a lot of ticks survive and hang out," Nesheiwat said.
Lots of anecdotal evidence of ALS developing after tick bites, or more concretely infection with Borrelia Burgdorferi.
Probably a genetic component, and other enviromental factors are also involved, but the only dramatic reversals of MND I have seen documented (or heard about) have been either with IV antibiotics [1][3], or years of Mercury chelation [2]
In the recent book "Chronic" by Dr. Stephen Philips, he's frustrated since he can only treat successfully (outcome similar to Dr. Martz), with antibiotics, about 15% of his ALS-like patients. Considering how uniformly fatal ALS diagnosis is otherwise, even considering how skewed of a sample he might get (patients that already know they are Lyme positive or suspect it), still find it astonishing.
Note that the author does not imply that Delta originated from a lab, but rather that Delta leaked from a lab at the end of 2021, and cites a supporting source.
My question would be how easy is for this molecule to cross the blood brain barrier. Perhaps if toxicity is very low you can diffuse it somewhat by maintaining high levels in blood, but my understanding is that molecules with a weight of more than 400daltons have trouble crossing it.
It might be also true that a certain percentage of lyme patients have some level of meningeal inflammation that might facilitate crossing more.