Griffith University research indicates that patients suffering from allergic rhinitis, otherwise known as hay fever, can specifically benefit from probiotic supplements.
In a study funded by Winclove Probiotics, Griffith’s research team at the Menzies Health Institute QLD found eight weeks of supplementation with a specific multi-species probiotic reduced symptoms of allergic rhinitis and medication use.
This study published in the Journal Genes, found most allergy patients (64%) responded with a clinical improvement in their QoL score, otherwise known as the quality of life scale.
Whilst noting that not all people with allergies respond similarly, Dr. Pete Smith of Queensland Allergy Services and a member of the study team said, “our study may allow us to personalize probiotic treatment for individuals with seasonal allergic rhinitis.”
Dr. Nic West of Griffith University adds that the evidence basefor the role of probiotics in allergy continues to increase.
“The results from our study will allow us to conduct targeted research to find strategies people can use during the pollen season,” said Dr. West.
Hay fever is a chronic disorder that has a serious impact on quality of life for up to 30% of the general population. Current treatment options are costly and do not tackle the underlying cause of the disorder.
With the aim of helping sufferers the research team examined the differences in the immune system between responders and non-responders and are currently undertaking a clinical trial of the probiotic supplement that involves further immune profiling of individuals with hay fever.
https://madisonarealymesupportgroup.com/2018/01/03/the-invisible-universe-of-the-human-microbiome-msm/Recitas, author of “The Plan,” calls MSM the wonder supplement for your gut. It can alleviate allergy symptoms, helps with detoxification, eliminates free radicals, and improves cell permeability. She states that with given time, MSM will start to actually repair damage caused by leaky gut – a common problem with Lyme/MSIDS patients. It can also help the body’s ability to absorb nutrients from food. Many Lyme patients struggle with paralysis of the gut where the muscles of the stomach and intestines stop being efficient. MSM helps this muscle tone as well.
Jenna clearly outlines the multi-layered complexities of the blocks causing difficulty in progressing best practise diagnosis and medical care with Lyme globally. Note: Jenna would also like to add that a Disulfiram protocol has been one of the very hopeful developments for both her and her husband. Jenna really benefited from this generic drug and her husband who was about to go on disability, is now in normal to high function including hiking and kayaking. There is hope for new treatments like this and more.
**Correction**: ‘a number of monkeys died from Ebola in the lab in my (then) home town of Reston VA; but no humans died’
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**Comment**
Jenna is truly a force to be reckoned with and the Lyme community is blessed to have her expertise in government corruption. In this video she explains the complicated saga behind why Lyme patients are not getting coverage for treatment. In brief it has to do with codes doctors use so patients obtain insurance coverage. Without these codes, patients will not get coverage.
I’m so thankful she and her husband are doing so well on Disulfiram. I would like to point out another side; however, so you as patient weigh the risk vs the benefit:
Most of us involved in this scandal are familiar with the faulty/misleading testing algorithm for Lyme disease as it is the root cause of unimaginable pain and suffering. Delayed diagnosis and treatment leads to serious health consequences.
Feel free to share the letter below and attachments to the uneducated public who are in denial that this couldn’t possible happen to them.
——— Original Message ———-
From: CARL TUTTLE <runagain@comcast.net>
To: tickbornedisease@hhs.gov
Cc: (82 Undisclosed recipients)
Date: January 11, 2020 at 11:54 AM
Subject: NH House Bill 490 and Serology for Lyme Disease
To: The Tick-Borne Disease Working Group,
Please see the letter below addressed to the New Hampshire Medical Society regarding House Bill 490.
In order to cut down on email size I have provided Dropbox storage links for the attachments listed in this message.
Carl Tuttle
Lyme Endemic Hudson, NH
Letter to the New Hampshire Medical Society:
———- Original Message ———-
From: CARL TUTTLE <runagain@comcast.net>
To: james.potter@nhms.org
Cc: (28 Undisclosed recipients)
Date: January 10, 2020 at 11:19 AM
Subject: NH House Bill 490 and Serology for Lyme Disease
Jan 10, 2019
New Hampshire Medical Society
7 North State Street
Concord, NH 03301-4018
ATTN: James G. Potter, CAE, Executive Vice President
Dear Mr. Potter,
I have reviewed the amended version of HB490 calling for a commission to study the role of clinical diagnosis and the limitations of serological diagnostic tests and I have to tell you that all Tuttle family members did not meet the CDC’s criteria for positive test results on the only FDA approved testing algorithm for Lyme disease (2 out of 3 IgM bands and 5 out of 10 IgGbands) and yet all of us were horribly ill.
