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The Ups & Downs of Exercise

Treatment & Research News

The Ups & Downs of Exercise

Exercise floods the body with feel-good endorphins, clears the mind, and ramps up the cardiovascular system. It’s invigorating, unless you have fibromyalgia. The processes controlling cardiovascular workouts do not work correctly, causing exercise difficulties in fibromyalgia patients.

Dane Cook, Ph.D., of the University of Wisconsin, says, “People with fibromyalgia show an abnormal response to gentle exercise.” 1 According to a report by Bruno Gualano, M.D., of Brazil, fibromyalgia patients do not accelerate their heart rates adequately during increased activity.2 And a study by Jose Parraca, Ph.D., of Portugal, shows that the oxygen supply to the muscles is impaired (even at rest) in people with fibromyalgia.3

The above studies highlight a variety of reasons why you encounter difficulties with overexertion. Yet, understanding what you are up against will help you tailor activities to accommodate your dysfunctional response to exercise.

System Controllers

Control of heart rate is based on input from two different nerve branches: your sympathetic (fight or flight) and your parasympathetic (rest and digest). Together, they make up your autonomic nervous system—it’s the network of nerves that communicate between your spinal cord and your peripheral tissues (e.g., your muscles and organs).

To ensure your organs respond appropriately to any challenge, your nervous system must be responsive and flexible. The control dials for either branch must be capable of going from zero to zoom in a split second. Let’s face it, your environment and activity levels are constantly changing, so a flexible autonomic system is essential.

The diagram shows how the two opposing on/off inputs from your sympathetic and parasympathetic nerves control your heart rate. Think of it like two kids on a seesaw that works best if balanced (i.e., both children weigh the same). Yet the timing from one lift off to the next varies, just like your heartbeat, because the system has built-in flexibility.

If you dash out of a burning house, your adrenaline-controlled sympathetic branch should kick in to get your body moving and your heart pumping. If you are digesting your dinner or trying to fall asleep at night, the calming actions of your parasympathetic branch should take over.

Low Heart Rate

People with fibromyalgia have too much sympathetic nervous system activity, even when relaxing.4 Mild challenges to the body, such as standing up or being exposed to cold, may also lead to unwanted symptoms. When switching from reclining to standing, your heart should pump more blood to the brain to prevent lightheadedness. Exposure to cold requires increased circulation of warm blood to your extremities to prevent Raynaud’s-like symptoms (painful spasms in the hands and feet).

Reduced heart rate in response to exercise is a risk factor for cardiovascular disease. This prompted Gualano to look at the differences in cardiac functions between fibromyalgia patients and healthy controls during exercise. Not only did he measure the heart rate at peak exercise capacity, but he also looked at how fast the heart slowed down after ceasing activity. Ideally, the heart rate should increase rapidly to adjust to the body’s physiologic demands, but once resting, its rate should drop quickly.

“Fifty-seven percent of the fibromyalgia patients exhibited slow heart rate response to exercise, but none of the healthy controls,” says Gualano. “The reduction in heart rate was also slower in the fibromyalgia group during the two minutes post-exercise.”

Why was the heart rate so low in people with fibromyalgia? Gualano says, “The autonomic nervous system is not as flexible as it should be.” Exercise ought to prompt the sympathetic system to get the heart pumping while forcing the calming parasympathetic branch to withdraw control. The reverse should occur during rest, yet an imbalance called dysautonomia exists.

The cause of dysautonomia remains unclear. Gualano emphasizes the sympathetic system is super-charged at rest and unresponsive when challenged. A hyperactive sympathetic system leads to a chronic pounding on the receptors in the heart that help regulate how fast it beats. After a while, these receptors become indifferent to the sympathetic system’s demands, which makes the heart less responsive to activity challenges.

Fibro is to Blame

Could Gualano’s finding be due to a lack of exercise or a reduced fitness level? Or could symptom severity play a role? The answer is no, based on two reports from another Brazilian team.

The first study compared fibromyalgia patients to healthy controls who were matched for their level of physical fitness.5 Despite the same fitness levels, the fibromyalgia group had a reduced heart rate response to an exercise challenge. The speed at which their heart rate returned to resting levels was also slower. In addition, measures of autonomic nervous system function revealed an imbalance between the sympathetic and parasympathetic branches.

