Anger affects blood vessel dilation

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Oliver3

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Personal attacks aren't really helpful. They're more likely to convince me that you can't support your arguments. I did ask to point me to a study that would convince me that endothelial dysfunction is a cause of ME. Maybe I was just unlucky in the studies I did bother to look at, and only found weak ones. Since you feel that there are so many good studies proving it, it shouldn't be difficult to point out one or more particularly convincing ones.
Literally whatever study one provides you..if it's not in the brain, it's not convincing
...so good luck
 

Wishful

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But it's a definite signal.
You posted the link I posted earlier in this thread, along with the flaws. They admit "In the present study, there was no clear relation between endothelial dysfunction and severity of disease symptoms,", which to me implies that it isn't involved in the disease. Since there are so many studies, it's possible that I've just sampled ones that are weak, so I asked for a link for a study that is considered convincing. To convince me, the study would have to show that measured differences aren't just between healthy active controls and inactive ill people in general. It would also have to show that it's a cause rather than an effect. PWME will probably have lots of factors that differ from healthy active people: typical PWME burn fewer calories and have lower cardiovascular fitness, but that applies to other equally inactive people, so that's not convincing as being a cause of ME, or that ME is caused by not burning enough calories.

I'm not absolutely set on ME being neuroimmunological, since the body is so complex and poorly understood, so the root cause of ME could be a complete surprise. However, from my personal observations and my reading of the studies and theories, the brain's immune system seems a critical part. If some study shows a clear involvement of the spleen or some yet-undiscovered microbiome in our kneecaps, I'll accept that. I just haven't seen that from the endothelial dysfunction papers that I've looked at, or the chronic viral infection theories, or the various other ones.

FWIW, I noticed that the Mayo Clinic's review (posted in another thread) describes ME as "a chronic neurologic disease". While I agree with that, I do think there's not enough evidence to make such a definite claim. We're still waiting for that evidence of what ME really is.
 

hapl808

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since the body is so complex and poorly understood, so the root cause of ME could be a complete surprise

Agreed.

Has anyone noticed a correlation between ME symptoms and anger?

Yes, as I've already said in this thread, anger makes my symptoms worse. Although to be more precise, like many things I will get a short increase in energy while I'm doing the thing, and then a crash that comes later - whether it's from anger, or cognitive exertion.

Yeah, not sure it's useful because I believe most LC or ME/CFS who are moderate or severe will say that anger makes them much worse.

I'm not sure the point of your thread. You asked if anyone has noticed a correlation. I said yes, I have - and many with LC or MECFS report the same. Unfortunately, lots of other stuff also worsens symptoms or leads to PEM, so I'm not sure what that means, if anything.

So are you asking if anyone's noticed a correlation (which I've answered and you ignored), or are you asking if there are definitive studies (as you point out, it's poorly understood so I don't think any definitive studies exist on any aspect).

Again, it's fine to inquire - but you don't seem to be inquiring, you seem to be trying to persuade about…something? I'm really not sure. That's why people might be getting annoyed (or at least it kind of annoys me because I answered in good faith and you ignored my entire answer except the last sentence when I said I wasn't sure the point of the study).
 

Wishful

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My reason for posting the link was that I saw it as a blood vessel changing factor that we all experience. With the interest in endothelial dysfunction and other blood flow abnormality hypotheses, it seemed like something that could show an effect on ME symptoms. It also had a time frame for the dilation-blocking (up to 40 minutes), which narrows down when to look for correlation. It's also so common that people might not pay attention to a correlation, and maybe being distracted by whatever made them angry. As I said, a lack of correlation doesn't disprove the hypothesis of blood flow rate affecting ME symptoms. A significant positive correlation would have been interesting. A positive correlation wouldn't prove that it's blood vessel changes, since there are so many other effects of anger, but a strong correlation, positive or negative, would be worthy of further study.

I didn't ignore your response. I wasn't looking for one or two responses of feeling better or worse during or after anger. It wasn't impossible that there would be dozens of responses of the same type, which would be interesting and possibly useful. The tiny chance of that made it worth posting the link and asking the question.


Amusing observation: this ended up testing the question. I inadvertently made cfs since 1998 angry and Oliver3 really angry, and they didn't report any noticeable effects on their ME, so I guess that's two "no" responses. Not a great example of good scientific testing, but I thought it was amusing.
 

