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Date:         Tue, 28 Jul 1998 16:28:11 -0400
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To:           Mark London <MRL@PSFC.MIT.EDU>

                  Alternative Treatments for Fibromyalgia

                           Updated July 27, 1998

                    Copyright (C) Steve Emerson 1997, 1998


   This document contains short descriptions of some alternative
   treatments for fibromyalgia (FM). Nearly all of these treatments are
   experimental (the exceptions being 5-HTP, Dr. Lowe's use of Cytomel,
   exercise, and acupuncture). My justification for the use of
   experimental therapy in the treatment of fibromyalgia can be found at
   this http://www.geocities.com/HotSprings/6028/altjust.htm


   Serotonin

   Studies have found PWFM (patients with FM) low in both tryptophan and
   serotonin. Serotonin is normally synthesized from tryptophan. A
   tryptophan deficiency with similar biochemical markers has been found
   in other diseases such as cancer and AIDS. As with most FM biochemical
   abnormalities, determining to what degree the low tryptophan is cause
   vs. effect is the challenge.

   Serotonin is a critical neurochemical and has a multitude of functions
   in the body. It plays a role in sleep, mood, appetite, immune
   function, pain sensitivity, and hormone regulation. A more complete
   discussion of serotonin can be found at this link.

   Many PWFM are taking melatonin for sleep. But since melatonin is
   normally synthesized from serotonin, a deficiency in melatonin, if it
   exists, is most likely the result of low serotonin.

   Non-pharmacological treatment approaches to increasing serotonin
   include: reducing immune load, increasing energy metabolism, and
   taking serotonin precursors.

   Dopamine/norepinephrine

   Dopamine and norepinephrine have a role in providing energy, vigor,
   interest/motivation/attentiveness, mental alertness, and have a role
   in memory and cognition/IQ. Deficiencies in these transmitters can
   cause depression, lethargy, fatigue, and poor thinking/memory. A study
   found PWFM low in these two neurotransmitters (in CSF) [7], but this
   finding is not as well-established as the low serotonin finding.
   Clinical success has been reported with the use of both phentermine
   and Ritalin, two drugs which specifically increase brain dopamine. Dr.
   Charles Lapp, a CFS specialist in North Carolina, recently said in a
   talk, "Just so that you will know, we've had the best success with
   Ritalin." These dopamine-enhancing drugs also have the effect of
   increasing metabolism in the brain and central nervous system, and
   this benefit may actually be one of the reasons why they are working
   for PWFM.

   Many PWFM are currently taking two kinds of treatments: the uppers and
   the downers (informally speaking). They are taking uppers of some kind
   to provide energy and alertness in the day, and they are taking
   downers of some kind to provide relaxation and sleep at night. These
   treatments, though often the most practical, are superficial solutions
   to a deeper problem of disturbed body function. For example, immune
   activation due to allergy or in response to a virus can cause both
   fatigue and insomnia. However, these treatments can sometimes help to
   break the cycle of illness because they can eliminate certain
   perpetuating factors (e.g. low ATP, unrefreshing sleep) which are
   holding the body down.

   Serotonin and dopamine crudely correspond to these two neurochemical
   influences: serotonin relaxes and dopamine stimulates. A treatment
   protocol which is based strictly on increasing serotonin and dopamine
   in a combined manner has been employed in the treatment for FM. This
   is discussed in a later section.

   Serotonin precursors.

   The two precursors are tryptophan and 5-hydroxy-l-tryptophan (5-HTP).
   Serotonin is produced in this way: l-tryptophan -> 5-HTP -> serotonin.

   Either l-tryptophan or 5-HTP is taken at bedtime on an empty stomach.
   In some individuals, once-daily before bedtime dosing may not be
   sufficient, and between-meal use throughout the day may be required.

   1) Tryptophan -- the "co-factors" vitamin C, B3, B6 (consider taking a
   B-complex), and magnesium are all utilized in the metabolism of
   tryptophan. Insulin enhances the transport of tryptophan to the brain.
   So taking tryptophan with juice or carbohydrates can increase
   transport. On the other hand, increased glucose level can reduce (via
   somatostatin) the release of Growth Hormone (GH). GH is normally
   released during stage 4 sleep. Studies have found PWFM low in both
   tryptophan and GH. Besides serotonin production, tryptophan is also
   used in the production of NAD/NADH (required for normal cellular
   energy), niacin, picolinate, and proteins.

