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RTM: Smith, Terpening, Schmidt, Gums:
full text: aspartame, MSG, fibromyalgia 1.17.2 rmforall

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The Annals of Pharmacotherapy: Vol. 35, No. 6, pp. 702–706.
Relief of Fibromyalgia Symptoms Following
Discontinuation of Dietary Excitotoxins
Jerry D Smith,
Chris M Terpening,
Siegfried OF Schmidt,
and John G Gums
BACKGROUND: Fibromyalgia is a common rheumatologic disorder that is
often difficult to treat effectively.
CASE SUMMARY: Four patients diagnosed with fibromyalgia syndrome
for two to 17 years are described.
All had undergone multiple treatment
modalities with limited success. All had complete, or nearly complete,
resolution of their symptoms within months after eliminating monosodium
glutamate (MSG) or MSG plus aspartame from their diet.
All patients were women with multiple comorbidities prior to elimination

of MSG. All have had recurrence of symptoms whenever MSG is ingested.
DISCUSSION: Excitotoxins are molecules, such as MSG and aspartate, that
act as excitatory neurotransmitters, and can lead to neurotoxicity when
used in excess. We propose that these four patients may represent a
subset of fibromyalgia syndrome that is induced or exacerbated by
excitotoxins or, alternatively, may comprise an excitotoxin syndrome
that is similar to fibromyalgia. We suggest that identification of
similar patients and research with larger numbers of patients must be
performed before definitive conclusions can be made.
CONCLUSIONS: The elimination of MSG and other excitotoxins from the
diets of patients with fibromyalgia offers a benign treatment option
that has the potential for dramatic results in a subset of patients.

EXTRACTO
OBJETIVO: La fibromialgia es una afección reumática que muchas veces es
dificil tratar efectivamente.
RESUMEN DEL CASO: Se describen cuatro pacientes con el síndrome de
fibromialgia por una duración de dos a 17 años. Todas fueron tratatadas
con varios tratamientos con poco éxito. En todas se observó completa o
casi completa resolución de los síntomas en unos pocos meses después de
eliminar el glutamato modosódico (MSG) ± aspartame de su dieta.
DISCUSIÓN: Las excitotoxinas son moléculas, como MSG y aspartato, que
actuan como neurotransmisores excitatorios y que, en exceso, pueden
causar neurotoxicidad. Los autores sugieren que las cuatro
pacientes descritas representan un
subconjunto de pacientes con síndrome de fibromialgia
inducido u exacerbado por excitotoxinas o, alternativamente, un
subconjunto con un síndrome de excitotoxina que es similar a la
fibromialgia. La identificación de otros pacientes similares y mucho
más estudio es necesario antes de llegar a conclusiones definitivas.
CONCLUSIONES: La eliminación de MSG y otras excitotoxinas
de la dieta constituye una opción terapeútica para pacientes con
fibromylagia.
Este tratamiento benigno tiene el potencial para producir resultados
positivos dramáticos en un subconjunto de pacientes.
Christina Dalmady-Israel

RÉSUMÉ
RÉSUMÉ DU CAS: Cet article décrit quatre cas de fibromyalgie pour une
période de deux à 17 ans. Tous les patients ont reçu de nombreuses
modalités de traitement avec des résultats limités. Cependant, tous les
malades ont eu une résolution complète, ou presque complète, de leur
symptômes dans les mois suivant l'élimination du glutamate monosodique
(MSG) ± aspartame de leur alimentation. Ce sont toutes des femmes,
atteintes de nombreux problèmes médicaux avant l'élimination du MSG.
Toutes ont une recrudescence des symptômes à l'ingestion du MSG.
DISCUSSION: Les excitotoxines sont des molécules, telles que le MSG et
l'aspartame, qui agissent sur les neurotransmetteurs excitatoires
et qui peuvent conduire à une neurotoxicité excessive.
L'hypothèse proposée ici est que ces quatre patientes
puissent présenter une forme de syndrome de fibromyalgie
induit ou exacerbé par les excitotoxines ou,
alternativement, puissent comprendre un syndrome d'excitotoxine
similaire à la fibromyalgie. L'identification d'autres patients
avec des symptômes similaires ainsi qu'une recherche poussée
sur un plus grand nombre de sujets doit être effectué avant
qu'on ne tire de conclusions définitives.
CONCLUSIONS: L'élimination du MSG et des autres excitotoxines de la
diète des patients atteints de fibromyalgie offre une option
thérapeutique bénigne avec un potentiel de résultats impressionnants
chez un certain nombre de sujets.
Louise Gagnon

KEY WORDS: aspartame, fibromyalgia, monosodium glutamate.
Ann Pharmacother 2001;35:702–706.

