ME Association funds development of new protocol for Dysautomnia

https://meassociation.org.uk/2024/06/me-association-professor-manoj-sivan-to-develop-new-protocol-for-dysautonomia-in-me-cfs-and-long-

sorry Dont know how to copy the text

 

Does not look like a very useful design, at first glance.

 

His comments in a letter to the BMJ in 2020 on the LC NICE GDL include some good comments:
"The guidance mentions screening blood tests (such as full blood count; clotting profile; renal, liver, and thyroid functions; and C reactive protein) and tests of both cardiac and lung function to capture reversible abnormalities, but it lacks detail on the management of serious life threatening complications such as a hypercoagulable state.10 The next update should prioritise how to screen for, diagnose, and manage medical complications11 reported in patients with long covid including silent desaturations; cardiac, respiratory, renal, hepatic, gastrointestinal, and neurological abnormalities; endocrine problems; autonomic dysregulation and postural tachycardia; and mast cell disorder. Missing these complications could result in serious adverse outcomes for patients."
https://www.bmj.com/content/371/bmj.m4938.short

 

Dysautonomia in its classical sense is not just a clinical syndrome. POTS is meant to be diagnosed based on subjective and objective features but there remain questions as to the relevance of the objective measures being used. And the "30-100%" estimate just tells you that we have no reliable prevalence data. The sequential intervention design introduces the potential for confounding carry-over effects. There's no mention of blinding for the pharmacological interventions. It's an 8 week trial with no mention of longer-term or post-intervention follow-up. Personalisation isn't explained in the linked document & may limit the generalisability of any findings. And an open question as to whether abnormal lean & active-stand tests do indeed constitute "objective evidence of dysautonomia".

I hadn't come across this home-based "aAP" ("adapted autonomic profile") test before - link.

I would be surprised if this tells us anything useful.

Something that reading this reminded me of: what's the evidence base look like for the common recommendation of increased salt intake in this group of patients? Perhaps useful advice for orthostatic hypotension but in POTS cohorts? The trials I've come across so far have been less than robust, and obviously high salt intake has well-known long-term risks.

Perhaps an unpopular suggestion on S4ME, but in view of the highly limited evidence base, perhaps the term "dysautonomia" should be left for PAF, Shy-Drager, etc?

 

That sentence to me is unimpressive. The way to screen for these is already established. What exactly is being said here? I fear it is 'Why don't we measure everything we can charge a fee for measuring? Send them along'.

 

That would be my thought. As far as I can see 'POT' is not dysautonomia (almost the opposite) because it is a sign of a competent autonomic response to a haemodynamic stress. I have not yet seen any evidence of dysautonomia in ME/CFS or LC. Unusual autonomic activity maybe, but that may have many origins.

 

I’m not a scientist but I’m learning. Not sure where the blame lies here, but the headline on this story made me feel something was off, hence I posted here.

So, dysautonomia is usually an umbrella term for some kind of issue with the autonomic nervous system (Google tells me) occurs in a number of illnesses and diseases and the most common is POTS (thank you Wikipedia) https://en.wikipedia.org/wiki/Dysautonomia

So as a general citizen, I’d think - oh good, POTSand OI are a problem in ME/CFS and probably LC, yes dysautonomia should be looked at, it’s good the MEA are funding this.

Now, as a cynical, more educated S4ME member, I’m thinking this sounds a bit 6th form A-Level science project. Surely there’s a wealth of existing research in POTS/OI (which are distinct, and only two of the items under the large dysautonomia umbrella) given that the issues also arise in such well-studied diseases as Parkinson’s, HIV, eDS, Dementia with lewy bodies.

I don’t know if they’ve “dumbed down” the language for the press release?

 

It’s talking about leading to a bigger NIHR study 25/26. I think there’s little there that could not have been done ten / twenty years ago, especially if the significant POTS component /co morbidity with ME Had been more Acknowledged .The “let’s make a start in ‘24” shows the dearth of genuine commitment to managing the field In any medical Way vs behavioral management of fatigue before. If the interest wasn’t there, which it probably was because Julia newton was keen to do research but said she’d been limited by funding (&was bizarrely funded by afme to study effects of drinking more water or something) , it could have been included in a ring-fenced funding call to stimulate it, as long covid.

 

It used to be that Orthostatic Intolerance (OI) was an umbrella term that covered several different diagnoses, including POTS, NMH, and others. So at least at one time POTS was considered one type of OI.

But autonomic specialists often don't agree on this terminology. Plus I think it has changed over the past 20 years.

I have no particular attachment to any particular terms! But I do wish there was more agreement and better definitions so it would not be so confusing.

 

I think what irked me was the sentence in bold at the start of the press release “…managing dysautonomia POTS (Postural Orthostatic Tachycardia Syndrome and OI Orthostatic Intolerance)…” reads as if dysautonomia is just POTS and OI, and from then on it’s as if dysautonomia can be used interchangeably to represent POTS/OI. Whearas POTS and OI are both distinct and not the full range of dysautonomia types.

I note the study outline doesn’t refer to OI, but OH (orthostatic hypotension)

 

I have heard several autonomic specialists say that autonomic neuropathy is the most common form of dysautonomia. (They might in fact specify diabetic autonomic neuropathy – please forgive my aging memory.)

I'm not sure that POTS is even the most common form of othostatic intolerance. We don't have great figures for POTS prevalence and orthostatic hypotension (OH) might give POTS a run for its money given that OH is common in older people and the aging population.