The above findings run counter to what is known about exercise and fitness levels, at least in healthy people. When a healthy person becomes sedentary, their sympathetic and parasympathetic systems become unbalanced, but they can correct this with exercise. So, the same research team sought to answer another question: could the dysautonomia in fibromyalgia be related to symptom severity?

Dividing fibromyalgia patients into two groups based on symptoms, moderate and severe, they compared fitness measures and autonomic functions to a healthy group.6 Although the level of physical fitness was worse for the severe fibromyalgia group (compared to the moderate), their autonomic nervous system function was equally impaired. 

What does this mean for you? Lack of exercise or symptom severity do not appear to contribute to your level of dysautonomia. In fact, the sympathetic dominance with reduced parasympathetic activity is likely adding to your fibromyalgia symptoms, rather than being the result of inactivity.

Altered Response

If exercise does not increase heart rate appropriately, what about the rest of your cardiovascular system? Cook’s team looked at how this system worked in fibromyalgia patients (compared to controls) while performing mild exercise. He found the heart pumps harder during exercise in fibromyalgia patients, and the rest of the cardiovascular system doesn’t keep up.

“These results indicate that exercise for fibromyalgia patients is more difficult than for healthy individuals on many levels … but it doesn’t mean that increasing physical activity won’t help some of these abnormalities.”

Muscles Lack Oxygen

To increase delivery of oxygen and nutrients to your muscles, your sympathetic constricts blood vessels to speed up the flow. However, your parasympathetic is responsible for relaxing or expanding the arteries so that a larger quantity of blood can be delivered.

Given the studies showing an overpowering sympathetic system with inadequate parasympathetic activity, are your muscles getting the oxygen they need? No.

Parraca’s team in Portugal assessed the amount of oxygen delivered before, during and after exercising the thigh muscle in fibromyalgia patients and healthy subjects. The healthy group showed an increase in oxygen consumption during the exercise, while there was virtually no change in the fibromyalgia group. Even at rest, the oxygen supply was significantly less in the patients.

Another finding by Parraca’s team shows that people with fibromyalgia experience a 50 percent drop in saliva secretion during exercise.7 Why is this important? Saliva flow is controlled by your parasympathetic system, and its dramatic decline is a sign of dysautonomia. It also explains why you may develop dry mouth when you exercise or overexert yourself.

Staying Active

Intense exercise will set you back, so the best you can do is move regularly at your preferred pace. If you maintain your own natural speed (which is much slower than healthy people), energy consumption is optimized. Moving too fast or vigorously may force your muscles to operate without enough oxygen and lead to more symptoms.

Another study shows that a self-paced program (on land or in the water) leads to slow improvements in speed over two to three months.8 Benefits in physical function take time and cannot be rushed. And if you can keep it up, you may also notice improved coordination and cognition.

One more point: make use of warm water. Heat invokes the parasympathetic system to relax your blood vessels to help your muscles receive more oxygen and nutrients. In addition, you have heat sensors in your tissues that work to help relieve pain. If you are struggling with an exercise program, warm water therapy may be the solution for you. If this is not feasible, the next best thing is taking a hot shower or bath just before working out.

  1. Cook DB, at al. Med Sci Sports Exerc 44(6):1186-93, 2012.
  2. Da Cunha Ribeiro RP, Gualano G, et al. Arthritis Res Ther 13:R190, 2011.
  3. Villafaina S, Parraca JA, at al. Biomedicines11:132, 2023.
  4. Lerma C, at al. Arthritis Ther Res 13:R185, 2011.
  5. Schamne JC, et al. J Clin Rheumatol 27(Suppl 2):S278-S283, 2021
  6. Sochodolak RC, at al. J Exerc Rehabil 18(2):133-40, 2022.
  7. Costa AR, Parraca JA, at al. Diagnostics 12:2220, 2022.
  8. Tiinus PM, at al. J Sports Sci Med 1(4):122-27, 2002.

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Giving LDN Your Best Shot

Treatment & Research News

Giving LDN Your Best Shot

There is no roadmap for test driving low-dose naltrexone (LDN), so this article offers navigation advice to minimize the bumpy road ahead. If you have not heard of LDN,  check the trial funded by AFSA. Basically, LDN works to quiet the immune cells in the central nervous system (the microglia) that are magnifying your symptoms. The side effects of LDN are mild. All other drugs prescribed for fibromyalgia target the neurons and cause a slew of side effects.

