This is such cheery stuff…sigh. Spend a little time away from a thread, and there’s SOOO much to catch up on
Joanne, I remember discussing the likelihood of non-IgE-mediated allergic reactions around 30 years ago with an immunologist friend. IIRC, her take was that the orthodoxy was that there was no such animal, but that what they really knew about immunology at that point would fill a thimble with plenty of room for a stiff drink.
Edited to add: Somehow, the last two-thirds of my comments has disappeared!DAMMITTOHELL !!!
Edited again: , I just added a post script to this and it never made it when I hit “Submit”.
We are starting to see data showing the effects of COVID-19 infections on overall cognitive function going forward after surviving it. This study focused on people aged 66-74 years old. However, the 3 factors cited below have been shown to happen regardless of the patient's age. The first factor listed below, cardiovascular harm, has shown up in even the milder cases causing several heart conditions in younger patients. I've culled out those items from the discussion section of the paper and posted them below. Oxygen deprivation, inflammation, and blood vessel clots/tears all contribute to what may become an epidemic of dementia countries are not equipped to handle withing the net decade.
The mechanisms of the long-term effects of COVID-19 on cognition are multifaceted. First, neurovascular elements might be involved in the development of postinfection cognitive decline in COVID-19 survivors,30,31 as reinforced by our findings that vascular risk factors, such as stroke, coronary heart disease, and hypertension, were associated with longitudinal cognitive decline.
Second, long-lasting hypoxia may also contribute substantially to postinfection cognitive decline, as neurons are sensitive to hypoxic injury, and individuals with severe cases may be under a more severe hypoxic status after infection than those with nonsevere cases.32,33 This hypothesis is supported by our finding that COPD was associated with an increase in risk of longitudinal cognitive decline.
Third, inflammatory factors have been shown to not return to normal status months after recovery, especially in individuals with severe COVID-19.34 Chronic systemic inflammation after SARS-CoV-2 infection exacerbates neurodegeneration, thus potentially leading to long-term cognitive deficits.35
It is also possible that the virus can directly invade the brain and damage neurons.40
Wear a mask. Please make every effort to avoid contracting COVID.
Since cognitive function is now a major focus of mine I also wanted to highlight the limitations the authors spoke of. They don't negate the findings but do give reasons for both muting the response to them as well as acknowledging that these data could be underestimating COVID's impact.
This study has some limitations.
First, owing to the emerging infection risk, telephone questionnaires were used to follow up on the cognitive functions of participants. This method of follow-up may not be as accurate as face-to-face interviews, although telephone-based questionnaires have been validated.9,15,17
Second, the lack of cognitive information before SARS-CoV-2 infection is an inherent limitation of this study that may lead to an overestimation of the impact of COVID-19 on postinfection cognitive decline. As cognitive decline might be affected by both preexisting cognitive impairment and COVID-19, we excluded participants with known preexisting cognitive impairment and a family history of dementia. However, this reduced the generalizability of the findings.
My comment on this [[[Unlike yearly physicals, people don't tend to undergo neuropsychiatric evaluation until *after* some event gives cause for concern.]]]
Furthermore, this study lacks information about biomarkers of neuronal injury; thus, the etiology of cognitive decline could not be determined. [[[The exact cause of each individual's cognitive decline is unknown. It also means that they don't know if some people did not suffer a decline in spite of one or more indicators of a present injury.]]]
In addition, the mismatch of sample sizes between survivors and control individuals and the relatively high rate of loss-to-follow-up weakened the power of the findings. [[[If people drop out of the study for whatever reason, their data cannot be included.]]]
^^^ Re your comment that people tend not to test test for cognitive injury/function and retest for signs of decline, I’m actually wondering how much this will change over the next few years. There’s been so much emphasis on the (literal) impacts of head knocks and even very mild concussions from school sports, through to various varsity sports, road incidents etc and now we’re seeing all kinds of incidents in workplaces, or via illnesses previously thought ‘harmless to the brain’ - it’s relatively easy to get a general functional baseline and then a few years later compare to that as necessary.
Plus, the things we’re learning in brain health anyway. I reckon pretty soon some of these caveats won’t be needed. (Am sitting on a brain injury consumers group for a research & recovery lab. Wow)
I've been saying this to whoever will listen.
Covid-19: Even mild infection can cause 'significant' changes to brain
Avoid Covid-19 if you can. Your brain may thank you.
https://www.medscape.com/viewarticle/969901?src=soc_tw_220310_mscpedt_news_mdscp_longcovid&faf=1Combined blood biomarker evidence of neuronal damage activation of glial cells, indicating brain inflammation, correlated with symptoms of anxiety in long COVID patients.