Fibromyalgia syndrome occurs in 3–6 million patients in the
US. [1] It is the third most commonly diagnosed rheumatologic disorder
(after osteoarthritis and rheumatoid arthritis).
Most patients are women, with
a median age of onset of 29–37 years;
the median age of formal diagnosis is 34–53 years. [2]
This disabling disorder is characterized
by widespread pain and tenderness, fatigue, morning stiffness,
and sleep disturbance
Diagnosis criteria have been developed by the American College of
Rheumatology [Appendix 1] [3],but, unfortunately,
the cause of fibromyalgia syndrome is unknown.

Theories have included alterations in neurotransmitter regulation
(especially serotonin); hormonal control problems (especially of the
hypothalamic–pituitary–adrenal and growth hormone axes); immune system
dysfunction; problems in sleep physiology; abnormal perception of
bodily sensations; stress; viral pathologies; local hypoxia;
and disturbances in
muscle microcirculation, adenosine monophosphate, and creatine
concentrations. [1]

Current evidence most strongly supports a
neurochemical or neurohormonal hypothesis. [4-6]

We describe four patients who experienced a dramatic recovery from
fibromyalgia syndrome by eliminating certain preservatives and food
additives, mainly monosodium glutamate (MSG), from their diet. All four
patients had fibromyalgia syndrome characterized by tenderness and pain
at all tender points, fatigue, sleep disorders, and irritable bowel
syndrome. [Table 1]
This appears to be the first such report in the medical
literature, based on the absence of results in a MEDLINE search.

CASE REPORTS
CASE 1
A 40-year-old white woman was diagnosed in 1987 with moderately
aggressive fibromyalgia symptoms that had been very difficult to manage
with traditional approaches.
She also had atypical chest pain and carpal tunnel syndrome.
This patient did a tremendous amount of reading in the
lay press regarding fibromyalgia, allergies, food allergies,
and “food toxins.”
She treated her daughter, who had a number of skin allergies, with a
diet that was basically additive-free,
with an emphasis on corn derivatives and MSG.
When her daughter's allergy problem resolved,
the woman decided to follow the same dietary regimen.
The patient had, over time, what she and her
physician considered complete resolution of fibromyalgia symptoms. The
carpal tunnel symptoms disappeared, she began to sleep better, and
believed that her memory improved as well. The patient rechallenged
herself with the food products she felt were the offending agents, and
the symptoms returned. She restricted her diet again, and the symptoms
resolved.

CASE 2
A 37-year-old white woman, the sister of the patient described above,
had multiple medical problems including fibromyalgia syndrome
affecting all 18 tender points,
allergic rhinitis, irritable bowel syndrome, dysuria,
stress reaction, depressive disorder, temperomandibular joint (TMJ)
disorder, facial pain, carpal tunnel syndrome, anxiety, mitral valve
prolapse, and dyslexia. She underwent a total hysterectomy in 1991 and
surgery to open her left nasal passage. This woman was in a basically
nonfunctional condition, much worse than her sister. She reported pains
she had experienced since she was 15 years old. She did not recall a
traumatic or emotional event prior to the onset of the pain.
The pains progressively worsened, especially after the birth of her
first child in 1979, and never completely resolved. She underwent
several tender point injections with bupivacaine,
with temporary relief.
The patient then began a corn-free diet
and was able to decrease her amitriptyline dose
from 100 to 25 mg/d and discontinue sertraline and lorazepam.
After several months of using a diet free of aspartame and MSG,
she had no pain in any of the tender points,
no further abdominal or facial pain, no carpal tunnel syndrome,
and no further depression or anxiety;
a reevaluation also showed no sign of dyslexia.
The woman also reported
improvement in her memory. Symptoms of fibromyalgia recur when she
unknowingly eats foods that contain MSG or aspartame. At times, she
experiences an episode for 24–48 hours, and then researches if
anything in her foods could have caused it.
She often calls a food manufacturer to
learn more details about the ingredients.
Both the number of medications and
number of office visits were markedly reduced after elimination of
aspartame and MSG. On reevaluation, she had no further
findings consistent with fibromyalgia,
allergic rhinitis, irritable bowel syndrome, dysuria,
stress reaction, chronic depressive disorder, TMJ disorder, or chronic
fatigue issues.