Success Rate

What are the odds that LDN benefits you? Sean Mackey, M.D., Ph.D., a pain specialist at Stanford University in Palo Alto, CA, was one of the investigators on AFSA’s LDN trial. He found that three out of ten patients achieved at least a 30 percent improvement in pain. The drug produced similar benefits in fatigue and sleep, but the study included only 30 people.

Nicholas Aitcheson, M.D., a rehabilitation and pain specialist in Queensland, Australia, says, “Around 200 patients have been tried on LDN in our chronic pain clinic. Anecdotally, one-third have reaped significant positive results in pain reduction and improved function.” Reports by other pain clinics involving anywhere from ten to 70 fibromyalgia patients give similar findings.

Symptoms Treated

Aside from pain, LDN helps with cognition (reduces brain fog), sleep, mood, and fatigue. “Fatigue is a major complaint for people with fibromyalgia,” says Mackey, and it’s difficult to find anything to alleviate this symptom. Pain specialist Michael Fishman, M.D., of Lancaster, PA, adds that LDN also reduces postural hypertension (lightheadedness upon standing) and burning symptoms. While not every patient has these symptoms, they are tough to treat.

“When choosing patients for a prescription of LDN, I like to ensure that they have fibromyalgia and not just pain in a few areas,” says Aitcheson. “The presence of other symptoms like cognitive clouding, fatigue and unrefreshing sleep tends to shift me towards the use of LDN.”

Must Be Compounded

LDN appears to work as well, if not better, than other drugs to treat fibromyalgia. Unfortunately, your local pharmacy only dispenses 50 mg tablets of naltrexone. To get the tiny dose needed, you must go through a compound pharmacy. Insurance companies won’t pick up the tab, but the cost of LDN is $1/day … and possibly less.

“Some patients and physicians may be nervous when using a medication that needs to be compounded,” says Aitcheson. To ease concerns, he points out, “Naltrexone has been used safely for at least 40 years and we are prescribing it at less than one tenth of the minimal normal dose.”

Working with a compounding pharmacy sometimes presents hurdles for patients or physicians. However, Anne Marie McKenzie-Brown, M.D., a pain specialist at Emory University in Atlanta, GA, offers advice on Compounding Pharmacies in the last section.

Dosing Strategy

The most common dose of LDN is 4.5 mg/day, but the range is from 1.5 to 9 mg. Just like all medications, one dose doesn’t work for everyone. LDN is usually taken as a single dose at bedtime because if side effects occur, they won’t impact daytime function.

“I just recommend that patients start at 4.5 mg at night,” says Mackey. “I don’t think that there is anything magical about that dose.” This was the dose used in the fibromyalgia trial and it happens to be the average dose patients end up taking.

According to Fishman, “If nightmares or vivid dreams are present, they improve with taking LDN in the morning instead of the evening.” Other side effects, such as headaches, nausea and anxiety are mild and occur infrequently. However, if they persist, you can drop down to a 3 mg dose and these side effects will usually go away. 

If you are drug sensitive, other dosing schedules may be used. “I start patients at 1.5 mg/day for the first week, increase it to 3 mg/day the second week, and move patients to a stable dose of 4.5 mg/day the third week,” says Aitcheson. He prescribes 1.5 mg compounded capsules during the titration phase.

McKenzie-Brown uses a similar titration schedule, but instead of capsules, she prescribes 3 mg tablets that are scored. This form of LDN is available from a few mail-order pharmacies. “I start with 3 mg tablets and ask patients to cut them in half for one to two weeks to make sure there are no side effects. Then they go to 3 mg. If they have relief and want to stay at 3 mg, we stay at this dose. Otherwise, I have patients increase to 4.5 mg. Many stay at 3 mg.”

Be Patient

LDN is not a fast-acting treatment. Patients in the fibromyalgia trial took a month to notice improvements. Both Aitcheson and McKenzie-Brown recommend being on LDN at 4.5 mg/day for three months before giving up. In fact, McKenzie-Brown published a study on the use of LDN at her chronic pain clinic. She found that 12 percent of patients did not get pain relief until after three months.

“I ask patients to reserve judgement on LDN efficacy until the end of three months,” says McKenzie-Brown. “Many patients have told me that they would have stopped LDN, but they are glad they did not.”

Complimentary Therapies

Getting a handle on fibromyalgia requires combination of therapies, so don’t view LDN as your only option. “I usually prescribe LDN as an add-on to other medications,” says Aitcheson. He recommends magnesium and duloxetine along with LDN. “These agents act on the pain amplification pathways in the brain and spinal cord.”

