Fibromyalgia and Low Blood Pressure

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Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

Latest posts by Adam Foster (see all)

• Hypermobile Neck Exercises - 8 November 2026
• Swollen legs and hypermobility: pooling, lymphoedema and lipoedema - 4 November 2026
• Walking with fibromyalgia - 2 November 2026

You stand up off the sofa and the room goes pale round the edges. You hold the worktop while the kettle boils, because you’ve learned, without ever really deciding to, that this is a thing you now do. At some point you mentioned it, somebody put a cuff on your arm, and you’re told your blood pressure is fine. Or better than fine. It’s low, and low is healthy, lucky you.

Then you go home and it happens again.

Before we go anywhere, two numbers, because this article is full of them and I’d rather you weren’t guessing. Blood pressure is written as one number over another, 120/80 being the one everybody has heard of. The top one, systolic, is the pressure inside your arteries at the moment your heart squeezes. The bottom one, diastolic, is what’s left in them while it refills. So 98/60 means 98 on the squeeze and 60 in between. They’re measured in millimetres of mercury, shortened to mmHg, which is a leftover from when the gauge really was a column of mercury in a glass tube.

Here’s where this is going though, so you don’t have to hold four thousand words in your head to get to the point. Fibromyalgia doesn’t reliably give you a low blood pressure. What it hands you is a blood pressure held loosely, so your lowest readings go lower than they ought to, while your average sits there behaving impeccably. One reading, taken once, in a chair, is close to the worst possible way of catching that, and it’s the only way most people ever get checked.

One thing before we get going: If you take amitriptyline, there’s a section near the bottom with your name on it.

What Fibromyalgia Actually Does to Your Blood Pressure

15,869 people with a first recorded diagnosis of fibromyalgia, 82% of them women. Each one of them was paired with five people of the same sex and roughly the same age who didn’t have it, so the comparison group came to 79,345. Then every routine blood pressure reading in all of those records was pulled out, in some cases 20 years’ worth ^[1].

Average systolic came out about 1 mmHg apart between the two groups ^[1]. That’s nothing. On the averages alone you would close the file and just go home.

The averages are hiding the interesting part though. The lowest systolic each person had ever recorded sat 3.5 mmHg lower in the fibromyalgia group, their lowest diastolic was down by just over 2, and their fastest recorded heart rate ran just under 3 beats a minute quicker ^[1]. Their highest systolic, meanwhile, was slightly higher than the controls’ ^[1].

So, the floor dropped, the ceiling lifted, and the average sat in the middle looking perfectly respectable. The spread got wider, while the middle stayed where it was, which is exactly the shape an average is worst at showing you.

The low floor was already there in readings taken 15 to 20 years before anybody wrote the diagnosis down, by a shade under 3 mmHg ^[1]. The authors are careful about what this means, and they give two reasons. The first is that a diagnosis date isn’t an onset date, so those early readings sit before the label rather than before the symptoms ^[1].

The second is that the people who went on to be diagnosed, had noticeably more blood pressure readings taken in the first place, and by the authors’ own calculation that alone inflates the effect somewhere between a third and a half ^[1]. Take more readings, catch more low ones. They re-ran the whole thing capping everybody at their first 3, 5 and 10 readings, and the differences shrank and held ^[1].

Which leaves us with something real and something small. A few mmHg off your lowest reading isn’t, by itself, a thing to be frightened of. What makes it worth knowing is the company it keeps: a faster maximum heart rate, more variation within the same person from one reading to the next, a lower minimum body temperature ^[1]. Pressure, pulse and temperature are all run by the same bit of background housekeeping, and all three of them look loose.

Why Standing Up Is the Hard Bit

Standing up is a surprisingly difficult thing to do, and nobody ever really mentions it, because most people’s bodies get it right first time.

When you stand, blood drops out of your chest and down into the veins of your legs and your gut, which stretch to take it. Blood is a liquid, you’ve just made your legs the lowest point, and gravity doesn’t make exceptions. Less blood coming back to the heart means less going out of it, and the pressure at the top of you, where your brain is, starts to fall.