It is not necessary to meet these strict criteria as it was originally developed for surveillance/reporting purposes only but there is no disclaimer on the test to inform the physician that a negative test result does not necessarily mean that the patient does not have Lyme disease.
The confusion over this has caused untold pain and suffering as delayed diagnosis will lead to dire health consequences. The uneducated PCP will see “Negative” on the lab report and inform the patient that he or she does not have Lyme disease.
Had we not met Dr. Sam Donta of BU School of Medicine (Currently a member of the Tick-Borne Disease Working group) who spent a career studying Lyme disease, none of us would have been treated.
This is a serious problem!
For your review, I have attached a copy of my 2009 letter addressed to Salim E. Kabawat, M.D. Medical Director of Quest Diagnostics outlining the problems with current serology. Nothing has changed.
In addition, I am attaching a copy of my wife’s Western blot showing only one single positive test band and no disclaimer.
I mean no disrespect Mr. Potter but what we have here in New Hampshire (and across the country) is a plague of ignorance and House Bill 490 is looking to address this.
Included with this correspondence is a copy of a 2009 tick study here in New Hampshire conducted by UMass Amherst and you will see in the town of Litchfield, 77% of the ticks tested are carrying tick borne disease. You or a loved one is a single tick bite away from experiencing this travesty.
Respectfully submitted,
Carl Tuttle
Lyme Endemic Hudson, NH
Attachments:
1. 2009 letter addressed to Salim E. Kabawat, M.D. Medical Director of Quest Diagnostics
Summary: Gentamicin and G418, two aminoglycoside antibiotics, were effective at correcting genetic mutations associated with a specific form of frontotemporal dementia. The findings are promising for the treatment of frontotemporal dementia.Source: University of Kentucky
Researchers at the University of Kentucky’s College of Medicine have found that a class of antibiotics called aminoglycosides could be a promising treatment for frontotemporal dementia.
Results of their proof of concept study, which was a collaborative effort between UK’s Department of Molecular and Cellular Biochemistry and the University of California San Francisco’s Department of Pathology, were recently published in the journal, Human Molecular Genetics.
Frontotemporal dementia is the most common type of early onset dementia. It typically begins between ages 40 and 65 and affects the frontal and temporal lobes of the brain, which leads to behavior changes, difficulty speaking and writing, and memory deterioration.
A subgroup of patients with frontotemporal dementia have a specific genetic mutation that prevents brain cells from making a protein called progranulin. Although progranulin is not widely understood, its absence is linked to the disease.
A group led by Haining Zhu, a professor in UK’s Department of Molecular and Cellular Biochemistry, discovered that after aminoglycoside antibiotics were added to neuronal cells with this mutation, the cells started making the full-length progranulin protein by skipping the mutation.
“These patients’ brain cells have a mutation that prevents progranulin from being made. The team found that by adding a small antibiotic molecule to the cells, they could ‘trick’ the cellular machinery into making it,” said Matthew Gentry, a co-author of the study and the Antonio S. Turco Endowed Professor in the Department of Molecular and Cellular Biochemistry.
The researchers found two specific aminoglycoside antibiotics – Gentamicin and G418 – were both effective in fixing the mutation and making the functional progranulin protein. After adding Gentamicin or G418 molecules to the affected cells, the progranulin protein level was recovered up to about 50 to 60%.
These results could be promising to drug development. Currently, there are no effective therapies for any type of dementia.
After this preclinical proof of concept study, the next step is to study the antibiotics’ effects on mice with the mutation that causes frontotemporal dementia, Zhu says. Another focus is to possibly develop new compounds from Gentamicin and G418 that could be safer and more effective. Although Gentamicin is an FDA-approved medication, its clinical usage is limited as it is associated with a number of adverse side effects.
“If we can get the right resources and physician to work with, we could potentially repurpose this drug. This is an early stage of the study, but it provides an important proof of concept that these aminoglycoside antibiotics or their derivatives can be a therapeutic avenue for frontotemporal dementia,” said Zhu.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: University of Kentucky Media Contacts:
Elizabeth Chapin – University of Kentucky Image Source:
The image is in the public domain.
Frontotemporal dementia nonsense mutation of progranulin rescued by aminoglycosides
Frontotemporal dementia (FTD) is an early onset dementia and is characterized by progressive atrophy of the frontal and/or temporal lobes. FTD is highly heritable with mutations in progranulin accounting for 5-26% of cases in different populations. Progranulin is involved in endocytosis, secretion and lysosomal processes, but its function under physiological and pathological conditions remains to be defined. Many FTD-causing nonsense progranulin mutations contain a premature termination codon (PTC), thus progranulin haploinsufficiency has been proposed as a major disease mechanism. Currently, there is no effective FTD treatment or therapy.
