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Serotonin & Blood Flow in Fibromyalgia & Chronic Fatigue Syndrome

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We hear a lot about low serotonin in fibromyalgia (FMS) and chronic fatigue syndrome (ME/CFS), and it’s usually in relation to its function as a neurotransmitter (chemical messenger in the brain.) However, serotonin is also busy within the rest of your body as a hormone, and body-wide serotonin dysregulation is believed to contribute to many of our symptoms and comorbid conditions.

The name serotonin is derived from its earliest discovered function, which is too narrow the blood vessels — sero means serum, which is a component of blood.

Blood flow irregularities have been noted in both of these conditions:

  • In FMS, research shows abnormal blood-flow patterns in the brain, with more than normal in some areas and less than normal in others. We don’t know the specific effects of this, but researchers do know that blood flow has a significant impact on brain function.
  • Also in FMS, some researchers theorize that the horrible burning pains we get are due to ischemia (impaired blood flow), which basically means the area “falls asleep” and then gets those painful pins and needles as the blood, and therefore feeling, returns.
  • In ME/CFS and to a lesser degree in FMS, some research has shown low blood volume, which results in cells that are starving for oxygen and nutrients. Picture being at a high altitude and struggling to catch your breath after not eating all day. That’s what every cell in your body may be going through.

I feel like a broken record saying this, but at this point, we don’t have specific research on the possible relationship between serotonin dysfunction and these irregularities, but it’s certainly a connection that seems logical.

The relationship of serotonin to fibromyalgia isn’t fully understood but appears to be fairly straight forward. Not so for ME/CFS. This is one area where we have to look at the conditions separately.

Fibromyalgia & Serotonin

One of the most consistent findings in FMS is low serotonin. It’s possible that our bodies don’t produce enough, that they don’t use it properly, or both.

Many of us are helped by the supplement 5-HTP (tryptophan), which our bodies use to create serotonin. Some of us are helped by serotonin-increasing foods. Most of the drugs used to treat us change the way our brains use serotonin in order to make more of it available. (For a detailed look at this see Understanding Reuptake.)

Low serotonin is also linked to migraine, which is considered a related condition. In migraines, low serotonin causes the blood vessels to dilate (open wide,) which causes inflammation in surrounding tissues. That makes for a lot of pressure and results in throbbing pain. FMS pain isn’t exactly the same as migraine pain, but it’s theorized that similar mechanisms may be involved.

Then consider this — we all have a secondary set of nerves on our blood vessels and sweat glands that primarily deals with blood volume and sweat. Research published in late 2009 revealed that, at least in some people, these nerves also appear to transmit information about temperature. Researchers hypothesize that these often-ignored nerves may play a role in pain conditions including FMS and migraine.

It makes a lot of sense, since we have blood flow problems and excessive sweating in addition to temperature sensitivity and heightened pain response. Hypersensitivity in those nerves could also help explain why ischemia could lead to such intense pain.

Chronic Fatigue Syndrome & Serotonin

Then there’s ME/CFS. The common belief is that it, like FMS, involves low serotonin. The symptoms are consistent. The fact that serotonin-impacting treatments work for some people with this condition also lends support. However, it’s not that simple. In fact, researching the role of serotonin in this condition is enough to short circuit your every brain cell.

We have some evidence showing that the serotonin-creation system is in overdrive, and some showing two serotonin-based subgroups — one with high levels, one with normal levels. You’d think that would mean that, at least for the first subgroup, we’d need to lower serotonin levels. Like usual, ME/CFS is determined to defy logic.

That’s because we also have evidence showing weak serotonin-related signal transmission in the central nervous system. The condition appears to feature hyperactive production but low function.

Is the body producing extra to compensate for an impairment in how it’s used, like a type-2 diabetic who needs extra insulin to continue normal function? If so, are some areas getting flooded with too much serotonin while others are deprived? Is too much serotonin constricting blood vessels so the blood can’t get around properly? We don’t have answers yet, and research could well be muddled by the lack of proper, consistent subgrouping, in spite of research suggesting that several subgroups exist and are vastly different from each other. This could certainly explain the differences in how people with ME/CFS react to serotonin-affecting treatments (which I’ll cover later in this series.)

What Does It All Mean?

The bottom line is that, in some way, most of us have serotonin dysregulation of some kind, and it seems likely that it contributes to blood-flow abnormalities that may cause a variety of our symptoms. This is something to keep in mind as you gauge the effects of treatments, which is really the only way for us to learn our individual degrees of serotonin dysregulation. (It’s not something doctors test for outside of a research setting.)

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