   2) 5-HTP -- a more direct precursor to serotonin. 5-HTP is available
   over-the-counter in supplement form.

   Some people respond better to tryptophan than to 5-HTP and vice-versa,
   and dose sensitivity varies across people as well. So experimentation
   may be required. According to the neurobalancing practitioners,
   increasing serotonin by itself (using the precursors) may improve
   sleep but may aggravate other symptoms (e.g. allergy, brain fog), and
   in this case additional dopamine/norepinephrine is needed to balance
   the serotonin and avoid the symptoms of a serotonin excess. This has
   not been scientifically established but is based on clinical
   experience. Whether or not this relative serotonin excess will occur
   is, according to theory, dependent on the person's unique
   neurochemical status.

   FM research suggests that, for PWFM, tryptophan is being metabolized
   into kynurenine[15] rather than 5-HTP and serotonin. Some folks
   therefore recommend against taking tryptophan for this reason, as it
   may simply increase kynurenine/quinolinic acid levels, and recommend
   5-HTP instead. A comparison of tryptophan and 5-HTP from a pro-5-HTP
   perspective can be found at:
   http://www.shaysnet.com/~wmson/5htp.htm

   A double-blind study found 5-HTP to be effective in the treatment of
   FM [1].

   3) 5-HTP + carbidopa -- carbidopa is a drug which prevents amino acids
   from being metabolized by the liver, so that instead they will enter
   the brain. So the purpose of the drug is to potentiate the effect of
   the precursors. However, there is debate whether carbidopa combined
   with 5-HTP truly increases 5-HTP transport to the brain, and carbidopa
   also produces side-effects. This is discussed at:
   http://www.life-enhancement.com/n31/n315htp.html

   Dopamine/norepinephrine precursors

   The amino acid precursors are phenylalanine and tyrosine. These
   transmitters are synthesized in the following way:
   l-phenylalanine -> l-tyrosine -> l-dopa -> dopamine -> norepinephrine

   L-phenylalanine OR l-tyrosine is taken in the daytime on an empty
   stomach. Another alternative supplement is DLPA, or DL-phenylalanine.
   It contains two different forms of phenylalanine, which, besides
   providing the dopamine precursor, is believed to raise the level of
   PEA and inhibit endorphin-degrading enzymes, thus having the potential
   to reduce pain. A study found DLPA just as effective at reducing
   depression as the anti-depressant drug imipramine. The rate-limiting
   step in the synthesis of dopamine is in the conversion from l-tyrosine
   to l-dopa, and this conversion step is more "saturated" than the
   tryptophan conversion. So dopamine levels may be more difficult to
   influence using the amino acids l-phenylalanine and l-tyrosine. On the
   other hand, l-dopa, the most direct dopamine precursor, bypasses this
   rate-limiting step. L-dopa is only available by prescription and is
   called Levodopa. Sinemet is a medication which combines l-dopa with
   carbidopa and is most often employed in the treatment of Parkinson's
   disease.

   Combined serotonin/dopamine precursors

   The combined use of serotonin and dopamine precursors is being
   employed in the treatment of FM. Dr. Pieter Hitzig in Maryland has
   developed a protocol called PHENFOUR which utilizes the serotonin and
   dopamine precursors with or without carbidopa. Dr. Hitzig has devised
   a way of taking the precursors so that they bypass the liver and more
   easily reach the brain. Dr. Dan Malone at the University of Wisconsin
   is employing a similar treatment protocol and is formerly researching
   this protocol for the treatment of FM. These neurobalancing protocols
   require that the patient manage her own serotonin/dopamine levels by
   monitoring her symptoms and taking the precursors as needed. Serotonin
   and dopamine are both powerful and significant neurochemicals which
   strongly impact brain and body function. They impact energy
   metabolism, hormone regulation, immune function, GI function, brain
   function, and pain sensitivity. Experimentation with this protocol is
   not recommended without supervision and training from a doctor who
   understands the specifics of the protocol, namely how to recognize
   symptoms of a serotonin vs. dopamine deficiency and excess.

