Differentiating POTS from ME - Harder than it sounds.

[taniaaust1]

@Murph

Very good point, in fact you're right, I could probably do some really light exercise and not experience PEM as long as I have rest days in between. I'm just a bit scared to start proper exercise again after my last few failed attempts, I do try to go on regular walks of about 1-2 miles per day and don't get PEM from that.

if you are regularly doing 1-2 miles walks per day.. I personally wouldnt think you need any more exercise esp since I think you also do have ME/CFS. I think from you saying this that you should not worry about doing more exercise.

If u want to do more.. low rep weight training can be okay for many who have ME/CFS and may be fine for you. (very low rep.. say 3-5 lifts) or training with those elastic bands. Keep in mind to start very low with things, its better to always find u can build up to more then jump in doing too much and suffer ill affects.

I suggest as I personally think you probably have tendancy to over do your exercise, I suggest to get yourself a heart rate monitor and stay under what is said to those with ME/CFS should stay under (there are some threads about here on monitoring oneself with monitor to make sure not doing to much). Some here use heart beat monitoring to stop themselves from ME crashing.

Seeing you havent been sick for long, you really should take care to not make yourself worst as you have the best chance of recovery currently. So take precautions such as a monitor. (too many overdos can be disastous to your possible recovery).

 

[taniaaust1]

A medical professional I know told me that "Dr Raj has said in one of his other papers that lying to standing 27 point increase is equivalent to 30 points on tilt test."

The Dr Satish Raj paper in question I think may be this 2006 one, which says:


However, I appreciate that this 2006 paper might now be a bit out of date. Would you have links to more up-to-date authoritative sources for POTS diagnosis criteria? I'd like to put any more up-to-date info in my roadmap document, which details POTS testing.

yeah 2006 is way out of date for POTS.. but sorry I dont know off my head where active links are on this. There may still not be an actual set diagnostic criteria still (so it could further change and toughen up further for diagnoses) but the general strong medical consensus now is that 30 beats per minute (higher for children) shift.

Possibly my lack of POTS symptoms on standing might relate to the wiry physique and taut muscles I have, which may compress my blood vessels and prevent blood pooling in my lower limbs on standing.

maybe.. one of my drs had me doing calf strengthening exercises.. squats, in attempt to help stop the blood pooling and to help the POTS symptoms. Unfortunately this didnt work for me at all.

 

[taniaaust1]

Your workout looks good ! Just readjust if need be (do less) and most of all don't be tempted to increase once you've found the right combination. You most probably won't progress once you've found it, so try not to have any expectations.

Sometimes I can increase a little bit for a short period, but it never lasts. Most of the time I need to tone it down...

If you do want to progress in exercise... you need to be completely okay with what you are doing for at least 3 weeks before any increase. (Ive found can take up to 3 weeks if one is very slightly over doing to show)

 

[adreno]

@AdamS

That looks like a good workout. Important points:

1. Low reps (you have that)
2. Long rest pause between sets; HR return to baseline (you have that)
3. No full body workouts; with POTS you likely have hypovolemia so don't include too many big muscle groups (you have that)
4. Sitting exercises preferable to standing (I think you have that too)
5. No PEM before training again, i.e. return to baseline between sessions

I'm trying a schedule of just one large muscle group per workout session, example:

Day 1: (Chest) Dips and shoulder press
Day 2: (Back) Row and chinups
Day 3: (Legs) Some leg and core exercises

 

[AdamS]

@adreno

Thanks! Yeah the workout seems to tick a lot of the boxes. I actually woke up today feeling reasonably good, so hopefully that's a positive sign. It sounds obvious but it was just nice to be back in the gym from a psychological perspective because it made me feel like i'm getting a tiny bit of control back.

I like the look of your programme, it hits all the main muscle groups, I hope I can build up to 3 sessions per week after a few months. You're braver than me attempting chin ups and dips though good luck!

 

[AdamS]

I've personally found that anything involving sustained cardio effort is bad. I can do some cardio, but it is better to be stop-start activity.

For example, in one of my "remissions" I could trigger PEM by jogging for 30 minutes, but playing a 90 minute soccer game would not trigger PEM, because even though there are high intensity moments, there are moments where you're just standing there. Those rests are apparently crucial for me.

