I have given this link to my daughter, as she was just stating today that she thinks she may have ME also. It may just be the Autism. We have noted several times that both she and I share certain “traits” in our illnesses. This may explain why.
I follow “Onward Through the Fog,” a blog on blogspot, authored by Erica Verrillo, a talented person who suffers from ME (Myalgic Encephalomyelitis). Her reports and research are top notch.
In this particular posting, Erica reports on the similarity of some findings affecting Autism and ME/CFS. These findings have to do with brain inflammation.
A John Hopkins study acts as confirmation that excitotoxicity caused by chronic inflammation is central to autism.
A great question asked by Sunshinebright – #ME Where are we? A question I would like a great answer to.
Alas, I am doomed to be disappointed. As Sunshine pointed out, 2015 started out with a lot of optimism. M.E. was officially declared a real, physical disease by the IOM. This was a big win, as an estimated two million sufferers in the U.S alone, including myself, have been treated horribly by the medical establishment. M.E. had never been taught in medical school and doctors typically would “poo-poo” the symptoms effecting M.E. patients. We have been labeled as hypochondriacs and being mentally ill. The outcome of the IOM’s report would surely change things for the better – this was the hope. More research dollars to find a biomarker and, hopefully, a treatment that works (if not a cure.)
The truth: Doctors still have no clue what M.E. is. Money for research is still not coming from the NIH. Just this month, Dr. Ian Lipkin , a researcher, resorted to eating hot peppers in a challenge to raise funds. Very sad.
During the first half of this year, there was much going on in the Health and Human Service (HHS) Department and regarding ME (Myalgic Encephalomyelitis): we had the IOM’s (Institute of Medicine) outstanding, positive report (in my opinion) and then there was the P2P (Pathways to Progress) report. The former was indicative of forward movement in the cause of ME and the latter, was not.
We’ve been ignored.
There were stand-offs, delays, and hidden refusals when the FOIA was used to obtain documents vital to the ME cause.
And where are we? After all the hullabaloo and interviews of patients including Laura Hillenbrand, author of “Seabiscuit,” Jen Brea, co-developer of a movie, “Canary in a Coal Mine,” I ask again:
Where are we?
It looked like we had some strong headway for a while, in getting ME recognized as a VERY SERIOUS disease (which it is of course), and…
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As someone with ME, and as someone with a daughter on the Autism Spectrum, this discovery is one of the most important medical events in recent history. Times are changing and researchers are finally picking up the pace studying neuro-immune issues. As my ME progresses, the hope for better understanding of the disease and better treatments may see fruition. Many with ME, MS, and Autism, to mention some of the many misunderstood neuro-immune diseases suffered by millions, might see a flicker at the end of the tunnel.
“They’ll have to change the textbooks.” This statement, by Kevin Lee, PhD, Chairman of the UVA Department of Neuroscience, is the result of a study at the University of Virginia School of Medicine. The study, awarded to the UVA Health System and funded by the National Institutes of Health (NIH), has shown there are heretofore undetected lymphatic vessels connecting the brain to the immune system.
Researchers knew there was a connection between the brain and immune system, but the vessels were completely hidden. Now, there are many new angles to exploring neurological disease.
This is a stunning discovery. It is difficult to explain how these vessels in the brain were overlooked when the lymphatic system was explored. New avenues of discovery are now possible and beneficiaries might be MS, Autism, Alzheimer’s and maybe even…
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The next time someone at your office lets out a “silent but deadly” emission, maybe you should thank them. A new study at the University of Exeter suggests that smelling farts could prevent disease and even cancer.
The study, published in the Medicinal Chemistry Communicationsjournal, found that flatulence could be a key factor in treating diseases.
“Although hydrogen sulfide gas is well known as a pungent, foul-smelling gas in rotten eggs and flatulence, it is naturally produced in the body and could in fact be a healthcare hero with significant implications for future therapies for a variety of diseases,” Dr. Mark Wood, a professor at the University of Exeter, said in a statement.
While hydrogen sulfide gas is harmful in large doses, smelling it in small amounts could reduce the risk of cancer, strokes, heart attacks, arthritis, and dementia by preserving the body’s mitochondria. Dr. Matt Whiteman, a University of Exeter professor who worked on the study, said in a statement that researchers are even replicating the natural gas to reap its health benefits.
Thoughts on the Mental Health and ME misconception.
One of the most common misconceptions regarding ME is the idea that it is psychosomatic. This assumption stems in part from the fact that there is as yet no universally reliable diagnostic test, so it is often diagnosed on the basis of self-reported symptoms following the exclusion of other possible explanations. The problem is compounded by a large and very vocal group of psychiatrists who dismiss biomedical evidence of a physical cause of ME in favour of bio-psychosocial theories, claiming that ME is a form of personality disorder characterised by depression, exercise phobia and false illness beliefs.
Despite official recognition that ME is a neurological disease, the treatments sanctioned on the NHS (anti-depressants, graded exercise and behavioural therapies) have a primarily psychiatric focus, thereby reinforcing the perception that ME symptoms must be ‘all in the mind’. What little money the government spends on research into ME (far less than for…
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There are good reasons for thinking that central nervous system pathology is important in ME/CFS, and some indications that inflammation of the brain (neuroinflammation) might be involved. However, proving the existence of neuroinflammation requires specific neuroimaging methods, and these had never been applied to ME/CFS patients – until Japanese researchers bit the bullet.
The team at Osaka City University in Japan, which has been studying ME/CFS for many years, have used PET imaging to try to obtain direct evidence of neuroinflammation. In essence, they measured the density of the ‘translocator protein’ (TSPO) produced when certain brain cells are activated – it’s the activation of these cells which indicates that inflammation is taking place. In this case, the brain cells were microglia (thought to be the main form of active immune defense in the central nervous system) and astrocytes (the most numerous brain cells, with functions including nutrient supply, repair, and nerve impulse transmission). The researchers recruited 9 people with ME/CFS (Fukuda 1994 and ME-ICC 2011 definitions) and 10 healthy controls, who underwent PET scanning involving the injection of a tracer followed by dynamic scanning over 60 min. Participants also completed questionnaires about symptoms, including fatigue, pain, and neurocognitive problems.
Their report in the Journal of Nuclear Medicine reveals that protein levels (indicating inflammation) were higher in ME/CFS patients than controls in “widespread brain regions”, including the cingulate cortex (199% higher), hippocampus (81%), thalamus (66%), midbrain (47%), and pons (45%). And, intriguingly, protein levels in some brain regions were significantly associated with the severity of particular symptoms; some of these associations were quite striking (despite the small number of patients), as in the correlation between protein level and cognitive impairment scores (r=0.94, p<0.0002).
The authors conclude that “neuroinflammation is present in widespread brain areas” in ME/CFS patients compared with healthy people. As they point out, this may be due to an immune response to an underlying infectious process, or possibly to over-activation of nerve cells (for whatever reason). There are two things to bear in mind, however. First, numbers are small (in essence, this is pilot data), and would need replication – one swallow doesn’t make a summer, and one scientific report does not convince, though it might fascinate. Second, protein levels were relatively low in absolute terms, raising intricate methodological issues associated with standardization in PET imaging. The authors are to explore this particular aspect in the next phase of their work on ME/CFS patients, an international collaboration study that will use a different, second-generation tracer and have a refined methodology.
If these dramatic and fascinating results can be reproduced, objective evidence of an inflammatory process in the brain of people with ME/CFS will become readily available for diagnostic and treatment-monitoring purposes, with enormous consequences for patients and their families.