   GABA

   GABA, like serotonin, is an inhibitory neurotransmitter which, when
   enhanced or increased, causes a sedative effect, and many PWFM are
   taking GABA to induce sleep. Alcohol and tranquilizers like valium are
   both known to enhance or stimulate GABA receptors in the brain. GABA
   is also available in supplement form. Twinlabs GABA Plus is one such
   product. Although people claim that GABA in this form does not pass
   the blood-brain barrier, my own experience with this supplement is
   that it does indeed produce intended effects. GABA is also an
   anti-convulsant, and it can be used to stop myoclonus or the "muscle
   jerks" which some PWFM suffer. The dopamine precursor l-dopa is also
   employed to treat myoclonus. GABA is also a muscle relaxant. However,
   those people who are suffering from chronic involuntary contraction of
   the muscles may wish to investigate therapies for magnesium deficiency
   and ATP deficiency, which are both documented in PWFM and are both
   known to cause this problem.

   GHB

   GHB, or gamma-hydroxybutyrate, is a natural biochemical produced by
   the body. It can now be synthesized and has been produced by
   compounding pharmacies for medicinal uses. One of those uses is sleep
   enhancement. GHB both induces sleep and promotes deep stage 4 sleep.
   GHB has unfortunately caught the interest of recreational drug users,
   and as a result several states have prohibited its use. As a result of
   the increasing governmental involvement in outlawing GHB, compounding
   pharmacies in the US have ceased to produce it. Proponents of GHB have
   argued that GHB has been stigmatized and the ban does not have any
   basis in scientific findings. A thorough discussion of the science,
   medicinal benefits, and politics of GHB from a pro-GHB perspective can
   be found at:
   http://www.ceri.com/ghbpage.shtml

   Arginine and Ornithine

   Arginine and ornithine are amino acids which are precursors to the
   synthesis of Growth Hormone (GH). Studies have found PWFM low in GH.
   Studies have also shown that use of arginine can increase the levels
   of GH in the body (though I don't know if stage 4 sleep was a factor
   controlled for). GH is released by the body during stage 4 sleep.
   (N.B. Of note to herpes sufferers, Arginine inhibits L-Lysine. One may
   need to increase L-Lysine to prevent reactivation of herpes. MJK)

   Deprenyl citrate

   This is a drug which is a selective MAO inhibitor, i.e. an MAO-B
   inhibitor. This drug inhibits the MAO-B enzyme which is known to break
   down dopamine. Use of this drug can thus raise one's
   dopamine/norepinephrine level. Since this drug is a selective MAO
   inhibitor, it does not require special dietary measures to avoid
   tyramine-containing foods like cheese. This drug actually destroys
   MAO-B enzymes, and this is one fact to consider in the decision to
   take it. The recommended brand for deprenyl is Discovery brand
   citrate, not Eldepryl, which supposedly produces more side-effects.

   Energy Therapies

   A 1994 study by I. Jon Russell[15] found in PWFM abnormal levels of
   biochemicals related to energy metabolism. Levels of ATP, NADH, NADP
   were found to be low, and earlier studies have found pyruvate levels
   to be high. These findings also relate to the abnormalities in
   tryptophan metabolism mentioned earlier.

   A theory of FM which has been advocated in some quarters is the
   hypometabolism hypothesis. This theory states that the body is
   producing an inadequate amount of energy (ATP). All the functions of
   the body are dependent on ATP, including immune function, brain
   function, and hormone regulation. An ATP deficiency, i.e. insufficient
   energy metabolism, can produce the symptoms we typically see in
   hypothyroidism, which include brain fog, Attention Deficit Disorder,
   dry skin, depression, low resistance to infections, sleep disorders,
   cold extremities, allergy, etc. A good discussion of the possible role
   of reduced energy metabolism in the etiology of various diseases,
   including FM, can be found at:
   http://www.ceri.com/mito2.htm It is the similarity of the symptoms of
   FM and hypothyroidism which has led some to suspect hypometabolism as
   a cause or factor in FM. If hypometabolism does play a role in FM, it
   is not clear to what extent it is a result of abnormalities (such as
   infection or immune dysfunction or disordered sleep), and to what
   extent it produces them.

   Several treatment approaches along these lines are being pursued (some
   more direct than others):
   1) supplemental thyroid hormone ,
   2) mitochondrial support factors, 3) dopamine-enhancing therapies
   (there are dopamine receptors on the mitochondria), 4) guaifenesin
   (based on Dr St. Armand's hypothesis), 5) improving adrenal status, 6)
   reducing immune load and immune dysfunction , 7) investigation of
   anemia/hypoxia, 8) direct treatment of the sleep disorder.