This study shows that "some patients with long COVID have evidence of brain damage or brain inflammation, which gives validity to the symptoms that these patients present with," Igor Koralnik, MD, head of the Neuro COVID-19 Clinic at Northwestern Memorial Hospital, Chicago, Illinois, said during a media briefing.
This is the full text journal article.
Barbara A. Hanson, View ORCID ProfileLavanya Visvabharathy, Sareen T. Ali, Anthony K. Kang, Tulsi R. Patel, Jeffrey R. Clark, Patrick H. Lim, View ORCID ProfileZachary S. Orban, Soyoon S. Hwang, Dawn Mattoon, View ORCID ProfileAyush Batra, View ORCID ProfileEric M. Liotta, View ORCID ProfileIgor J. Koralnik
This article is more of a long discussion.
Alzheimer’s, Parkinson’s, and traumatic brain injury can cause changes in behavior by altering brain anatomy. Now it seems the coronavirus can too.https://www.nationalgeographic.com/science/article/can-covid-19-alter-your-personality-heres-what-brain-research-shows
This NPR story was very interesting. It points to the immune system's possible role in that group of mental illnesses. Lot's of new things to learn there.
A higher risk of developing diabetes has now been shown a statistically significant consequence of COVID infections./fulltext" rel="nofollow" target="_blank">https://www.thelancet.com/journals/landia/article/PIIS2213-8587(22)0007/fulltext
this thing is a true bastard
drummerboy said:this thing is a true bastard
Yes. Now that there have been several months for longitudinal studies to come out we're seeing some odd and nasty things going on. Long COVID also causes vascular problems that can have unpredictable effects all over the body. Anti-MAS-1 antibodies are part of an autoimmune response that messes up endothelial cells' ability to produce and release nitric oxide. That compound (NO) plays a key role in relaxing arteries and increasing blood flow wherever those arteries lead. MAS-1 is involved in the same signaling process the Angiotensin Converting Enzyme II (ACE2) is active in. The COVID spike protein binds ACE2 as part of its infectious cycle and now it seems that some people wind up with antibodies that attack a "bystander" by mistake.Angiotensin II constricts blood vessels and MAS-1 binds it, reversing that effect. So, if a person's MAS-1 receptors are bound up by autoantibodies against it, blood flow can be reduced to a region of tissue. So, reduced NO release means less blood vessel dilation and more Angiotensin II means more vasoconstriction - those two things combined can make that tissue O2-deprived, CO2-saturated and accumulate metabolic byproducts that normally get flushed away. The brain and the heart are the two absolutely critical parts of the body that cannot tolerate that for very long. In the brain it will cause a general fatigued feeling and cognitive slowing - fogginess.If you're wondering about whether this long COVID **** could be happening with you, go out and buy some beet juice. That juice is very high in NO and see if it has any noticeable effect within a couple of hours of drinking a big glass of it. If it seems to help, speak with your doc. There is a blood test that checks for the presence of these Anti-MAS-1 autoantibodies.
It took a whole year to discover SARS COV2 wasn't transmissable on surfaces so I imagine a whole lot more will be discovered in the coming years. Scary stuff indeed..
it IS transmittable on surface, just not highly transmittable compared to breathing it in
jmitw said:it IS transmittable on surface, just not highly transmittable
it IS transmittable on surface, just not highly transmittable
It was not treated that way at ALL, over the first year was the point. None the less you got me.
To be fair, that property isn't monolithic. The omicron variants have shown a much better survival rate on surfaces compared to the earlier renditions of COVID-19. We were washing the hell out of hands and faces and surfaces then but now that it is more important for these current variants, that's considered almost passé.
From the Boston Globe, a piece on how COVID causes neurological problems resembling other commonly seen conditions. They could have overlapping mechanisms.
An article cited:
Another one from the piece:
One more. This describes oxidative damage that occurs due to a shift towards a condition where it is not countered by reductive (free radical eliminating) activity.
Ampligen reportedly worked in CFIDS. Its approved in Europe from what I heard, but never made it out of trials in the YS
I could probably tell you more than you’d want to know about the back story on Ampligen and HemiSpherix, its manufacturer. I’ve still got the info in storage boxes. I was involved in a number of medical conferences back in the day, when it was being promoted by Drs. Daniel Peterson, Paul Cheney and a number of others for CFS/CFIDS/ME. One conference, in particular, in Milwaukee where info came to light that looked like they “cooked the books” on a supposedly double-blinded study.