CASE 3
A 57-year-old white woman had a past medical history of chronic
musculoskeletal pain (very diffuse), chronic fatigue, migraine and
tension headaches, irritable bowel syndrome, allergic rhinitis,
gastroesophageal reflux disease, anxiety and depressive disorder,
as well as a diagnosis in 1994 of fibromyalgia syndrome involving 16 of
18 tender points. Despite a major workup and extensive therapies,
including physical therapy,
electro-acupuncture, chiropractic treatment, injection treatment,
counseling, medication, and lifestyle adjustment, her condition
severely worsened, and she was placed on a diet to eliminate MSG and
aspartame.
Within two months, she improved partially with no further headaches,
allergic symptoms, or irritable bowel syndrome symptoms. Within three
months, she had no further diffuse musculoskeletal pain and
only continued to have very localized lower back
and bilateral shoulder pain attributed to osteoarthritis.
By seven months, she experienced no pain, but had
achieved marked improvement of the chronic fatigue, and reported
feeling “very good.”
If she inadvertently uses MSG, the symptoms recur.
The number of medications she takes was reduced from 15
to only estrogen for hormone replacement.

CASE 4
A 37-year-old African-American woman was diagnosed with fibromyalgia
syndrome involving all 18 tender points in 1985. Furthermore, she had
ongoing diffuse multiple symptoms including severe fatigue, epigastric
pain, retrosternal pain, precordial pains, symptoms consistent
with some reflux (none could be substantiated with a 24-h pH study),
major depressive episodes, chronic migraine and tension headaches,
chronic musculoskeletal pain with costochondritis
and myofacial pain component,
chronic TMJ dysfunction, emphysema, chronic postnasal drip,
hyper chol esterolemia, hypertriglyceridemia, and obesity.
At that time, she was receiving fluoxetine,
triamterene/hydrochlorothiazide,
nasal triamcinolone, fluticasone metered-dose inhaler (MDI),
ipratroprium bromide MDI, albuterol MDI as needed, ranitidine twice
daily, isosorbide dinitrate, buspirone, lorazepam, simvastatin, and
propoxyphene/acetaminophen,
along with repeated trigger point injections of bupivacaine.
The patient was told to try to eliminate MSG from her diet. After two
months, she stated that she had improved dramatically. The headaches,
as well as shoulder, neck, and abdominal pain,
decreased from 8 of 10 to 3 of 10 in severity.
After another month of elimination of MSG, the woman
experienced even further pain improvement and believed that she was at
70% of her normal health. Her ranitidine dose was cut to once daily,
the buspirone dose was decreased by half,
propoxyphene/acetaminophen use decreased,
and isosorbide dinitrate was discontinued. Secondary to her
financial situation, she was unable to adjust her diet completely;
whenever she uses certain foods, especially those that include MSG, she
develops recurrent pain. She intermittently tried to stop buspirone
completely, but felt very anxious and restarted the medication.

Discussion
MSG, the sodium salt of the amino acid glutamic acid or glutamate,
is an additive used to enhance the flavor of certain foods.
It does not have a flavor of its own,
but is believed to enhance the taste of other foods
by stimulating glutamate receptors on the tongue.

MSG was classified by the Food and Drug Administration (FDA) as a
generally recognized as safe (GRAS) substance in 1959, after the 1958
Food Additives Amendment to the Federal Food, Drug, and Cosmetic Act
required approval for new food additives.
This classification meant that MSG and other GRAS substances,
such as salt and baking powder,
were grandfathered as harmless food substances
due to their history of safe use.
Since then,
several expert committees have investigated MSG and determined that it
is safe for use by the general public.[7-9]

Between 1980 and 1994, the Adverse Reaction Monitoring System in the
FDA's Center for Food Safety and Applied Nutrition received
600 reports of problems due to MSG.
Complaints, since verified in susceptible individuals, [10]
included symptoms such as headache, weakness, muscle
tightness, numbness or tingling, and flushing. Collectively, these
symptoms have been termed the MSG symptom complex.
The complaints submitted to the FDA, several books, and a television
news show reporting the possible dangers of MSG
prompted a review of the safety of the additive by the Federation of
American Societies for Experimental Biology (FASEB). The 1995 FASEB
report [11] reaffirmed the FDA's belief that MSG and related substances
are safe food additives for most people.