   Thyroid hormone

   Dr. John Lowe in Texas believes that FM is a result of hypometabolism
   due to various forms of hypothyroidism. In his practice Dr. Lowe has
   found a subset of patients who have documented hypothyroidism. But he
   has also found a different subset of patients who have normal thyroid
   tests but suffer the same set of hypothyroid symptoms. Moreover, these
   patients improve upon administration of thyroid hormone. Dr. Lowe has
   postulated that this is form of hypometabolism caused by a cellular
   resistance to thyroid hormone, i.e. the body isn't properly responding
   to it. A discussion of the problem of hypothyroidism in FM, including
   Lowe's approach, can be found at:
   http://thyroid.miningco.com/library/weekly/aa090897.htm

   Dr. Lowe's treatment consists of T3/T4 thyroid hormone being given,
   with dosages customized for the patient, with the addition of
   mitochondrial support factors. Some doctors have opposed this
   treatment on the grounds that it is a risky use of T3 hormone, and can
   possibly cause a heart attack if overstimulation occurs. In any case,
   the supervising doctor and patient should monitor blood pressure and
   agitation and irritability.

   Proponents of a more general theory of ATP deficiency have argued that
   supplemental thyroid hormone is effective (in patients with normal
   thyroid tests) simply because it upregulates the activity of the
   mitochondria so that more ATP is produced, not because it addresses a
   problem specific to thyroid hormone. Dr. Lowe however believes that
   only thyroid insufficiency can explain the known facts.

   Mitochondrial support factors

   ATP is produced by the mitochondria, which reside in all the cells in
   the body. In order to properly produce ATP, the mitochondria require a
   number of biochemical factors. If there is a deficiency in one or more
   of the required factors, then mitochondrial function may become
   depressed. So another therapy being explored is to provide those
   specific factors which are required by the mitochondria to produce ATP
   (energy). These include: magnesium, B vitamins, malic acid,
   alpha-lipoic acid, fatty acids (e.g. fish oil or flax seed oil),
   l-carnitine, branched-chain amino acids, CoQ10, NADH, and various
   trace minerals. Mitochondrial function also requires normal oxygen
   transport, and so the problem of hypoxia/anemia is something which can
   be addressed. This includes addressing B-12, folic acid, iron, vitamin
   E, and hemoglobin status.

   CoQ10 and NADH are metabolic intermediates which play a significant
   role in mitochondrial function. Both have anecdotal support from some
   patients but also provide no beneficial effect for others. This may
   due to a variability in CoQ10 and NADH levels in the FM population.
   Many PWFM report that benefits of CoQ10 are not obtained until the
   dosage reaches 100 to 200 mg/day. A general explanation of energy
   metabolism and the function of the mitochondria can be found at:
   http://www.nadh.com/site7/GTactl05.htm#Top
   Although this is part of an infomercial from an NADH supplier, I
   believe it has some valuable educational information.

   Vitamin B-12 is another mitochondrial support factor which is
   receiving anecdotal support. Besides its role in oxygen transport,
   B-12 is also a "methyl donor" in a biochemical process which supports
   energy metabolism. A recent 1997 study indicates that B-12 may be
   deficient in PWFM[33]. The study found increased amounts of
   homocysteine in the cerbrospinal fluid (CSF) of patients, and also
   found that the B-12 levels in the CSF correlated with severity of
   symptoms. The authors of the study suggest that a B-12 deficiency
   exists in PWFM, since excess homocysteine is known to result from
   insufficient B-12, and symptoms were found to correlate with B-12
   levels.

   Several clinical studies have found that the combined use of magnesium
   and malic acid is effective in the treatment of FM. In addition, many
   FM/CFS specialists, such as Drs. Cheney, Lapp, Goldstein, and Flechas,
   include this supplement in their treatment regimen. Both substances
   play an integral role in mitochondrial function and the production of
   ATP. In addition, magnesium has been found deficient in PWFM and is
   discussed in a later section. The combination of magnesium and malic
   acid has also received anecdotal support from many PWFM. Often the
   maximum dose is required, i.e. 600mg magnesium and 2400 mg of malic
   acid. This combination is available in several speciality brands, such
   as SuperMalic, and also as magnesium malate. Patients report that not
   all brands are the same.