In my current, mild state, I find I can walk my dog most days, but I feel much better after "city" walks where I pause at a lot of traffic lights, than "country" walks where I just trudge along non stop.

If I were you (and of course everyone is different) I would not aim for anything like keeping your HR in X zone for for Y amount of time. I think being able to regularly walk 2 miles a day is pretty damn good and maybe if you add in some light strength work you'll be doing more than 90% of the entire population!

So the tl;dr what works best for me is exercise broken up with rests.

Thanks for this! Really good advice about breaking up exercise with resting/pausing, it's amazing that these breaks can mean the difference between triggering PEM and not. Haha, your comment about doing more than 90% of the population made me chuckle!

 

[AdamS]

@AdamS I was reading some of Dr Hyde's material today and according to him, ME is caused by an Enterovirus, mainly, that causes chronic infection resulting in dysfunction of the brain (hypoperfusion) and the overall body functions. The area of the brain responsible for dysautonomia (POTS is a type of dysautonomia) is the operculum, which is affected in most cases in severe ME patients. My brain has been tested for hypoperfusion, which I have, but my operculum (insular lobe) isn't affected, which explains why I don't have POTS.

Interesting stuff, thanks for bringing this to my attention, i'll have a look at Dr Hyde's work today!

 

[Dechi]

If you do want to progress in exercise.. you need to be completely okay with what you are doing for at least 3 weeks before any increase. (Ive found can take up to 3 weeks if one is very slightly over doing to show)

Not in my case. I've been doing this for almost 2 years now and I've reached a plateau. As long as I have this illness, my body can't take more than what I've been doing. I can always do less, but not more.

 

[Hip]

yeah 2006 is way out of date for POTS.. but sorry I dont know off my head where active links are on this. There may still not be an actual set diagnostic criteria still (so it could further change and toughen up further for diagnoses) but the general strong medical consensus now is that 30 beats per minute (higher for children) shift.

Would you know if that 30 bpm threshold definitely applies to the active standing test, as well as the tilt table test? I know for the tilt table test, it is definitely 30 bpm.

In the 2006 Dr Satish Raj paper I quoted above, it says that when you stand using your own muscle power (active standing), this acts to compress the blood vessels more than when you are passively placed in an upright position using the tilt table. The paper says that is due to the skeletal muscle pump, which is important in countering orthostatic intolerance when standing.

So via this skeletal muscle pump, active standing compensates a little bit for your POTS, whereas the tilt table does not compensate.

So that's why I believe in the 2006 paper, Dr Raj refers to the criteria used by Streeten et al, which is a 27 bpm threshold for POTS diagnosis on the active standing test, to account for the effects of the skeletal muscle pump.

But yes, this is back in 2006, so this criterion may well be out of date now. It would be nice to find an up-to-date paper detailing the criteria for both the tilt table test and the active standing test.

 

[Strawberry]

Looks like there's some overlap. Which ones were you positive on?

Alpha1, M3 and M4. Note I am only mild to moderately affected, I would expect others worse than me to have more, but that is only a guess. I was surprised to have those 3. Actually, M3 is borderline, called "at risk," so 2 and a half.

 

[AdamS]

Do you know which antibodies relate to POTS and which relate to ME? I have 3 positives to the CellTrend test and am curious.

Thanks in advance!

According to this Antibodies against β2, M3 and M4 receptors were significantly elevated in CFS patients compared to controls.

I'm tempted to get a test myself now. I've tried Midodrine (Alpha Agonist) & Propranolol (Beta Blocker) together and isolation with minimal benefit. This begs the question...are the Muscarinic receptors the real culprits? I know that Dr. Light found autoantibodies to at least one of the receptors (beta adrenergic / muscarinic) in almost all (15/18) of the ME/CFS/FM patients. In his video he actually talks about the M2 receptor specifically too.

I wonder whether the autoantibodies are agonising or antagonising the Muscarinic M2, M3 & M4 receptors though? Perhaps @Hip knows about this?

Anyway, what I found even more interesting is what these Muscarinic Receptors do:

M2: The M2 muscarinic receptors are located in the heart, where they act to slow the heart rate down to normal sinus rhythm after positive stimulatory actions of the parasympathetic nervous system, by slowing the speed of depolarization.