Oliver3

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You posted the link I posted earlier in this thread, along with the flaws. They admit "In the present study, there was no clear relation between endothelial dysfunction and severity of disease symptoms,", which to me implies that it isn't involved in the disease. Since there are so many studies, it's possible that I've just sampled ones that are weak, so I asked for a link for a study that is considered convincing. To convince me, the study would have to show that measured differences aren't just between healthy active controls and inactive ill people in general. It would also have to show that it's a cause rather than an effect. PWME will probably have lots of factors that differ from healthy active people: typical PWME burn fewer calories and have lower cardiovascular fitness, but that applies to other equally inactive people, so that's not convincing as being a cause of ME, or that ME is caused by not burning enough calories.

I'm not absolutely set on ME being neuroimmunological, since the body is so complex and poorly understood, so the root cause of ME could be a complete surprise. However, from my personal observations and my reading of the studies and theories, the brain's immune system seems a critical part. If some study shows a clear involvement of the spleen or some yet-undiscovered microbiome in our kneecaps, I'll accept that. I just haven't seen that from the endothelial dysfunction papers that I've looked at, or the chronic viral infection theories, or the various other ones.

FWIW, I noticed that the Mayo Clinic's review (posted in another thread) describes ME as "a chronic neurologic disease". While I agree with that, I do think there's not enough evidence to make such a definite claim. We're still waiting for that evidence of what ME really is.
I'm guessing you didn't read the bit where it says endothelial dysfunction appears to be a clinical presentation in m.e. sufferers.
I mean, all m.e. science is very theoretical right now, but they clearly say it appears to be a clinical presentation in people with m.e.
It's a misinterpretation by you to assume that because it MAY not alter disease severity that it is not a major part of the illness. You're just dancing on the head of a pin
Clinical presentation s without conclusive data are...in part

The brain

the stomach.

Etc etc
So when you're talking about convincing evidence,even the greatest minds on this are still inconclusive.

You did this before when we talked about eds like tissue type playing a role in this disease and you said eds didn't present with symptoms in the brain.
So I posted you links that says eds does cause many brain issues.
You never replied.
So I just took the first study on endothelium that was recent they said what I thought it said...that it appears to be a clinical manifestation

That's all we've got with m.e
Research at the moment.

I don't want to " other you" . We've all had enough of that. Just you consistently pick and choose and don't reply or poo poo research.

It's great to keep an open mind on all this.
I don't care where this disease comes from. I just want it ended as I'm sure you do.

Like other posters have said. What are you trying to to get from making strange suppositions. I mean in a way, it's good science to want to ask questions, but you want to chip away at stuff for the sake of a reaction?
Endothelium is one of the things I'm most sure about, but it's not smthg I champion. It's a definite part of my personal experience and many of the sufferers I know. We should listen to our symptoms. Especially when they occur in large numbers. They can be misleading, but experience is all we've got in terms of science sometimes. The existing science does support our feelings. You seem to just not compute the conclusion of that study. Why?


Making the anger connection has zero points to it. It proves nothing about endothelial dysfunction in me.
So why plug away at that?

I think you have to be happy with a certain degree of uncertainty in m.e. research. The anger idea is kind of a misplaced attack on the endothelium dysfunction thing.bthats why you've got a reaction. Almost a cheap shot?

No I'm not angry at all .the fact that that amuses you gets to the core of what I think may be going on with your posts tho
 
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Rufous McKinney

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I was thinking about people like me who have the coloring and circulatory system which means I turn BEET RED after a sauna. Today I am going to research heat rashes, as I wonder why I am so vulnerable?

Red Head GENETICs is suspected.

We are considered genetically YANG and overheated which could be considered a form of inflammation.

In my body, heat is pouring out.

so with anger, more heat pours out too.

People who flush red alot, can do so from embarrassment.

I take herbs to build Yin, to try to reduce this Yang energy.
 

Wishful

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I'm guessing you didn't read the bit where it says endothelial dysfunction appears to be a clinical presentation in m.e. sufferers
Read it, wasn't impressed. Is 5.1% vs 8.2% likely to have a major effect on body function? I'm just guessing that FMD varies more than that from daily activities. It varied 25% between individuals in the sample, so 3% just doesn't seem "markedly". Furthermore, that's the difference between healthy active controls and people who have limited activity, so it's not proof that it's due to ME directly. Maybe the difference in FMD between athletes and couch potatoes is much greater.