   Guaifenesin

   Discussed in Dr. Devin Starlanyl's FAQ. You may view it at:
   http://www.sover.net/~devstar

   The following are also sites which discuss this controversial
   treatment:

   Nancy Medeiros' Fibromeet Web Site:
   http://www.csusm.edu/public/guests/nancym/fibromt.htm

   this will point you to the study by Dr. Bennett.

   this will point you to the critics of Dr.Bennett:
   http://www.csusm.edu/public/quests/nancym/Contraversies.htm

   Herbs

   Two herbs, ginseng and gotu kola, have both been found to improve
   energy and mental alertness. Ginseng is known to contain a steroid,
   however.

   St. John's Wort is an herb which has been found to both relieve
   depression and improve sleep. It produces relatively few side-effects.
   It has been postulated that St. John's Wort produces its effect by
   enhancing both serotonin and norepinephrine, so this herb may have
   potential benefit for PWFM. For more information on this herb, see
   http://www.hypericum.com

   Valerian root has a relaxing and sedative effect. Gingko biloba
   enhances circulation and may be helpful for the problem of low blood
   flow and hypoxia, which may play a role in FM. Proanthenols (though
   not herbs per se) such as grape seed extract are antioxidants which
   provide an anti-inflammatory and antihistamine effect, and may help to
   reduce immune load. Herbalists have stated that this is a very
   simplistic assessment of herbal compounds, and that long-term use of
   these herbs may not be wise, and a competent herbalist can help the
   patient to better select appropriate herbs.

   Licorice is an herb which is known to increase cortisol, which is
   deficient in PWFM. Its use is recommended only for people suffering
   low cortisol and low blood pressure. Licorice is discussed in more
   detail in the cortisol section.

   Cortisol

   Several studies have found PWFM low in cortisol. The condition of low
   cortisol is called hypoadrenocorticism, hypocorticism, or adrenal
   insufficiency. Cortisol is a hormone produced by the adrenal gland,
   and has a role in the regulation of immune function, inflammation,
   blood sugar, and blood pressure. Cortisol is also the body's "stress
   hormone"; and the adrenals, in response from the brain, increase their
   secretion of cortisol upon stress, both psychosocial stress and
   physiological stress. Since FM is known to be "triggered" upon the
   incidence of trauma and infection, some researchers have argued that
   failure of the stress response system, which includes adrenal
   insufficiency, plays a major role in the pathophysiology of FM. The
   symptoms of low cortisol include low blood pressure, fatigue,
   dizziness, inflammation, and hypoglycemia. A helpful description of
   the adrenals and cortisol and adrenal insufficiency can be found at:
   http://pw1.netcom.com/~klkramer/Adrenal.htm

   A technical summary of adrenal insufficiency can be found at:
   http://blue.temple.edu/~pathphys/endocrine/adrenal%20insufficiency.htm
   l

   Dr. Jacob Teitelbaum, in his book From Fatigued to Fantastic, reports
   that he treats the hypocorticism with low doses of a supplemental
   cortisol (hydrocortisone) called Cortef. Testimony from patients
   on-line who have tried Cortef has been mixed. The medical profession
   has generally avoided hormone replacement therapy for adrenal
   insufficiency due to concerns about its safety. Dr. Teitelbaum
   responds to these concerns in his book and defends the use of Cortef.
   I simply pass this professional disagreement on to the reader.

   Another treatment option for cortisol enhancement is licorice extract.
   Licorice extract contains a compound called glycyrrhizin, which
   inhibits the enzyme in the body which breaks down cortisol. As a
   result, licorice extract can effectively increase cortisol levels both
   in the kidney and periphery. This makes licorice a potentially
   valuable therapy for adrenal insufficiency, since it is an alternative
   to supplemental hydrocortisone therapy and may avoid the problems of
   steriod use. Many licorice products sold at health food stores contain
   wildly varying amounts of glycyrrhizin. It is recommended that a
   quality brand is sought which indicates glycyrrhizin content, so that
   appropriate dosing can be achieved.

   Since licorice extract increases cortisol in the body (including
   increased blood pressure), its use is unsafe for people with normal
   cortisol levels and blood pressure. Licorice therapy is intended only
   for those suffering a cortisol deficiency and low blood pressure.
   Licorice extract should not be taken without a doctors approval if you
   have any medical problems other than fibromyalgia such as heart,
   liver, or kidney disease. Licorice extracts are also contradicted with
   many medications that PWFM now take daily so one must be sure to check
   with a professional or read up on the potential reactions of potent
   licorice extracts with other drugs.