What causes Alzheimer’s? Not toxic amyloid, new study suggests
Many researchers have argued that the accumulation of toxic beta-amyloid in the brain causes Alzheimer’s. However, a new study offers some evidence contradicting this sequence.
New research is questioning the predominant hypothesis that a buildup of beta-amyloid causes Alzheimer’s disease.
Yet, researchers are still at a loss as to why this condition — which is characterized by memory impairment and many other cognitive problems — occurs in the first place. And until they fully understand the cause, investigators will remain unable to devise a cure.
So far, the prevailing hypothesis among experts has been that the excessive accumulation of a potentially toxic protein — beta-amyloid — in the brain causes Alzheimer’s.
Researchers have argued that beta-amyloid plaques disrupt the communication between brain cells, potentially leading to cognitive function problems.
Now, a new study from the University of California San Diego School of Medicine and the Veterans Affairs San Diego Healthcare System suggests that while the buildup of beta-amyloid has associations with Alzheimer’s, it may not actually cause the condition.
In a study paper that appears in the journal Neurology, the researchers explain what led them to reach this conclusion.
“The scientific community has long thought that amyloid drives the neurodegeneration and cognitive impairment associated with Alzheimer’s disease,” says senior author Prof. Mark Bondi.
He notes that “[t]hese findings, in addition to other work in our lab, suggest that this is likely not the case for everyone and that sensitive neuropsychological measurement strategies capture subtle cognitive changes much earlier in the disease process than previously thought possible.”
What comes first?
In their study, the researchers worked with a total of 747 participants with different levels of cognitive health. All of the study participants agreed to undergo neuropsychological assessments, as well as PET and MRI brain scans.
Of the participants, 305 were cognitively healthy, 289 had mild cognitive impairment, and 153 displayed markers of what the investigators call “objectively-defined subtle cognitive difficulties (Obj-SCD).”
Experts define mild cognitive impairment as a state of cognitive impairment that is more severe than what one would normally experience with age, but not yet severe enough for a dementiadiagnosis.
But what are Obj-SCD? In their paper, the investigators define them as “difficulties or inefficiencies on some sensitive cognitive tasks even though the overall neuropsychological profile is in the normal range.”
That is, they are a measurement of experienced, subtle cognitive functioning problems that occur in the absence of any visible signs of brain or psychological issues. To find out whether someone is experiencing Obj-SCD, researchers assess, among other factors, how efficiently that person can learn and retain new information.
Previous research has suggested that individuals with Obj-SCD are at a higher risk of mild cognitive impairment and forms of dementia.
In the current study, Prof. Bondi and the team found that beta-amyloid built up at a faster rate in the participants with Obj-SCD compared with those who were deemed cognitively healthy. Moreover, brain scans of people with Obj-SCD showed that these individuals experienced a thinning of brain matter in a region called the entorhinal cortex.
Past research has shown that the entorhinal cortex decreases in volume in people with Alzheimer’s disease. This is significant because this brain region plays a role in memory and spatial orientation.
The researchers also found that while people with mild cognitive impairment had higher quantities of beta-amyloid in their brains at the beginning of the study, this protein did not seem to build up any faster in these participants than it did in cognitively healthy individuals.
But why do the current findings potentially contradict a decades-old hypothesis about the development of Alzheimer’s? Prof. Bondi explains:
“This work […] suggests that cognitive changes may be occurring before significant levels of amyloid have accumulated. It seems like we may need to focus on treatment targets of pathologies other than amyloid, such as tau, that are more highly associated with the thinking and memory difficulties that impact people’s lives.”
“While the emergence of biomarkers of Alzheimer’s disease has revolutionized research and our understanding of how the disease progresses, many of these biomarkers continue to be highly expensive, inaccessible for clinical use, or not available to those with certain medical conditions,” adds first author Kelsey Thomas, Ph.D.
The new study’s findings could help change that by refocusing the research approach on more subtle markers of Alzheimer’s, such as those assessing for Obj-SCD.
“A method of identifying individuals at risk for progression to [Alzheimer’s disease] using neuropsychological measures has the potential to improve early detection in those who may otherwise not be eligible for more expensive or invasive screening,” says Thomas.
NEUROSCIENCE NEWS