M3: Because the M3 receptor is Gq-coupled and mediates an increase in intracellular calcium, it typically causes constriction of smooth muscle, such as that observed during bronchoconstriction. However, with respect to vasculature, activation of M3 on vascular endothelial cells causes increased synthesis of nitric oxide, which diffuses to adjacent vascular smooth muscle cells and causes their relaxation and vasodilation, thereby explaining the paradoxical effect of parasympathomimetics on vascular tone and bronchiolar tone. Indeed, direct stimulation of vascular smooth muscle M3 mediates vasoconstriction in pathologies wherein the vascular endothelium is disrupted.
***NOW THIS IS EXCITING STUFF*** Nitric Oxide, Intracellular Calcium, endothelial cells.

M4: Not 100% sure, need to do more research.

I wonder if targeting these receptors with agonists/antagonists would be useful for a subset with autoantibodies to them?

 

[Hip]

I wonder whether the autoantibodies are agonising or antagonising the Muscarinic M2, M3 & M4 receptors though? Perhaps @Hip knows about this?

The only paper I have seen that found muscarinic receptors autoantibodies in POTS is this one, but it is not clear whether they agonize or antagonize this receptor.

There are a couple of papers finding adrenergic receptors autoantibodies in POTS: here and here.

There are also a couple of papers finding muscarinic and adrenergic receptor autoantibodies in orthostatic hypotension (another type of orthostatic intolerance found in ME/CFS), see: here and here.

 

[Hip]

@AdamS if you are talking about ME/CFS rather than POTS, then the following papers found muscarinic receptors autoantibodies in ME/CFS patients: here and here, and also the following paper:

Antibodies to the Muscarinic Acetylcholine Receptor in CFS

Presented In: International Conference on Fatigue Science 2005; Karuizawa, Japan, 2005. David E. Bell, BS, Aristo Vojdani, PhD, David S. Bell, MD

Patients with chronic fatigue syndrome experience severe fatigue, orthostatic intolerance and numerous other symptoms that are similar to known illnesses of the autonomic nervous system. Because of these similarities it is possible that disruption of autonomic nervous system nerve transmission may play a role in the symptoms of the illness. In a recent paper, researchers noted that 50% of patients with CFS had antibodies to the muscarinic acetylcholine receptor (Tanaka S, et al. Autoantibodies against muscarinic cholinergic receptor in chronic fatigue syndrome. Int J Mol Med 2003;12:225-230.) The presence of an autoimmune dysautonomia with autoantibodies to the muscarinic acetylcholine receptor is a theoretical etiology for some patients with CFS. If autoimmune dysautonomia exists and can be effectively recognized, therapeutic implications for this group of patients may be developed.

Objective: The present study was designed to examine IgG, IgM, and IgA antibodies to the neuromuscular acetylcholine receptors (AR) and to muscarinic receptors (MR) in patients with chronic fatigue syndrome (CFS) and healthy matched controls.

Methods: Twenty five adults with CFS were matched with healthy community controls for age and sex. After informed consent, venous blood samples were drawn and sent to Immunosciences Laboratory in a blinded manner. The testing procedure was the same as previously described.

Results: Five of the antibodies studies (IgA_AR; IgM_AR; IgG_AR; IgM_MR; and IgG_MR) showed no differences between patients and controls. However the IgA_MR was statistically higher in patients than in controls (0.43 vs. 0.33, p = 0.031).

Conclusions: Our studies are in agreement with the studies of Tanaka et al (1) that autoantibodies against muscarinic receptors may be an important marker in a group of patients with CFS. Further studies should be undertaken to further characterize these autoantibodies and to determine specifics of the subgroup to which they may apply. If this proves to be a consistent finding, therapy directed toward the acetylcholine neurotransmitter system may be of benefit in this group of patients.

I don't know whether these were agonist or antagonist autoantibodies, but if you get the full paper from Sci Hub, that info might be buried somewhere in the paper. But quite often these studies do not determine whether the autoantibodies are agonists or antagonists; all they determine is whether the autoantibody has affinity for the receptor.

 

[AdamS]

Thanks @Hip - What i'm wondering ultimately is whether the use of agonists/antagonists would help those who have autoantibodies to such receptors.

Just found this from Fluge & Mella here:

Interestingly, recent studies have indicated a possible autoimmune basis for Postural Tachycardia Syndrome (POTS) with autoantibodies to autonomic receptors [27]. Studies have also suggested that in subsets of Chronic Regional Pain Syndrome (CRPS) patients, associations to partly agonistic autoantibodies to β2-adrenergic receptors and to muscarinic-2 receptors were reported.