   A good reference site listing all the therapeutic effects of licorice
   can be found at:
   http://www.uspharmacist.com/issues/1998/apr/licorice.htm

   A recent study has found that grapefruit juice has similar effects on
   cortisol as licorice, namely to inhibit the enzyme which degrades
   cortisol and effectively increase cortisol levels[34]. The inhibition
   in this case is brought about by bioflavonoids in the grapefruit.

   Licorice extract and grapefruit juice increase cortisol and blood
   pressure. They are intended here for people with low cortisol and low
   blood pressure. Dosage recommendations and warnings for licorice are
   based on studies and observations on the effects of licorice in people
   with normal cortisol and blood pressure, not people with
   hypocortisolism. One method for determining the necessary dosage is to
   start at a low dose, and then gradually increase the dose while
   monitoring blood pressure, and find the dose which produces a normal
   blood pressure. Those who wish to undertake this therapy are strongly
   urged to first have lab work done to verify hypocortisolism. One good
   test is a temporal adrenal profile, in which the patient takes regular
   saliva samples during a 24-hour period. The lab then produces a
   24-hour cortisol profile for the patient. This test is useful because
   it allows the doctor/patient to isolate when during the 24-hour period
   cortisol is actually low. This may be important because PWFM have been
   found to have low cortisol in the day but high cortisol at night. The
   test results can help the doctor determine a proper dosing schedule.

   It should be noted that the use of licorice and grapefruit juice are
   experimental therapies and have not been widely used for cortisol
   enhancement. The reason why licorice has been avoided is because its
   side-effects have been falsely attributed to a supposed
   aldosterone-like property of licorice, when in fact the hypertension,
   salt retention, and potassium loss from licorice are now believed to
   be caused by the excess cortisol it produces in people with normal
   cortisol. But in the context of FM, licorice is intended for people
   with low cortisol and hypotension.

   It is recommended that those undertaking these treatments monitor
   their blood pressure. A blood pressure increase is desired to correct
   the hypotension, but a high blood pressure should obviously be
   avoided. Besides hypertension, an additional symptom of excess
   licorice/grapefruit consumption is fluid retention and edema
   ("puffiness"). If this symptom occurs, the dosage should be reduced.

   DHEA and Pregnenolone

   A 1993 study found PWFM low in DHEA[19]. DHEA and Pregnenolone are two
   hormone precursors which have been found to improve immune function
   (both reduce allergy and strengthen immune defense), and improve brain
   function and metabolism. Pregnenolone is synthesized from cholesterol
   in the cells' mitochondria, and DHEA is produced from Pregnenolone by
   the adrenal gland. All human steroid hormones are produced from
   Pregnenolone and DHEA, including Progesterone, Estrogen, Testosterone,
   Cortisol, and Aldosterone.

   An introduction to Pregnenolone can be found at:
   http://www.smartbasic.com/glos.news/preg.plieotropic.html

   An introduction to DHEA can be found at:
   http://www.levo.com/moredhea.html

   A more technical introduction to DHEA can be found at:
   http://www.ceri.com/dhea.htm

   An interview of Steven Fowkes on DHEA and Pregnenolone can be found
   at:
   http://www.smartbasic.com/glos.news/DHEA.Pregnenolone.html

   The liberal use of hormones for the treatment of disease has some
   detractors. An argument against the hormone fad can be found at:
   http://www.jrthorns.com/Chall em/DHEA.html

   The transdermal form of DHEA has been recommended over the oral form.
   This is because much of the DHEA, when ingested, is broken down and
   eliminated by the liver. Secondly, excessive levels of Testosterone
   have been attributed to oral DHEA. The transdermal form is a gel which
   is applied to the skin. A DHEA-S test is strongly recommended before
   supplementation.

   DHEA secretion by the adrenals is known to be stimulated by Growth
   Hormone (GH), which has been found low in PWFM. Therefore, a DHEA
   deficiency may be secondary to a GH deficiency. However, GH
   supplementation is expensive and has not been generally pursued. Since
   GH is normally released by the brain during Stage 4 sleep, efforts to
   normalize GH have concentrated on restoring normal sleep function.
   However, DHEA supplementation, when DHEA-S has tested low, is being
   increasingly employed in treatment.

