I will add some links at the bottom of this for you to print out and take to your doctor.

A large percentage of people, including PWP, have a colony of bacteria in their stomach called Helicobacter pylori (HP). Among other things, it causes ulcers. The two Australians who discovered it won a Nobel Prize two years ago. It is that important.

HP belongs to a family called "gram negative" bacteia, named for the way they stain in the lab. These bacteria produce a neurotoxin called lipopolysaccharide (LPS) and use it as a part of their cell wall. It is harmless there. But when the bacterium dies, it sends out a tiny cloud of a major toxin. And sometimes when it detects particular antibiotics and knows that it is under attack, some strains ramp up their toxin production. Two hundred fold.

One of the leading factors that set the stage for later PD is exposure of the fetus to LPS. This sets up a chain of events that sensitizes the adult to further exposure and leads to the brain's immune cells (microglia) over reacting and damaging neurons. Plus, LPS is, itself, a potent neurotoxin.

So, with all that preamble, your husband may be drowning in poison from the dead bacteria. I don't want to be overly dramatic, but if this scenario is true then certain steps must be taken as quickly as possible to get the toxin out of the bowel and to dampen the immune response. If your husband is constipated that makes it easy. Your doctor can just flush him out good. If he is not then it gets tougher and changing antibiotics might be in order.

Two things that have research behind them to calm the microglia and that you can start right now are green tea extract and silymarin.

I learned this the hard way and have two wonky fingers on my right hand to remind me. This is something each and every one of us could run into tomorrow. Wlk into the hospital with a bad bug and come out in a wheel chair.So everyone print this out and keep a copy in your wallet and give each of your doctors one. This is not something they are going to know. If they do then you have an unusually good doctor.


Here is an abstract for your doctor. I did not notice if you were in USA or UK, but Dr. Sylvia Dobbs at King's College in London might be worth your doc's call if it gets complicated. Good luck and let us know how it goes.


: Helicobacter. 2005 Aug;10(4):276-87.

Erratum in:
Helicobacter. 2005 Oct;10(5):557. Bjarnason, Inguar T [corrected to Bjarnason,
Ingvar T].

Role of chronic infection and inflammation in the gastrointestinal tract in the
etiology and pathogenesis of idiopathic parkinsonism. Part 2: response of facets
of clinical idiopathic parkinsonism to Helicobacter pylori eradication. A
randomized, double-blind, placebo-controlled efficacy study.

Bjarnason IT, Charlett A, Dobbs RJ, Dobbs SM, Ibrahim MA, Kerwin RW, Mahler RF,
Oxlade NL, Peterson DW, Plant JM, Price AB, Weller C.

Section of Neuropharmacology, Institute of Psychiatry, London, UK.

BACKGROUND: Links between etiology/pathogenesis of neuropsychiatric disease and
infection are increasingly recognized. AIM: Proof-of-principle that infection
contributes to idiopathic parkinsonism. METHODS: Randomized, double-blind,
placebo-controlled efficacy study of proven Helicobacter pylori eradication on
the time course of facets of parkinsonism. Intervention was 1 week's triple
eradication therapy/placebos. Routine deblinding at 1 year (those still infected
received open-active), with follow-up to 5 years post-eradication. Primary
outcome was mean stride length at free-walking speed, sample size 56 for a
difference, active vs. placebo, of 3/4 (between-subject standard deviation).
Recruitment of subjects with idiopathic parkinsonism and H. pylori infection was
stopped at 31, because of marked deterioration with eradication failure. Interim
analysis was made in the 20 who had reached deblinding, seven of whom were
receiving antiparkinsonian medication (long-t(1/2), evenly spaced) which remained
unchanged. RESULTS: Improvement in stride-length, on active (n = 9) vs. placebo
(11), exceeded size of effect on which the sample size was calculated when
analyzed on intention-to-treat basis (p = .02), and on protocol analysis of six
weekly assessments, including (p = .02) and excluding (p = .05) those on
antiparkinsonian medication. Active eradication (blind or open) failed in 4/20,
in whom B-lymphocyte count was lower. Their mean time course was: for
stride-length, -243 (95% CI -427, -60) vs. 45 (-10, 100) mm/year in the remainder
(p = .001); for the ratio, torque to extend to flex relaxed arm, 349 (146, 718)
vs. 58 (27, 96)%/ year (p < .001); and for independently rated, visual-analog
scale of stance-walk videos (worst-best per individual identical with 0-100 mm),
-64 vs. -3 mm from anterior and -50 vs. 11 lateral (p = .004 and .02).
CONCLUSIONS: Interim analysis points to a direct or surrogate (not necessarily
unique) role of a particular infection in the pathogenesis of parkinsonism. With
eradication failure, bolus release of antigen from killed bacteria could
aggravate an effect of ongoing infection.



PMID: 16104943 [PubMed - indexed for MEDLINE]




By the way, that first bold part is "Scientese" for "We scared ourselves silly and backed off real quick because we were afraid someone was going to get hurt."