However, that report [11] identified two groups of people who may
develop complications from MSG.
One group may be intolerant of MSG when the substance is eaten in large
quantities, and develop the MSG symptom complex.
The second group contains
patients with severe, poorly controlled asthma, whose asthma may worsen
after they eat foods containing MSG, in addition to being prone to MSG
symptom complex.

Aspartame was first marketed in 1981. It is a dipeptide of aspartate
and phenylalanine used in foods, beverages, and drugs.
[Along with the 10 % methanol (wood alcohol) component)...]
In animal models, aspartame has been associated with an increased
incidence of brain tumors. [12]

Anecdotally, aspartame use in humans has been linked with head aches,
seizures, dizziness, movement disorders, urticaria, angioedema, and
anaphylaxis. However, in placebo-controlled trials, only the potential
for headache has been verified, even among self-identified susceptible
patients. [13]

With the discovery of excitatory amino acid (EAA) transmitter systems
and identification of EAA receptor subtypes (N-methyl-d-aspartame
[NMDA],
kainic acid, and amino-3-hydroxy-5-methyl-isoxazole-4-proprionic acid)
and their antagonists, it has become widely accepted that glutamate,
aspartate, and other environmental substances have neurotoxic
(excitotoxic) effects in the human nervous system. [14]

The adverse reactions to MSG have been theorized to be due to MSG's
actions at glutamate receptors in glutamate-responsive tissues. Studies
have shown that glutamate acts as a neurotransmitter in the brain, and
abnormal function of glutamate receptors has been linked to neurologic
disorders such as Alzheimer disease and Huntington's
chorea. [15] Injections of glutamate in laboratory animals have
resulted in damage to nerve cells in the brain.

Aspartate is equipotent to glutamate in destroying hypothalamic neurons
and has additive neurotoxic effects when the two are combined.
Aspartate is derived from the gut hydrolyzation of aspartame. It is a
much more
potent flavoring agent than glutamate and is, therefore,
used in smaller doses.
However, even in small amounts,
aspartate has additive effects to any glutamate. [14]

Normally, people can consume large amounts of dietary glutamate,
and the body can produce and eliminate glutamate efficiently.
Glutamate is rapidly absorbed
into the bloodstream after oral administration.
In fact, when compared with mice and monkeys,
humans demonstrated higher plasma peaks
and AUCs after receiving MSG 150 mg/kg. [14]

Glutamate crosses the blood–brain barrier only by active transport, and
concentrations in the brain are kept low and independent of plasma
concentrations. However, glutamate freely enters brain regions that
lack blood–brain barriers (circumventricular organs, e.g., the
hypothalamus).

It has been shown [14] that glutamate can destroy circumventricular
organ neurons by an excitotoxic mechanism (via the NMDA receptor)
in all animal models appropriately tested
(cats, chickens, guinea pigs, hamsters, mice, monkeys, rabbits).

In fact, much of the research performed proving that
glutamate was safe for human consumption may have been flawed.
Tests using infant monkeys anesthetized these animals with
phencyclidine, now known to inhibit the neurotoxic effects of glutamate
on the hypothalamic neurons
by its potent antagonism of the specific subtype of NMDA receptor. [14]

As the etiology of fibromyalgia remains unclear, it is difficult to
pinpoint an exact role for glutamate in its exacerbation or induction.
However, several potential hypotheses can be envisioned. For example,
when glutamate enters the endocrine hypothalamus, it interacts with EAA
receptors on the surface of the hypothalamic neurons, which then
stimulate the release of hypophysiotrophic-releasing factors.
These factors trigger the release of pituitary hormones
into the general circulation, which
can disturb hormonal biorhythms. The use of intravenous glutamate or
related analogs in prepubertal monkeys induces a release of growth
hormone, luteinizing hormone, and prolactin. [14]

However, recent tests [16] in healthy adult humans
showed no increases in pituitary or cortical
hormones in response to orally administered MSG.