Their exact wording of their conclusion is: "ME/CFS patients had reduced macro- and microvascular endothelial function, indicating that vascular homeostasis may play a role in the clinical presentation of this disease." I could do a study comparing number of calories burned between PWME and healthy controls, find a difference (probably higher than 3%) and say that "caloric metabolism may play a role in clinical presentation in ME", but "may" doesn't mean "very likely".

I agree that the lack of correlation between FMD and disease severity doesn't disprove a link, but I consider it strong counterevidence, meaning that it doesn't appear to be a hot trail to follow. There are limited resources for research, so supporting evidence and counterevidence is important for deciding what studies should be funded. The study we're discussing doesn't convince me that it's more worthy of a followup than a study of vagus nerve bidirectional communication of immune signals.



I was thinking about this thread, and there are two reasons why I appear to be anti-any-theory-not-brain-related:

1) Most of the other theories are contrary to my personal observations of ME. It would, for example, be hard to convince me to accept a theory of ME being due to weak connective tissue when I don't have any noticeable weakness of mine. How we view studies is influenced by our personal observations, experiences and education.

2) I can't point out flaws in neurological hypotheses or studies with the same frequency due to the lack of them. There's a lot of mystery there and it's difficult to study live brains in detail, so there just aren't a lot of studies available. However, as "uncharted territory", it's a good place for the root cause of ME to be hiding.
 

Oliver3

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It doesn't matter if you weren't impressed. It was a definite scientific conclusion.
No I think you just enjoy the friction more than anything. M.e. is a hard disease to live with so I get the frustration.
The majority of m.e. sufferers feel smthg is wrong with their vasculature. The science back that..as this conclusion shows.
Are we saying it's for definite. Nope.
Btw health rising did a piece recently on the burgeoning interest in tissue type.
Have you seen the tissue in your brain. How do you know that the tissue is not localized to your brain and is not more systemic in others.
Subclinical EDS is a definite possibility

In short you just keep saying the same thing, with no evidence...so yeah...that's why we respond like that.

You keep telling us about your personal bias..we get it.
I don't think anyone here would dispute the brain is involved. Guess what's in the brain. Vasculature.
This is a phenotypic illness most likely. No one knows. I'll go back to just not commenting because your arguments are just empty
 

Rufous McKinney

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This diagram seems useful for visualizing aspects of the vascular system.

Seems like considerable opportunity exists for ME affecting the various proteins which provide some of this important structure.

Figure 1. Structure of the vascular wall. Schematic representation showing the three layers of the vascular wall: tunica intima, tunica media, and tunica adventitia, as well as the components of each layer. VSMC: vascular smooth muscle cells (from Bkaily et al., 2021 [2]).
Ijms 24 01998 g001
 

hapl808

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I didn't ignore your response. I wasn't looking for one or two responses of feeling better or worse during or after anger. It wasn't impossible that there would be dozens of responses of the same type, which would be interesting and possibly useful. The tiny chance of that made it worth posting the link and asking the question.

You posted because you were looking for 'dozens of responses' here? First of all, put your question in a poll. Second of all, this isn't a high traffic posting site. You expected 'dozens of responses' to a weirdly phrased vague question with no stated purpose?

I have seen few people on MECFS twitter who don't have a correlation between strong emotions (including anger) and MECFS symptoms. And I follow hundreds of MECFS people there. It's a frequent topic - eg. "I'm so angry at XX but I can't afford to be angry because I'll crash."

1) Most of the other theories are contrary to my personal observations of ME. It would, for example, be hard to convince me to accept a theory of ME being due to weak connective tissue when I don't have any noticeable weakness of mine. How we view studies is influenced by our personal observations, experiences and education.

Which, TBH, is a bit weird because your own personal case of MECFS seems highly unusual. I can't remember if you still experience PEM?

Mine is unusual as well, so I actively try not to focus on the most unusual portions. I have incredibly weak connective tissue, inability to walk without crutches or some support, constant injuries from minor physical exertion, permanent declines from physical activity, etc. I don't spend a lot of time talking about being unable to stand without assistance, because that's not a traditional hallmark of MECFS. It is pretty common to see EDS comorbid with MECFS, though, so I don't rule out connections. We still don't know if MECFS is a bucket diagnosis that will actually be 20 diseases with differing etiologies, or one unifying disease.