You have a couple of seconds. In those seconds, sensors in your neck and the top of your chest register the pressure dropping and fire off a correction: heart rate up, and the blood vessels in your legs and gut squeeze down to push the blood back where it’s wanted. That whole loop is the baroreflex, baro meaning pressure. It’s worth knowing which half of it does the heavy lifting, because it matters later on for you reading. The faster heart rate doesn’t make up for the blood that has left your chest, so the amount your heart shifts per minute still falls. It’s the squeeze in the vessels that holds your pressure up ^[2]. In most people the whole thing happens so fast that standing up feels like nothing at all.

270 people with hypermobile Ehlers-Danlos syndrome (which many with Fibromyalgia have) went through full autonomic testing, which included being tilted upright on a motorised table while an ultrasound probe held against the side of the skull measured how fast blood was actually moving through the arteries feeding the brain ^[3]. Then came the question of which of those measurements predicted who went lightheaded and dizzy during the tilt itself.

How far the brain blood flow fell predicted it (along with age). Whether the blood pressure dropped didn’t, and neither did a racing heart rate, nor the carbon dioxide in their breath, nor general autonomic failure ^[3].

Pressure is a rough stand-in for flow, and in this group it turns out to be a poor one. You can hold your pressure and still be short of what your brain is asking for, which is something you’ve probably half suspected for years without actually being able to put a name to it.

Their tilt results say the same thing, just from another angle. Brain blood flow on tilting was outside the normal range in 79% of them ^[3]. Sorted into named patterns, POTS, where the heart rate climbs steeply on standing without the pressure falling, showed up in around a third. Two separate patterns of reduced blood flow to the brain turned up in roughly a fifth each. Orthostatic hypotension, the actual pressure drop, came up in about 1 in 7 ^[3]. Heart rate and flow problems were common. Pressure problems weren’t.

The limitations are real ones and the authors put them plainly. Everybody in it had been referred to one specialist autonomic lab in the first place, so it isn’t a picture of hEDS generally ^[3]. The probe measures how fast blood is moving rather than how much is reaching the tissue, so it wants confirming with more direct methods ^[3]. And they can’t yet say why one person ends up with one pattern and somebody else another ^[3].

What you can take to an appointment is this. If you’ve been told your dizziness can’t be circulatory because your blood pressure held, the reasoning behind that is a good deal weaker than it sounds.

So What Counts as Low?

This is what most people land on the page looking for, usually with their own numbers in hand, so here’s a straight answer. A resting number on its own isn’t really the thing that gets diagnosed. What gets defined, measured and acted on is what your pressure does when you stand up ^[2].

98/60 is a thoroughly ordinary reading for a lot of healthy young women. It’s also a number that arrives with genuinely miserable symptoms in somebody else. The reading on its own tells you very little, which is maddening when the reading is the only thing anybody has offered you.

What clinicians look for instead is orthostatic hypotension. Orthostatic means to do with standing up, hypotension means low blood pressure, so the phrase means a pressure that drops specifically when you stand, measured rather than guessed at. Three things about how it behaves are worth knowing ^[2].

In the neurogenic kind, meaning the kind driven by the nerves that control the blood vessels rather than by dehydration or a drug, symptoms track the lowest pressure you reach while standing, rather than the size of the fall ^[2]. Which explains something that confuses people a lot. You can have an impressive looking 25 mmHg drop and feel completely fine, because you started high and landed somewhere comfortable. Somebody else drops 12 mmHg and has to sit down on the floor, because they started low and landed under what their brain needs.

Up to half of those with that neurogenic kind report no symptoms at all despite very low standing pressures, though somebody watching them may see their thinking slow down ^[2].

And timing matters. A drop inside the first minute of standing was more strongly linked to long term risks than one that appeared between 1 and 3 minutes ^[2]. A normal bedside test with no symptoms on the day doesn’t rule it out either, because readings taken at a few separate moments can miss mild and short lived drops completely ^[2].