 

[Hip]

Thanks @Hip - What i'm wondering ultimately is whether the use of agonists/antagonists would help those who have autoantibodies to such receptors.

Yes, I had the same thought myself; it seems like a reasonable idea.

I listed some muscarinic agonists/antagonists in this post. Choosing one is a bit hit and miss though (unless you have been tested for the autoantibodies you have).

I didn't really get down to trying many of these drugs and compounds, except for some brief experiments with oxybutynin, scopolamine (hyoscine), ginger, linalool and muscarine.

In this post there is the story of one Lyme patient who took low dose fly agaric mushrooms (which contains the M1 muscarinic agonist muscarine), and this dramatically improved her brain fog and mental clarity. She said: "fly agaric has changed my life. It's taken me from being an exhausted cripple with severe dementia-like symptoms to being pretty much a 'normal' person again".

But I understand that when other Lyme patients tried low dose fly agaric, most were not able to repeat her good results. I did not get any improvements in brain fog from low dose fly agaric.

 

[AdamS]

Yes, I had the same thought myself; it seems like a reasonable idea.

I listed some muscarinic agonists/antagonists in this post. Choosing one is a bit hit and miss though (unless you have been tested for the autoantibodies you have).

I didn't really get down to trying many of these drugs and compounds, except for some brief experiments with oxybutynin, scopolamine (hyoscine), ginger, linalool and muscarine.

In this post there is the story of one Lyme patient who took low dose fly agaric mushrooms (which contains the M1 muscarinic agonist muscarine), and this dramatically improved her brain fog and mental clarity. She said: "fly agaric has changed my life. It's taken me from being an exhausted cripple with severe dementia-like symptoms to being pretty much a 'normal' person again".

But I understand that when other Lyme patients tried low dose fly agaric, most were not able to repeat her good results.

Very interesting thanks for sharing this. When my cognitive problems were particularly bad about 3 months ago I looked into a Muscarinic M1 agonist called 77-LH-28-1. Looks super potent, no idea how you'd get hold of it though haha. Fortunately my brain fog has improved a little after avoiding PEM/crashes for a month or so.

Do you think that Rituximab responders benefit because B-cell depletion lowers autoantibodies or because of something else? Sorry I realise this is not an easy question to answer.

 

[Hip]

Do you think that Rituximab responders benefit because B-cell depletion lowers autoantibodies or because of something else? Sorry I realise this is not an easy question to answer.

We can only guess, but a theory on the cause of ME/CFS that I have been toying with is that enteroviral infection triggers the production of autoantibodies against the mitochondria, thereby making our energy metabolism dysfunctional.

This theory is based on the findings that in chronic heart muscle infections (myocarditis), enterovirus does precisely that: the virus seems to trigger an autoantibody attack on the mitochondria of the heart muscle, thereby weakening the muscle in terms of its energy supply.

Given that studies have shown many ME/CFS patients have chronic enterovirus infections of the skeletal muscles, my idea is that you may get the same autoantibody attack on mitochondria in the skeletal muscles of ME/CFS patients.

I detailed this enterovirus-induced autoantibody attack on mitochondria in this post and this post.


In addition, viral infection may cause other autoantibodies, such as the adrenergic and muscarinic receptor autoantibodies, thereby further exacerbating the problem in ME/CFS. So there may be a range of autoantibodies involved in ME/CFS, which rituximab would address.


Other speculation as to why rituximab helps involve changes in immune signaling: the idea is that the dysfunctional energy metabolism of ME/CFS may be due to certain aberrant signals send by the immune system, and that somehow rituximab rectifies those aberrant signals via its depletion of B cells.

 

[TrixieStix]

this was just posted online... "Postural Tachycardia Syndrome Diagnosis and Management in Adolescent and Young Adults"

http://www.healio.com/pediatrics/jo...nd-management-in-adolescents-and-young-adults

 

[Somer]

Thanks @TrixieStix for the link

I'm still wondering how the exercise treatment recommended for POTS sits with a diagnosis of M.E.
I've heard that exercising horizontal can be a less load so I guess some lying down exercises (if you can manage them) or even possibly something like hydrotherapy if you were well enough??

 

[Kenjie]

What is me?