The last I heard, back when I was actively running the NJ CFS Association, was that the Japanese were using it as an adjuvant in an influenza vaccine. It’s an interesting treatment, in that, IIRC, it was characterized as a mismatched RNA strand used as an immunomodulator. Or something like that. For years, it was a treatment in search of a disease and HemiSpherex’s only product. It’s been a lot of years since then.
Peter, I just caught up on your last two weeks of posts. Some heavy-going stuff there, in neurology land. The depth of the research is remarkable, especially the evidences of glial damage being wrought.
As a virology fanboy, I’m always falling behind, and certainly wading beyond my depth. I’ll have to review current details on its structure. Way back in the EBV research days, two nuclear antigens and a viral capsid antigen were of primary interest, but here I see that a nucleocapsid antigen is being measured along with plasma neurofilament light chain (pNfL) and plasma glial fibrillary acidic protein (pGFAP).
Lastly, I see that Tony Komaroff is one of the authors on the Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome paper on PNAS.
I knew him well, back in the day, and he was responsible for some of the most insightful studies done on CFS. I’m glad to see he’s involved in COVID research. He can bring a lot to the table.
metaphysician said:I could probably tell you more than you’d want to know about the back story on Ampligen and HemiSpherix, its manufacturer. I’ve still got the info in storage boxes. I was involved in a number of medical conferences back in the day, when it was being promoted by Drs. Daniel Peterson, Paul Cheney and a number of others for CFS/CFIDS/ME. One conference, in particular, in Milwaukee where info came to light that looked like they “cooked the books” on a supposedly double-blinded study. The last I heard, back when I was actively running the NJ CFS Association, was that the Japanese were using it as an adjuvant in an influenza vaccine. It’s an interesting treatment, in that, IIRC, it was characterized as a mismatched RNA strand used as an immunomodulator. Or something like that. For years, it was a treatment in search of a disease and HemiSpherex’s only product. It’s been a lot of years since then.
How do you explain the reports of many people claiming to feel a lot better while getting the treatment? even if the studies were faked. were the reports of improvement faked also?
jmitw said: How do you explain the reports of many people claiming to feel a lot better while getting the treatment? even if the studies were faked. were the reports of improvement faked also?
Right now I just don't have the time to examine this study but there are some contributing factors. It's a delicate process if there isn't any hard physiological data that is rock-solid to quantify for interpretation.
1) The placebo effect. Yeah, it is controversial but sometimes believing you're getting effective treatment can change how you're feeling within the context of your condition. If it is self-reported data rather than clinical measures like blood tests or other physiological things such as muscle strength or fatigue/limit trials a patient's feelings and expectations may play a role.
- being unsure of their progress and wanting to believe they got better might bias their thinking when filling out a survey, especially with a Likert score that isn't broad enough with the choices.
- the patient may not have been given any notion of how it would look/feel if a drug that is supposed to help them actually does or doesn't so they report their imagination and/or hopes.
- if the patient does indeed feel a difference and they happen to be receiving the drug under investigation they could exaggerate the impact in a self-reported manner, especially if they aren't medically educated or haven't looked into the condition out of frustration after not getting relief or so long.
2) The scientists themselves or the blinded evaluators might have their own biases or agendas that will influence how self-reported data is interpreted.
I'm sure that none of the reports of improvement were faked. The code was broken by people outside the study, which made the statistics of the result somewhat suspect.
Having also co-chaired an older CFS group at Beth Israel in Manhattan, I can tell you of some patients who found any particular substance that improved their condition immensely, but worked for almost no one else. The NJ CFS Assn. had more than 700 members at its peak and I worked with leaders in MN, KS, MO, AZ, MA, Canada, New Zealand, and more, so I've known a lot of patients in my time. Spontaneous improvements and remissions are not uncommon. There are also patients with cyclic disease, which makes it even harder to match improvement with a substance.
A syndrome, by its very nature, is not a disease. It's a collection of signs and symptoms where the causation has yet to be determined, with a few notable exceptions, like purple urine bag syndrome . Look it up, it's amusing.
The placebo effect is very real; it's not someone's imagination. The nocebo effect is also real. When people are TOLD that they're being given a placebo, a small but significant number will also improve. This is the point of a double-blind study: to prove that a substance actually has the intended effect.
If we ever manage to understand the biological mechanisms behind the placebo effect, so that it's more reproducible, medicine will have made an enormous stride towards helping our bodies to cure themselves.
I'm sorry if I'm taking this off-topic, but post-viral syndromes have been studied over many decades. All differ in some respects, but resemble each other in most others. If the $1.5 billion that NIH has dedicated towards Long COVID bears fruit, then all of us will profit from it.
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