McKenzie-Brown refers patients to physical therapy, aquatic therapy, and acupuncture, in addition to prescribing nonopioid medications. The point is, you don’t have to wait for LDN to work to get relief from your fibromyalgia.

Increasing the Dose

If LDN is reducing your symptoms, it’s natural to wonder if a higher dose might be better. “I take it on a case-by-case basis,” says Mackey, adding “there aren’t any guidelines to direct us in this phase.”

“For the vast majority of people,” says Aitcheson, “going above 6-8 mg per day is not likely to be worth it.” Trying a higher dose requires a new script, so talk it over with your physician at a follow-up visit.

Will LDN Stop Working?

It’s possible, but physicians seldom encounter patients who develop tolerance to LDN.

Drugs that target the neurons (mostly the receptors that produce transmitters) often lead to tolerance. Returning the microglia to their normal resting state should not cause tolerance, but no one knows for sure.

“Lifestyle measures (exercise, sleep, diet, etc.) must be put in place when the effect of LDN is good,” says Aitcheson. “This strengthens people’s reserve, so if LDN stops working, it won’t be so devastating.” He also points out that patients may not be experiencing a loss of LDN efficacy, but rather a symptom flare.

LDN and Opioids

Naltrexone blocks the action of opioids, so do you have to abstain from taking this class of meds while trying LDN? Maybe not if you are only taking an opioid on an intermittent basis during the day and you take the LDN at night.

“One of two things may happen,” says Mackey. “Patients may not notice any difference in the opioid’s effectiveness, or they may experience a reduced benefit of the opioid due to the LDN.” If you are on an opioid, Aitcheson adds, “Expect more gastrointestinal side effects for the first few weeks of LDN.”

Whether you take an opioid on bad days or are on tramadol (a weak opioid), Fishman still recommends LDN. However, his standard dosing schedule is to start at 1 mg and increase 0.5 mg per week until 4.5 mg/day is reached. If a person is on an around-the-clock opioid, very low-dose naltrexone (0.5 mg or less) may be used as the starting dose.

“In this era of the opioid epidemic where opioids were prescribed when all else failed for chronic pain,” says Fishman, “we need to consider positioning alternative strategies early on, including LDN.”

Compounding Pharmacies

LDN needs to be compounded as an immediate-release, short-acting formula. If you take LDN at bedtime, it is out of your system by morning.

Whether you use a local compounding pharmacy or a mail-order company, make sure it is PCAB accredited. This means the pharmacy meets the Pharmacy Compounding Accreditation Board standards set forth in the United States. If you live outside the US, be sure your pharmacy meets the highest standards set forth by your country.

Naltrexone is dirt cheap. The cost of LDN has to do with the labor involved in making the capsules or tablets. Typically, local compounding pharmacy only offer LDN in capsule form, while a few mail-order companies dispense scored tablets.

“The price range is substantial,” says McKenzie-Brown. “When I found a pharmacy that compounded scored tablets, it substantially reduced cost.” She uses one-half tablets during the titration phase, then she switches patients to the more economical 90-day supply.

While going through a dosing up phase minimizes concerns about side effects, there are two disadvantages: increased cost and the inconvenience of requiring a second script for the target dose (usually 4.5 mg).

If you don’t want to hassle with mail-order pharmacies (or they are not available in your country), expect to pay about $1/capsule. Shop around though, because some places will charge you double.

Getting LDN

How does your doctor write the scripts for dosing up and testing LDN? Whether you work with a local or a mail-order compounding pharmacy, the information you need to know is below.

Local Pharmacies

If your local compounding pharmacy dispenses LDN capsules at a reasonable price, use them for the first three months. If LDN provides symptom relief, you can switch to a mail-order pharmacy for the long run.

If you want to dose up, rather than start out at 4.5 mg at bedtime, you will need two scripts (get both from your doctor in the same visit). Assuming you start at 1.5 mg per day, your physician will need to write the following two scripts:

Script #1
1.5 mg capsules of immediate-release naltrexone – quantity 21
Instructions: take one capsule at bedtime for the first week, then take two capsules at bedtime for the second week.

Script #2
4.5 mg capsules of immediate-release naltrexone – quantity 90
Instructions: take one capsule at bedtime

NOTE: If you are really drug-sensitive, ask your physician to change the dosing schedule for Script #1 to two weeks and increase the quantity to 42. Just keep in mind that Script #1 is an added expense to your LDN trial period.