One limit on that review: it covers orthostatic hypotension across the board, and a lot of the outcome data in it comes from older adults and from people with neurodegenerative conditions, where the risks under discussion are a different conversation entirely. Don’t read those figures as being about you. What carries over is how to measure the thing, not what it predicts.

Practically, then: what gets a low reading taken seriously, is a drop you can reproduce on standing, measured at a few points across a few minutes rather than once, and with symptoms that line up with it.

When It’s High Instead

A fair number of people reading this have the opposite problem, or have been told both at different times, and are wondering which of the two they’re supposed to believe.

In that same population study, coded diagnoses of hypertension were more frequent in the fibromyalgia group ^[1]. When the researchers looked at measured readings rather than diagnostic codes, grade 1 hypertension, the mild end of it, was no more common in fibromyalgia than in the controls, and grade 2 was actually less common ^[1]. More labels, the same pressures. The authors treat the coded diagnoses as supporting rather than independent evidence, for the obvious reason that the same route that gets you more appointments also gets you more labels ^[1].

The question underneath that one is usually whether any of this means something bad for the heart later on. Two large Taiwanese insurance databases have been mined for it. In one, covering more than 60,000 people with fibromyalgia against three times as many matched controls, coronary heart disease came out roughly one and a half times as likely once other factors were accounted for ^[4]. In the other, stroke risk overall came out about a quarter higher, and the whole of that increase sat in ischaemic stroke, the kind caused by a blockage, with no clear difference in the haemorrhagic kind, the kind caused by a bleed ^[5].

Both were built out of insurance records rather than designed as experiments, so they show things travelling together and can’t tell you what causes what. A raised relative risk also sounds a great deal more alarming than it usually is in absolute terms, particularly for the age group most of you reading this sit in. Take ordinary cardiovascular health seriously. Don’t take it as a prognosis.

If You’re Hypermobile As Well

Hypermobility and fibromyalgia overlap often enough, and if you’re hypermobile, the standing picture is different enough to need its own section. The short of it is that the sustained pressure drop everybody goes looking for is the least common thing on the list.

35 adults with joint hypermobility syndrome went through a battery of autonomic tests, though not one of them could finish the sustained handgrip, for pain and fatigue ^[6]. On head up tilt, 17 of the 35 met the criteria for POTS, 11 had orthostatic intolerance, meaning they felt dreadful upright without quite reaching the POTS threshold, and 7 came out normal. Exactly one of them had orthostatic hypotension, and the other 34 had a normal pressure response ^[6]. That’s a small group recruited through a specialist clinic, so the proportions won’t carry over cleanly to everyone. 1 in 35 is still a striking number for the mechanism the internet insists is the mechanism.

45 young women, 15 controls, 15 with generalised hypermobility spectrum disorder and 15 with hEDS, went through a head up tilt and an active stand. Not a single participant in any of the three groups met the criteria for orthostatic hypotension, on either test ^[7]. What most of them did have was initial orthostatic hypotension, a steep dip inside the first 15 seconds of standing, at least 40 mmHg off the top number or 20 off the bottom, which then rights itself: 13 of the controls, 10 of the hypermobility spectrum group and 14 of the hEDS group, with no difference between the three ^[7]. So the pressure does move. It just doesn’t stay down, and it does the same thing in women who aren’t hypermobile.

POTS during tilt was commoner in the hypermobility spectrum group, 6 of 14, than in the hEDS group or the controls, 1 of 15 in each ^[7]. The authors don’t make much of that and nor should you. It vanished when they counted POTS by a different threshold, it didn’t appear on the active stand at all, and their own conclusion is that POTS can’t be used to tell hEDS and hypermobility spectrum disorder apart ^[7]. 15 people per group is small and they say so themselves.

It runs the other way as well. Among 91 people who already had a POTS diagnosis from a clinician, just under a third met the clinical criteria for hEDS and another quarter had generalised joint hypermobility without meeting the full criteria ^[8]. They were recruited at a conference for people living with the condition, which selects fairly hard for those most involved in their own diagnosis, so read it as the overlap being substantial rather than as a figure for everybody with POTS.