These findings do not
preclude the possibility that a different response might occur in
subsets of fibromyalgia patients.
Up to 35% of subjects with fibromyalgia in
various studies demonstrate abnormal suppression to the nighttime
administration of dexamethasone. Additionally, patients with
fibromyalgia have reduced 24-hour free cortisol excretion in the urine,
loss of diurnal variation of cortisol concentrations,
and exaggerated adrenocorticotrophic hormone,
but blunted cortisol response to administration of
corticotropin-releasing hormone or to insulin-induced hypoglycemia,
and reduced adrenocortical activation
in response to exhaustive exercise. [17]

Another plausible explanation involves the role of glutamate in chronic
pain sensitization. [18]
Prolonged firing of certain peripheral nociceptor neurons causes
release of glutamate.
This acts on central NMDA receptors to produce chronic
sensitization at the level of the spinal cord. Perhaps exogenous
glutamate may act to produce similar sensitization in a small subset of
patients.

Alternatively, MSG may represent a specific chemical intolerance,
yielding a fibromyalgia-like picture as a result of some
cross-sensitization. [19]

Without further prospective studies in susceptible patients, clarifying
the mechanism of glutamate toxicity remains, at best, difficult.

Obviously, this case series does not establish a cause–effect
relationship between excitotoxins and fibromyalgia syndrome.
The potential relationship is further complicated by the often
inconsistent manner in which fibromyalgia syndrome is diagnosed and
documented in common practice.
However, the Naranjo probability scale [20]
places this drug reaction in or near the probable range.

As MSG is nearly ubiquitous in processed food,
appearing under many names, including
gelatin, hydrolyzed vegetable protein, textured protein,
and yeast extract, most people
in developed nations are exposed to it from a very young age.

The general population has less exposure to aspartame. None the
less, it is the dominant artificial sweetener on the market, and has
been since its approval in 1981.

In the four patients reported here, the
adverse reaction improved on discontinuation and reappeared under
retrial.

As the patient in case 4 reduced, but did not eliminate, MSG and
symptoms were reduced but not eliminated, one may argue a dose–response
effect.
Still, prospective, placebo-controlled trials are needed to verify the
finding.

Summary
As the mystery of fibromyalgia syndrome unfolds and the diagnosis gains
greater acceptance and awareness in both the medical and lay
communities, one should remember that multiple etiologies of this
syndrome exist. Our four patients were diagnosed with fibromyalgia
syndrome that met the typical criteria.
All also had allergic rhinitis symptoms and responded
to a diet of mainly MSG elimination, aspartame elimination, or both
with resolution of their symptoms.
This excitotoxin-induced or -exacerbated
fibromyalgia could be due to the mechanisms described above, but other
mechanisms may remain unknown.

We also do not believe that sensitivity to MSG
is the cause of all cases of fibromyalgia syndrome,
as many of our patients have not responded to
our recommendations of elimination of the excitotoxins.

There may also be many more yet unknown, or widely unrecognized,
excitotoxins that could also cause fibro myalgia syndrome. Even in the
patients described here, we cannot state unequivocally that MSG caused
their fibro myalgia. However, elimination of MSG and/or aspartame did
result in striking improvements in their symptoms. Identification of
similar patients and much more research must be performed before
definitive conclusions concerning causation can be made. This subgroup
of fibromyalgia syndrome patients needs to be identified by
physicians and other healthcare providers to initiate appropriate
dietary adjustments that may lead to
significant improvement of symptoms, and to further
delineate the mechanisms involved in their sensitivity.

References
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Fibromyalgia syndrome: a review.
Am Fam Physician 1996;53:1698–704.

2. Krsnich-Shriwise S
Fibromyalgia syndrome: an overview.
Phys Ther 1997;77:68–75.

3. Wolfe F, Smythe HA, Yunus MB, Bennett RM
Bombardier C, Goldenberg DL.
The American College of Rheumatology 1990 Criteria for the
Classification of Fibromyalgia.
Report of the Multicenter Criteria Committee.
Arthritis Rheum 1990;33:160–72.