If you want to just give 4.5 mg per day a try, you only need the second script above. However, you may ask your doctor to write Script #1, but not fill it unless you encounter side effects that can’t be managed.

Mail-Order Pharmacies
For Scored LDN Tablets

Care First Specialty Pharmacy in Mount Laurel, NJ provides scored LDN tablets in doses ranging from 0.5 mg to 6 mg. They are approved to ship to all 50 states plus the Virgin Islands, and their prices are excellent at $0.57/tablet. However, Avrio Pharmacy of Scottsdale, AZ offers a unique product: double-scored LDN “Quad” tablets. This means that you can dose up on 4.5 mg tablets and conveniently stay with the same script for the long run. Unfortunately, Avrio is not licensed to ship to 12 states.

Care First Specialty Pharmacy
www.cfspharmacy.pharmacy
TEL: (844) 822-7379
FAX: (844) 922-7379
Standard Shipping: $3.95; Cost for 90 scored tablets:
Any strength 0.5 mg – 4.5 mg is $46.95
5 mg is $48.95
6 mg is $59.95

Anything above 6 mg must be made into capsules; expect to pay closer to $80.

Dosing up in 1.5 mg increments requires 3 mg tablets; 135 costs $67.50
Patients on around-the-clock opioids may talk to their doctor about taking the 0.5 mg strength (each half tablet is only 0.25 mg). Care First also makes available “ultra” low dose naltrexone in micro-milligrams (mcg).

Patient registration forms, as well as prescriber forms, are available on their website. Or call to set up your profile for shipping address and payment info.

Avrio Pharmacy
avriorx.com
TEL: (480) 270-6700
FAX: (480) 270-6701
Standard Shipping: $8; Cost for 90 Quad tablets:
4.5 mg (1.125 mg segments) is $60.00
2 mg (0.5 mg segments) is $60.00
6 mg (1.5 mg segments) is $75.00

Three months at 4.5 mg/day is recommended before giving up on LDN. Many patients won’t encounter appreciable side effects at this target dose to warrant dosing up. However, if you want the safety-net of being able to drop down in dose for a few days without having to fill a second script, the 4.5 mg quad tablets may be ideal for you. Just keep in mind that Avrio does not ship to the following states: AL, AR, IA, LA, MD, MS, NJ, ND, OK, TN, VT, WV.

The following medical journal article is great for healthcare providers who are hesitant to let you try LDN:

Aitcheson N, et al. Aust J Gen Pract. 2023. Low-dose naltrexone in the treatment of fibromyalgia: A systematic review and narrative synthesis 52(4):189-195. Free Report

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Is Fibro an Autoimmune Disease?

Treatment & Research News

Is Fibro an Autoimmune Disease?

Could something in the blood be causing your fibromyalgia? Yes, says  Andreas Goebel, M.D., Ph.D., of Liverpool, UK, along with his collaborators at King’s College London and the Karolinska Institute in Sweden.* The researchers injected mice with serum from fibromyalgia patients and within two days the mice developed widespread pain. The immunoglobulin G (IgG) portion of the serum, which is loaded with antibodies, was found to be the pain-producing culprit. Serum without IgG had no impact.

Goebel suspects fibromyalgia may have an autoimmune basis and that autoreactive IgG might be responsible for the symptoms. But how could this occur in the absence of tissue damage that normally exists in autoimmune diseases? Goebel says the antibodies could be attacking the sensory nerves or nearby cells, which could increase the pain signals traveling to the spinal cord.

Examination of the serum-injected mice revealed IgG antibodies clustered around special immune cells called satellite glial cells or SGCs. As you can see from Figure 1, the SGCs surround the cell bodies of the sensory nerves. An attack on the SGCs can amplify sensory signals just before they enter the spinal cord. In addition, the chemicals secreted by the SGCs can enter the cerebral spinal fluid (which bathes the cord and brain) to cause more havoc.

Pain all over in the absence of obvious tissue destruction is a credibility nightmare for fibromyalgia patients. Yet, Goebel simply injected fibromyalgia serum into mice to cause pain, reduced activity (sign of fatigue?), sensitivity to cold, and reduced grip strength. Injecting serum from healthy subjects did not produce symptoms.