 

Dr Peter Novak calls them "orthostatic syndromes". This would be better as "orthostatic intolerance syndromes" in my opinion. I don't know whether other specialists like this term.

https://pubmed.ncbi.nlm.nih.gov/27525257/

 

I don't know whether it is a good study design or not, but Dr Satish Raj is doing this one:
https://live-research.ucalgary.ca/p...tic-tachycardia-syndrome-casa-pots-reb23-0779

 

Oh, I forgot to mention that increasing salt intake in POTS is presumed to address hypovolemia (chronic low blood volume), i.e. you want to move the patient from hypovolemia to euvolemia (normal blood volume).

Some of the dangers from increased salt consumption that have been found in the general population come from healthy people increasing their blood volume above normal levels, leading to high blood pressure and other adverse effects.

When medical organisations adopt this technology …
https://detalo-health.com/

… we will be able to measure blood volume, establish whether hypovolemia is really a problem in ME/CFS, POTS, and similar*, and then test individual patients to see whether they have it or not and treat accordingly. Also patients can be monitored to see whether they are under- or over-doing their volume expansion efforts.

On a personal note, my daughter spent a year trying volume expansion measures because no testing is available and specialists have to assume hypovolemia in orthostatic intolerance syndromes. Turns out she does not have low blood volume. We could have saved a lot of time and unnecessary medication trials, some of which cause lingering side effects.

The process could be streamlined by going straight to a short trial of IV saline. If that works, then you can start trialling the less-risky options with some clue that they are worth trying. But it doesn’t happen like that. You have to work your way up to the IV saline, potentially wasting a lot of time.

If I win the lottery, I’ll be donating a couple of the blood volume measurement devices to organisations that will make good use of them. Don’t even need to win big – the device is not that expensive to purchase or run.

*There are studies pointing this way, but only small ones, so lots more verification is needed.

EDIT: Apparently I caused a bit of confusion by not specifying that OI patients are advised to increase salt and fluid intake. I didn’t mention the fluid because nobody comes home from the doctor’s and says “Honey, the doctor told me to increase my salt and fluid intake. Is that guy crazy? Everyone knows extra salt and fluid gives you heart attacks.”

They come home concerned (and confused) about the increase in salt, because that is what is talked about in public health advice.

The water part doesn’t cause any concern, I don’t think, because people are familiar with the basic first aid advice that having a glass of water can help when you feel faint.

Phew.

 

As far as I know there is no physiological reason why eating salt should change blood volume. Salt passes readily by diffusion in and out of the circulatory compartment so it does not 'hold water' in the circulation. I have no idea where this idea has come from but I have never come across it in mainstream medicine. If someone is salt and water depleted then you want to give salt as well as water but just giving salt makes no sense to me.

 

Does it cause an increase in fluid volume somehow? That's what the heart heath/blood pressure charities seem to say, but I'm a bit unclear about it—it isn't very obvious whether it's been established, or is more a theory about how high sodium intake and hypertension are linked.

 

I have no idea why it should and I know of no evidence.
If you eat salt your kidneys reduce their reabsorption of salt in the tubules and within a short while you have peed it out. There may be a period of feeling thirsty because of a slight increase in body salt concentration. Total body water might increase a bit but that is no help to the circulation. You would just get swollen feet, or if lying down, face.

 

As far as I can tell from a quick search the evidence for an effect of salt on blood volume seems fairly scant. There is a 1996 paper in Heart of 31 postural syncope patients:

where the authors concluded:

Also, in the "24th International Symposium on the Autonomic Nervous System" (link) there is a short poster presentation ("Differential effects of dietary salt on blood volume regulation in postural tachycardia syndrome and healthy subjects") with 6 female POTS patients and 4 healthy controls where a high-salt diet was said to increase blood volume in the POTS patients but not in the controls:

 

I can see a problem there that if patients were more active as a result of expectation of improvement, their blood volume might changer as a result of that.

It looks as if high salt has no effect on blood volume in healthy people, which is what I would expect. The question is whether people with OI genuinely have some sort of salt sensitive lowering of blood volume other than due to spending more time recumbent. Unless they are just salt-starved for some reasons it doesn't seem very plausible. The alternative seems much more plausible, that researchers will always find what they expecting to find if their methodology isn't that good.

 

No, I was addressing two topics: one, that increased salt intake has been linked to health problems in the general population, and that that causes concern for people with orthostatic intolerance when their doctor suddenly tells them to eat more salt as opposed to the public health messages to cut back salt to recommended levels that we have all heard for many years.

And two, the reason for increased salt and water intake recommendations for people with orthostatic intolerance, and why that might overrule the “eat less salt” advice for the general population.

Presumably, nobody is going to come home from the doctor worried that they have been advised to drink more water, so I didn’t mention that. It’s the extra salt that gives them pause. Also, doctors seem to often omit to explain the purpose of the extra salt and fluid intake, adding to the confusion.


Are you saying that increased salt intake in the general population is not linked to high blood pressure through mild hypervolemia, and this type of information is incorrect? Presumably healthy people consuming high-salt foods get thirsty and take in extra fluids.

E.g.

“Your body responds to excess sodium by holding on to water to dilute the sodium. As a result, the amount of fluid in your blood vessels increases. That raises the pressure inside your blood vessels and makes the heart work harder.”

https://www.health.harvard.edu/heart-health/dietary-salt-and-blood-pressure-a-complex-connection

I see this simple connection has been questioned:
https://www.medicalnewstoday.com/articles/317099