So I do focus on the things that seem more universal - cognitive and physical exertion both causing PEM crashes, some PEM crashes leading to full 'recovery' to baseline and some being permanent, having the experience of 'mild' being a state of frequent crashes but then seeing that decline to housebound or bedbound, the initial trigger being hard to determine whether it was a virus or vaccine or something else, conversation (in-person or on phone/video) leading to PEM crashes, etc.

Those are all pretty commonly discussed things.
 

Wishful

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You posted because you were looking for 'dozens of responses' here?
No, I wasn't expecting a lot of responses. I thought the finding was somewhat connected to the hypothesis of vascular function and that there was a small possibility that someone might have noticed a correlation between being angry and their ME symptoms. Didn't cost much effort to post it. I certainly didn't expect the response.

Which, TBH, is a bit weird because your own personal case of MECFS seems highly unusual.
I see value in the outliers. They might study 10,000 subjects who are so average that they're practically identical, and not see anything useful in the data, but a single outlier could reveal an important pathway. Of course, studying only the outliers might give too much variation to see anything in common. So, both are useful for science.

I lack the physical reductions that are common in PWME, and several other people reported the same. To me that implies that those physical effects are downstream of the root cause rather than causative, and so I'm skeptical about studies claiming that ME is a muscle disease. Likewise, there are plenty of people without connective tissue problems, so that seem like a downstream effect too. There could be feedback from those, so that ME causes physical abnormalities which in turn feed back to the root cause, increasing the severity.

As for PEM, I still seem to have cognitively-triggered PEM, but not physically-triggered. I'm not sure whether I'm less sensitive to cognitive triggers since I lost the physical triggering, or just better at avoiding them.
 

Oliver3

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No, I wasn't expecting a lot of responses. I thought the finding was somewhat connected to the hypothesis of vascular function and that there was a small possibility that someone might have noticed a correlation between being angry and their ME symptoms. Didn't cost much effort to post it. I certainly didn't expect the response.


I see value in the outliers. They might study 10,000 subjects who are so average that they're practically identical, and not see anything useful in the data, but a single outlier could reveal an important pathway. Of course, studying only the outliers might give too much variation to see anything in common. So, both are useful for science.

I lack the physical reductions that are common in PWME, and several other people reported the same. To me that implies that those physical effects are downstream of the root cause rather than causative, and so I'm skeptical about studies claiming that ME is a muscle disease. Likewise, there are plenty of people without connective tissue problems, so that seem like a downstream effect too. There could be feedback from those, so that ME causes physical abnormalities which in turn feed back to the root cause, increasing the severity.

As for PEM, I still seem to have cognitively-triggered PEM, but not physically-triggered. I'm not sure whether I'm less sensitive to cognitive triggers since I lost the physical triggering, or just better at avoiding them.
You keep saying the same thing
 

cfs since 1998

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I haven't seen much evidence to support it. I checked one study ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9894436/ ) and while the tone of the paper was "major findings!", the data--to my inexpert eye--seemed fairly weak.

"Nevertheless, it is a significant and important finding that our group of ME/CFS patients had such markedly reduced vascular function compared to healthy individuals."

To me it seems reasonable that people with reduced activity levels would have reduced vascular function compared to healthy (active) controls. I wouldn't consider that "significant and important". To me the paper seems like it's puffing up a weak correlation in order to look good to get more funding.

Their second hypothesis was : "There could be a correlation between ME/CFS disease severity and FMD/PORH levels,". The discussion said: "There was also a tendency towards an association between vascular function and disease severity, which lends some support to our second hypothesis." ... but despite having the data, there wasn't any nice table or plot supporting the existence of this "tendency".

I didn't see any strong argument for this being a cause rather than an effect of ME. Since they have all that data, why didn't they show correlations between severity and blood flow? Maybe there was no correlation?

That study was funded by the government and other organizations, but it seems to be promoting use of rituximab, so there's plenty of potential for conflict of interest.

While that study "found endothelial dysfunction", I certainly don't see it as strong evidence. I haven't encountered any other studies with strong evidence of endothelial dysfunction being a cause of ME. If there is one, please point me to it.
Endothelial dysfunction studies can't be trusted because the authors are pushing rituximab? Does rituximab even treat endothelial dysfunction? No. Did flow-mediated dilation improve in patients who responded to rituximab? No. Grasping at straws to cast doubt and on any research you don't like for...reasons is not constructive. Your argument doesn't hold water.
 
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