Sunday, June 16, 2019
Mounting Evidence That Parkinson's Starts in The Gut - Not The Brain
There's Mounting Evidence That Parkinson's Starts in The Gut - Not The Brain
(c)DAVID NIELD
17 MAR 2019
Scientists have found mounting evidence that Parkinson's could start in the gut before spreading to the brain, with one study in 2017 observing lower rates of the disease in patients who had undergone a procedure called a truncal vagotomy.
The operation removes sections of the vagus nerve - which links the digestive tract with the brain - and over the course of a five-year study, patients who had this link completely removed were 40 percent less likely to develop Parkinson's than those who hadn't.
According to the team led by Bojing Liu from the Karolinska Instituet in Sweden, that's a significant difference, and it backs up earlier work linking the development of the brain disease to something happening inside our bellies.
If we can understand more about how this link operates, we might be better able to stop it.
"These results provide preliminary evidence that Parkinson's disease may start in the gut," said Liu.
"Other evidence for this hypothesis is that people with Parkinson's disease often have gastrointestinal problems such as constipation, that can start decades before they develop the disease."
The vagus nerve helps control various unconscious processes like heart rate and digestion, and resecting parts of it in a vagotomy is usually done to remove an ulcer if the stomach is producing a dangerous level of acid.
For this study, the researchers looked at 40 years of data from Swedish national registers, to compare 9,430 people who had a vagotomy against 377,200 people from the general population who hadn't.
The likelihood of people in these two groups to develop Parkinson's was statistically similar at first - until the researchers looked at the type of vagotomy that had been carried out on the smaller group.
In total, 19 people (just 0.78 percent of the sample) developed Parkinson's more than five years after a truncal (complete) vagotomy, compared to 60 people (1.08 percent) who had a selective vagotomy.
Compare that to the 3,932 (1.15 percent) of people who had no surgery and developed Parkinson's after being monitored for at least five years, and it seems clear that the vagus nerve is playing some kind of role here.
So what's going on here? One hypothesis the scientists put forward is that gut proteins start folding in the wrong way, and that genetic 'mistake' gets carried up to the brain somehow, with the mistake being spread from cell to cell.
Parkinson's develops as neurons in the brain get killed off, leading to tremors, stiffness, and difficulty with movement - but scientists aren't sure how it's caused in the first place. The new study gives them a helpful tip about where to look.
The Swedish research isn't alone in its conclusions. In 2016, tests on mice showed links between certain mixes of gut bacteria and a greater likelihood of developing Parkinson's.
What's more, earlier in 2017 a study in the US identified differences between the gut bacteria of those with Parkinson's compared with those who didn't have the condition.
All of this is useful for scientists looking to prevent Parkinson's, because if we know where it starts, we can block off the source.
But we shouldn't get ahead of ourselves - as the researchers behind the new study point out, Parkinson's is complex condition, and they weren't able to include controls for all potential factors, including caffeine intake and smoking.
It's also worth noting that Parkinson's is classed as a syndrome: a collection of different but related symptoms that may have multiple causes.
"Much more research is needed to test this theory and to help us understand the role this may play in the development of Parkinson's," said Lui.
The research was published in Neurology.
A version of this story was first published in April 2017.
Monday, June 3, 2019
Cranberry Compounds Help Prevent Antibiotic Resistance - The People's Pharmacy
Sunday, June 2, 2019
What is the future outlook for Lyme disease and tick-borne illnesses?
|
|
|
Thursday, May 30, 2019
More studies on the effectiveness of various Lyme disease prevention measures
Vázquez M, Muehlenbein C, Cartter M, Hayes EB, Ertel S, Shapiro ED
Emerging Infect Dis 2008 Feb; 2(14):210-6
Full Study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600214/
How can we prevent Lyme disease?
Hayes EB, Piesman J
N Engl J Med 2003 Jun 12; 24(348):2424-30
Emergence of Lyme disease in Hunterdon County, New Jersey, 1993: a case-control study of risk factors and evaluation of reporting patterns.
Orloski KA, Campbell GL, Genese CA, Beckley JW, Schriefer ME, Spitalny KC, Dennis DT
Am J Epidemiol 1998 Feb 15; 4(147):391-7
Full study here: https://pdfs.semanticscholar.org/300a/afcdabfd19e4a8cc17bba7ccf0b8b1177c16.pdf
Case-control study of risk factors for incident Lyme disease in California.
Ley C, Olshen EM, Reingold AL
Am J Epidemiol 1995 Nov 1; 9 Suppl(142):S39-47
Abstract only: https://academic.oup.com/aje/article-abstract/142/Supplement_9/S39/109581?redirectedFrom=PDF
Lyme Disease Prevention Results of a Population-Based Case–Control Study
Peridomestic Lyme Disease Prevention
Results of a Population-Based Case–Control Study
Neeta P. Connally, PhD, Amanda J. Durante, PhD, Kimberly M. Yousey-Hindes, MPH, James I. Meek, MPH, Randall S. Nelson, DVM, Robert Heimer, PhD
Background: Purpose:
Methods:
Results:
Conclusions:
Peridomestic Lyme disease–prevention initiatives promote personal protection, landscape modification, and chemical control.
A 32-month prospective age- and neighborhood-matched case–control study was con- ducted in Connecticut to evaluate the effects of peridomestic prevention measures on risk of Lyme disease.
The study was conducted in 24 disease-endemic Connecticut communities from 2005 to 2007. Subjects were interviewed by telephone using a questionnaire designed to elicit disease-prevention measures during the month prior to the case onset of erythema migrans. Data were analyzed in 2008 by conditional logistic regression. Potential confound- ers, such as occupational/recreational exposures, were examined.