A review of 10 papers on hypermobility and orthostatic intolerance puts lightheadedness and poor tolerance of standing at the top of the symptom list, with heart rate the most consistent thing to move ^[9]. It doesn’t say pressure stays put, though. In the small case series inside it, 10 of 12 adolescents met the criteria for POTS, 7 of those 10 went on to drop their pressure later in the same test, and 2 more dropped it without the racing heart rate ^[9].

An international expert committee looking at cardiovascular autonomic dysfunction in hEDS was blunt about what they had to work with. Nothing following a general hEDS population over time, one published comparison of symptom reporting, and no published trials of management at all ^[10].

Your Amitriptyline Might Be Doing This

Amitriptyline is a tricyclic antidepressant, an older class of drug which in fibromyalgia and in sleep gets prescribed at doses far below the ones used for depression. 69 randomised trials and more than 27,000 people have been pooled specifically to work out which drug classes make orthostatic hypotension more likely than a dummy pill does. Tricyclics came out at better than 6 times the odds, with the plausible range running from about 3 times up to 14 ^[11].

I want to be straight about how firmly that’s pinned down though. The tricyclic figure rests on 3 trials totalling 261 people, every one of them studying major depression rather than fibromyalgia, and the authors say there were too few studies to break the result down by dose or by anything else ^[11]. So the direction is solid and the size has a wide range around it. Dose is a genuine question here rather than a technicality, and it’s one to put to whoever prescribed it.

The direction, though, isn’t in dispute. A review of drug related orthostatic hypotension calls it the commonest cardiovascular side effect of tricyclics, and reports it in between 10% and 50% of those taking one ^[12].

None of which means stop taking it. Amitriptyline helps a great many people sleep and hurt less, and coming off a tricyclic abruptly is a problem of its own. What it means is that if your dizziness started, or got worse, after you started amitriptyline, that’s a known effect of the drug rather than a coincidence, and it’s a conversation to have rather than something to put up with quietly.

The other drugs that come up in fibromyalgia care are covered in the same review ^[12].

• SNRIs, the serotonin and noradrenaline reuptake inhibitors, came out strongly linked to orthostatic hypotension in one group of older adults already at high risk of falling, at better than 5 times the odds ^[12].
  
• Duloxetine on its own looks milder. Against a dummy pill it produced a small but real drop in systolic pressure and no increase in orthostatic hypotension at all, which if anything was slightly less common on the drug than off it ^[12].
  
• SSRIs, the selective serotonin reuptake inhibitors, showed no increase in the pooled trial data, where they were counted together with the other serotonin modulators ^[11].
  
• Venlafaxine moves pressure in both directions. The extended release form pushes it up in almost 6 people in 100, while orthostatic hypotension turns up around 3 times as often as that, and two thirds of the people who developed it were taking cardiovascular drugs as well ^[13].
  
• Beta blockers came out higher still in that same pooled data, at better than 7 times the odds, on a range running from 2.5 up to 24 ^[11]. If you take one for POTS or for migraine, that’s a legitimate prescription with its own reasoning behind it. It just isn’t a treatment for a pressure that falls when you stand.

What Actually Helps

Less than anybody selling you something would like. The authors of that orthostatic hypotension review make the general point first, which is that there are few good forward looking trials of the non drug management of this, and that our understanding of many aspects of managing it at all is poor ^[2]. Everything below sits inside that.

Water, and the way you drink it. This has the clearest mechanism of anything here. 500 ml of water, roughly a pint, drunk quickly over 2 or 3 minutes raises blood pressure within 5 to 10 minutes, and the effect lasts 30 to 45 minutes ^[2]. That’s a sympathetic response to a sudden volume of dilute water arriving, rather than to being topped up on fluid, which is why gulping it works and sipping it across an hour doesn’t. If you know you have to stand at a checkout or on a platform, a glass of water 15 minutes beforehand is doing something measurable.

Compression, with the expectations lowered. The same authors aren’t enthusiastic. Stockings worn up to the thigh take substantial effort to get on and have only a marginal effect on standing blood pressure ^[2]. That’s not a reason to bin yours if you find them useful, and plenty of people do. It’s a reason not to spend a lot of money expecting a transformation. Abdominal ones perform much better.