“Antibody-mediated immune processes in chronic primary pain (such as fibromyalgia) have been hiding in plain sight,” says Goebel. He adds that the antibody attack on the SGCs can’t be imaged, and standard lab tests cannot detect this process. Goebel’s findings also challenge the assumption that a person’s pain level corresponds to the degree of visible tissue destruction. 

Injecting serum from patients into rodents to see if the symptoms can be reproduced is called a passive transfer study. It’s only been done in a few other diseases. Although the current project involved patients from two different centers, the findings still need to be replicated. 

One last point: people are not mice. So how do the researchers know the SGCs are the cells under attack in humans? Goebel’s colleagues incubated the antibodies from fibromyalgia patients and healthy controls with SGCs taken from seven post-mortem subjects (none had fibromyalgia). Using a fluorescent dye and electron microscopy, the SGCs were heavily coated with antibodies from fibromyalgia patients. It’s as though the fibromyalgia antibodies are drawn to the SGCs like iron to a magnet.

Game Changer for Fibromyalgia

If Goebel’s work stands the test of time, fibromyalgia will be an autoantibody type of pain. This could be a game changer for fibromyalgia research because the condition is currently viewed as a dysfunctional central nervous system. Although plenty of evidence shows the brain and spinal cord do not operate properly, the cause remains unknown. However, if antibodies are attacking the SGCs, this could be the autoimmune trigger that causes the nervous system commotion.

Research points to multiple abnormalities in the central nervous system. The spinal cord contains too many pain messengers and not enough soothers. The pain control system doesn’t work, and the brain centers don’t provide a united front to contain the barrage of pain signals. Sleep is disrupted, hormones are dysregulated, and cognitive functions are diminished.

The foregoing findings are often packaged into the central sensitization theory to explain pain without a triggering source. It assumes that the central nervous system is hypersensitized to incoming sensory signals, but no one knows why. This, in turn, leads to an abnormally exaggerated response. In the case of fibromyalgia, a harmless trickle of nerve impulses might be transformed into widespread pain and other symptoms.

“Some say you don’t need a driving source to sustain central sensitization,” says Goebel, “but it has never been shown convincingly in any animal model. That’s why many of us (physicians and researchers) never really believed it.”

IgG autoreactive antibodies clustered around the SGCs may provide the missing piece to the fibromyalgia puzzle. As shown in Figure 2, activated SGCs form a pain-generating circuitry up and down both sides of the spinal cord (each red dot represents thousands of SGC/neuron units). Hurting from head to toe would be expected, not questioned! The spinal cord and brain would naturally be thrown into turmoil.   

Study Implications

Wondering why your body is generating antibodies that attack the SGCs? Examining the mice won’t answer this question. “Our model takes it from the point where the IgG antibodies are already produced,” says Goebel. However, dissecting the tiny fraction of the IgG that is pathogenic (autoreactive) could lead to a disease marker. Goebel’s colleagues in Sweden are working on this.

What about treatments? As the IgG antibodies work their way out of the mouse’s body, the symptoms go away. So, approaches that dislodge the IgG antibodies from the SGCs should work, even if they do not stop the antibody production.

Currently, therapies in this category are extremely expensive and not yet available to fibromyalgia patients. However, a small “proof-of-concept” type of trial is underway to test an intravenous drug called rozanolixizumab. 

Alternatively, tempering the SGC activation that leads to amplification of the sensory signals might work to reduce fibromyalgia symptoms. For example, low dose naltrexone targets specific receptors on the SGCs to quiet them down. This approach could never be as effective as removing the harmful antibodies from the SGCs, but it’s available and cheap.

Presuming autoantibodies to your SGCs are driving your symptoms, this may explain why medications that work in the spinal cord produce dismal results. Examples include the three FDA-approved drugs (pregabalin, duloxetine, and Savella) that operate downstream of the SGCs. Using them could be the equivalent to putting a bucket under a leaky faucet, while targeting the SGCs would be more akin to repairing the faucet.

Bottom Line

Once Goebel’s work is replicated and the word spreads about the passive transfer study, fibromyalgia will gain more credibility. And using Goebel’s mouse model will help researchers identify the mechanisms responsible for fibromyalgia and develop effective treatments. It could be a long road ahead, but at least research will be moving in the right direction.

*  Goebel A, Krock E, Gentry C, et al., 2021. Passive transfer of fibromyalgia symptoms from patients to mice. J Clin Invest. 131(13):e144201.

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