4. Russell IJ
Advances in fibromyalgia: possible role for central neurochemicals.
Am J Med Sci 1998;315:377–84.

5. Crofford LJ
Neuroendocrine abnormalities in fibromyalgia and related disorders.
Am J Med Sci 1998;315:359–66.

6. Neeck G, Riedel W
Hormonal perturbations in fibromyalgia syndrome.
Ann N Y Acad Sci 1999;876:325–38.

7. Select Committee on GRAS Substances.
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of protein hydrolyzates as food ingredients.
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SCOGS-37b-supplement 1980b. Prepared for the Food and Drug
Administration under contract no. FDA 223-75-2004 by the
Life Sciences Research Office,
Federation of American Societies for Experimental Biology.
Available from Special Publications Office, FASEB, Bethesda, MD.

8. Joint FAO/WHO Expert Committee on Food Additives
L-glutamic acid and its ammonium, calcium, monosodium and potassium
salts
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evaluation of certain food additives and contaminants.
New York: Cambridge University Press. 1987:97–161.

9. International Glutamate Technical Committee.
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Atlanta, GA: The Glutamate Association, 1991.

10. Yang WH, Drouin MA, Herbert M, Mao Y, Karsh J
The monosodium glutamate symptom complex:
assessment in a double-blind,
placebo-controlled, randomized study.
J Allergy Clin Immunol 1997;99:757–62.

11. Raiten DJ, Talbot JM, Fisher KD, eds.
Life Sciences Research Office Report.
Executive summary from the report.
Analysis of adverse reactions to monosodium glutamate (MSG).
J Nutr 1995;125 (suppl).:2892–906. s.

12. Olney JW, Farber NB, Spitznagel E, Robins LN.
Increasing brain tumor rates: is there a link to aspartame?
J Neuropathol Exp Neurol 1996;55:1115–23.

13. Van den Eeden SK, Koepsell TD, Longstreth WT, van Belle G, Daling
JR, McKnight B
Aspartame ingestion and headache: a randomized crossover trial.
Neurology 1994;44:1787–93.

14. Olney JW
Excitotoxins in foods.
Neurotoxicology 1994;15:535–44.

15. Choi DW
Glutamate neurotoxicity and diseases of the nervous system.
Neuron 1988;1:623–34.

16. Fernstrom J
Pituitary hormone secretion in normal male humans:
acute responses to a large, oral dose of monosodium glutamate.
J Nutr 2000;130 (suppl 4S).:1053–7. S.

17. Demitrack MA
Neuroendocrine correlates of chronic fatigue syndrome: a brief review.
J Psychiatr Res 1997;31:69–82.

18. Bennett GJ
Update on the neurophysiology of pain transmission and
modulation: focus on the NMDA-receptor.
J Pain Symptom Manage 2000;19 (suppl 1):S.:2–6.

19. Bell IR, Baldwin CM, Schwartz GE
Illness from low levels of environmental chemicals:
relevance to chronic fatigue syndrome and fibromyalgia.
Am J Med 1998;105 (suppl 3A).:74–82. S.

20. Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA
A method for estimating the probability of adverse drug reactions.
Clin Pharmacol Ther 1981;30:239–45.

Appendix I
American College of Rheumatology Diagnostic Criteria for
Fibromyalgia [3]
[History of Widespread Pain over most areas of body.
and Pain on digital palpitation in 11 of 18 (bilateral)
listed sites of tender points:]

Jerry D Smith PharmD, Clinical Pharmacist
Malcolm Randall Veterans Affairs Medical Center, Gainesville, FL

Chris M Terpening PhD PharmD, Clinical Pharmacy Fellow
Departments of Pharmacy Practice and Community Health & Family Medicine
University of Florida, Gainesville, FL

Siegfried OF Schmidt MD PhD, Clinical Assistant Professor
Department of Community Health & Family Medicine, University of Florida

John G Gums PharmD, Professor
Departments of Pharmacy Practice and Community Health & Family Medicine
University of Florida

Reprints: Chris M Terpening PhD PharmD, 625 S.W. 4th Ave.
Gainesville, FL 32601-6430, FAX 352/392-7766
cmt@...

Tables
Table 1. Fibromyalgia
Symptoms [1,3]
[Pain:
Prevalence
98 % widespread
85 neck
79 low back
72 posterior thorax
56 >= 15 painful sites
53 headache
41 dysmenorrhea

Other
81 fatigue
77 morning stiffness >15 min
75 sleep disturbance
63 paresthesias
48 anxiety
36 dry mouth
31 prior depression
30 irritable bowel syndrome
26 uninary urgency
17 Raynaud's phenomenon
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