Between April 2005 and November 2007, interviews were conducted with 364 participants with Lyme disease, and 349 (96%) were matched with a suitable control. Checking for ticks within 36 hours of spending time in the yard at home was protective against Lyme disease (OR0.55; 95% CI0.32, 0.94). Bathing within 2 hours after spending time in the yard was also protective (OR0.42; 95% CI0.23, 0.78). Fencing of any type or height in the yard, whether it was contiguous or not, was protective (OR0.54; 95% CI0.33, 0.90). No other landscape modifications or features were significantly protective against Lyme disease.
The results of this study suggest that practical activities such as checking for ticks and bathing after spending time in the yard may reduce the risk of Lyme disease in regions where peridomestic risk is high. Fencing did appear to protect against infection, but the mechanism of its protection is unclear.
(Am J Prev Med 2009;37(3):201–206) © 2009 American Journal of Preventive Medicine)
Thursday, May 16, 2019
Thursday, April 25, 2019
Three-antibiotic cocktail clears 'persister' Lyme bacteria in mouse study
https://medicalxpress.com/news/2019-04-three-antibiotic-cocktail-persister-lyme-bacteria.html
Wednesday, April 24, 2019
Mepron - Helps knock-off Babesia. But how much to prescribe?
"For mepron to work you have to push the dose- 5cc tid for 5 months minimum and must be taken with a huge amount of fat- in absorption studies, the test subjects had 23g of fat with each dose! I had ordered blood level measurements after the third week, goal being 20+, but this test may no longer be available.I use artemesinin SOD from Researched Nutritionals, but as with all artemesia products there must be a regular break in treatment- typically 3 weeks on and one off.Cryptolepis, green tea egcg and sida are commonly added.Specialty OTCs from Byron White and Susan McCamish help some but not others, and some have a hard time tolerating a full dose.I also like to add transfer factors."
Tuesday, April 23, 2019
Tiny, larval ticks can pack a wallop
Wed Mar 27, 2019 6:43 am (PDT) . Posted by:
"Rick Laferriere" ri_lymeinfo
/Lyme Science Blog/, by Daniel Cameron, MD, MPH, Mt. Kisco, New York
Dr. Cameron is a nationally recognized leader for his expertise in the
diagnosis and treatment of Lyme disease and other tick-borne illnesses.
March 25, 2019
http://danielcameronmd.com/study-finds-tiny-larval-ticks-can-transmit-borrelia-miyamotoi/
Nymphal and adult black-legged ticks, also known as deer ticks, harbor a
growing number of pathogens.
But researchers are now discovering that larval ticks, which are even
smaller, may pose an equal threat to public safety as a new study
describes larval ticks infected with the tick-borne bacteria /Borrelia
miyamotoi/.
*Read the Complete Blog Entry*:
http://danielcameronmd.com/study-finds-tiny-larval-ticks-can-transmit-borrelia-miyamotoi/
*Read more of Lyme Science Blog at*:
http://danielcameronmd.com/all-things-lyme-blog-archives/
<http://danielcameronmd.com/all-things-lyme-blog-archives/>
*Contact**Dr. Daniel Cameron*:
http://danielcameronmd.com/ <http://danielcameronmd.com/>
----------------------------------------------------------
Related reading:
*Vertical transmission rates of /Borrelia miyamotoi/ in /Ixodes
scapularis/ collected from white-tailed deer *
Han S, Lubelczyk C, Hickling GJ, Belperron AA, Bockenstedt LK, Tsao JI.
/Ticks and Tick-borne Diseases/. 2019 Feb 26. pii: S1877-959X(18)30088-8.
https://doi.org/10.1016/j.ttbdis.2019.02.014
Abstract
/Borrelia miyamotoi/is a relapsing feverspirochetetransmitted by ticks
in the /Ixodes ricinus/ complex. In the eastern United States, /B.
miyamotoi/ is transmitted by /I. scapularis,/ which also vectors several
other pathogens including /B. burgdorferi/sensu stricto.
In contrast to Lyme borreliae, /B. miyamotoi/can be transmitted
vertically from infected female ticks to their progeny. Therefore, in
addition to nymphs and adults, larvae can vector /B. miyamotoi/to
wildlife and human hosts. Two widely varying filial infection prevalence
(FIP) estimates - 6% and 73% - have been reported previously from two
vertically infected larval clutches; to our knowledge, no other
estimates of FIP or transovarial transmission (TOT) rates for /B.
miyamotoi/have been described in the literature. Thus, we investigated
TOT and FIP of larval clutches derived from engorged females collected
from hunter-harvested white-tailed deer in 2015 (n = 664) and 2016
(n = 599) from Maine, New Hampshire, Tennessee, and Wisconsin.
After engorged females oviposited in the lab, they (n = 492) were tested
for /B. miyamotoi/infection by PCR. Subsequently, from each clutch
produced by an infected female, larval pools, as well as 100 individual
eggs or larvae, were tested. The TOT rate of the 11 infected females was
90.9% (95% CI; 57.1–99.5%) and the mean FIP of the resulting larval
clutches was 84.4% (95% CI; 68.1–100%).
Even though the overall observed vertical transmissionrate (the product
of TOT and FIP; 76.7%, 95% CI; 44.6–93.3%) was high, additional
horizontal transmission may be required for enzootic maintenance of /B.
miyamotoi/ based on the results of a previously published deterministic
model. Further investigation of TOT and FIP variability and the
underlying mechanisms, both in nature and the laboratory, will be needed
to resolve this question. Meanwhile, studies quantifying the
acarological risk of /Borrelia miyamotoi/ disease need to consider not
only nymphs and adults, but larval /I. scapularis/ as well.
https://doi.org/10.1016/j.ttbdis.2019.02.014