Raising the head of the bed, properly. Small tilt angles don’t improve standing tolerance. What’s recommended is a steeper one, in the region of 20 to 30 cm of blocks under the head end ^[2]. If you tried this with an extra pillow and concluded it did nothing, you haven’t really tried it.

Movement, built slowly. This is where I’d normally give you an exercise prescription, and I’m not going to, because somebody has already gone looking for that evidence and come back nearly empty handed. Across 10 studies of exercise training for POTS, not one was set up to look at people with hypermobile EDS, and not one reported it in people who had both POTS and fibromyalgia ^[14]. One of the 10 had 8 people with hEDS inside a larger POTS group and never analysed them separately ^[14]. Where it was reported, POTS fell by between 53% and 77% after training, against 7% and 9% in the two studies that had a group doing no training ^[14]. Striking numbers. The same review says that, apart from one study, none of them recorded whether their participants had anything else wrong with them, so nobody can tell you how much those people resemble you ^[14].

The hEDS expert committee reported that after 3 months of moderate endurance and strength work, built up gradually, upright heart rate can come down, and baroreflex sensitivity, that correction loop from earlier, can improve, along with heart rate variability and quality of life ^[10]. They were pointing at two training studies done in POTS rather than in hEDS, and they said it in the same document in which they noted there were no published trials of management in hEDS at all ^[10].

So, graded movement is the thing with the most plausible mechanism and the most supportive signal behind it, and the direct evidence in people like you is thinner than anybody would like. Start lower than you think you need to, and go up slower than feels satisfying.

On the how, the orthostatic hypotension review is more specific than the POTS work is, and it’s worth having. Lower body strength work and moderate, non-strenuous activity are what it says to encourage, and the exercise that puts the least orthostatic stress on you is the kind done lying back, so recumbent or semi-recumbent cycling or rowing, which is tolerated even by people whose orthostatic hypotension is severe ^[2]. One thing in there that nobody ever mentions: pressure can drop after exercise as well as during it, so the first few minutes after you stop are the ones to be careful in ^[2].

Salt, and the caveat goes first on this one. Increasing salt is the traditional advice for orthostatic hypotension and there is a number attached to it: around 10 g of salt a day, with fluid at 2 to 3 litres, the reasoning being that it expands the volume of your plasma ^[2]. The conditions the same authors attach to it matter more than the number does. Only where nothing in your history rules it out, and cautiously if your pressure runs high lying down or sitting, because you can trade a standing problem for a different one ^[2]. Weighing yourself daily is how they suggest tracking whether it’s doing anything ^[2]. Salt also interacts with kidney function and with other medication, so this is a conversation with your GP, and that number is what to take into it rather than something to start on the strength of a blog post.

The Short Version

• Fibromyalgia doesn’t reliably give you low blood pressure. It gives you blood pressure held less tightly, which shows up as lower lows, a slightly faster maximum heart rate, and an average that looks fine ^[1].
• One reading in a chair can’t see that. A standing test taken at a few points across a few minutes can.
• Your dizziness may not track your blood pressure at all. In hypermobile EDS, how far brain blood flow fell predicted the dizziness, and whether blood pressure dropped didn’t ^[3].
• If you’re hypermobile, a sustained pressure drop is the least likely thing on the list. Heart rate and brain blood flow move far more often ^{[3] [6] [7]}.
• Best return for the effort: graded movement built up slowly, and 500 ml of water drunk quickly before you have to stand about ^{[2] [10] [14]}.
• Lower your expectations on: compression stockings, which have only a marginal effect on standing pressure ^[2].
• Raise your expectations on: the head of the bed, if you did it with a pillow rather than 20 to 30 cm of blocks ^[2].
• And if you take amitriptyline or another tricyclic, it’s a well evidenced cause of orthostatic hypotension ^{[11] [12]}. Worth raising with your prescriber, and not a reason to stop anything on your own.

References