   Estrogen/progesterone

   Many female PWFM report changes in severity of their symptoms with
   fluctuations in the menstrual cycle. Secondly, many report changes in
   symptoms during pregnancy: some feel better during pregnancy, others
   feel worse. Abnormalities in the female hormones estrogen and
   progesterone may play a role in this illness. In recent years more
   attention has been given to the role of progesterone, rather than
   estrogen, in the etiology of PMS and menopause. The health aid
   industry also promotes progesterone in its sale of progesterone creams
   and such. A discussion of estrogen and progesterone abnormalities
   causing symptoms, with an emphasis on progesterone, can be found at:
   http://www.worldworks.net/health/prgrev.html

   On the other hand, in an interview by Dr. Teitelbaum, Dr. Elizabeth
   Vliet, author of Screaming to be Heard, reports that estrogen
   deficiency rather than progesterone deficiency is more common in the
   CFIDS patients she sees. This interview can be found at:
   http://www.endfatigue.com/Newsletter/sample1-interview.html

   Adding more confusion to this is the fact that CFIDS patients on-line
   have reported benefits from topical progesterone! Perhaps scientific
   research is needed resolve this. The usual caveats about hormone
   supplementation apply to progesterone as well. Blindly increasing
   progesterone to cause a progesterone excess may not be safe. A visit
   to a knowledgeable gynecologist or endocrinologist may be helpful.
   Lastly, abnormalities in estrogen/progesterone may be symptomatic of
   other problems (such as reduced energy metabolism, disordered sleep,
   etc), and the usual questions about the degree of cause vs. effect
   apply here as well.

   Reduce immune load

   The tryptophan deficiency findings and I. Jon Russell's findings on
   kynurenine [15] suggest that immune system activity might play a role
   in the etiology of FM. The depletion of tryptophan due to excess
   activity of the kynurenine pathway is known to occur upon immune
   system activation, (infection, allergy, inflammation). Dr. Russell
   says, "There is reason to believe that both of these abnormalities in
   the kynurenine pathway could result from an excess of gamma interferon
   activity."[5] Gamma interferon is a cytokine (chemical messenger)
   produced upon immune system activation due to infection or immune
   dysfunction. Unfortunately, few FM studies have been undertaken in the
   area of cytokines, especially interferon cytokines, and no FM findings
   on gamma interferon (to my knowledge) exist, however a study did find
   gamma interferon high in CFS. Interleukin-2[2], a different cytokine,
   has been found high in FM. But FM and CFS research on cytokines has
   yielded conflicting results. This may be due to the documented
   difficulties in obtaining accurate cytokine measurements. Immune
   activation and elevated cytokine production can be caused by immune
   dysfunction (e.g. due to adrenal insufficiency, mitochondrial
   insufficiency, disordered sleep, magnesium deficiency [17][18]);
   infection (viral, bacterial); or both.

   With respect to the problem of sleep, the FM researcher Harvey
   Moldofsky noted that immune activation can both cause and result from
   disordered sleep:

     The chronic fatigue syndrome and fibromyalgia have similar
     disordered sleep physiology, namely an alpha rhythm disturbance
     (7.5-11 Hz) in the electroencephalogram (EEG) within non-rapid eye
     movement (NREM) sleep that accompanies increased nocturnal
     vigilance and light, unrefreshing sleep. Aspects of cytokine and
     cellular immune functions are shown to be related to the sleep-wake
     system. The evidence suggests a reciprocal relationship of the
     immune and sleep-wake systems. Interference either with the immune
     system (e.g. by a viral agent or by cytokines such as
     alpha-interferon or interleukin 2) or with the sleeping-waking
     brain system (e.g. by sleep deprivation) has effects on the other
     system and will be accompanied by the symptoms of the chronic
     fatigue syndrome.[6]

   A 1992 study by allergists investigated the coexistence of
   fibromyalgia with allergy. They evaluated 47 consecutive patients
   visiting an allergy clinic with rhinitis (sinus inflammation). They
   found that roughly half of the patients suffered aching, tiredness,
   and the 11 tender points of fibromyalgia [12]. This is a significant
   finding and indicates that immune activation is likely a factor in
   many cases of FM.

   A treatment approach along these lines is to reduce the immune system
   activity which may be possibly producing cytokines and disrupting body
   function and sleep. The general strategy employed is to reduce immune
   load, and this includes: 1) improving immune strength, 2) reducing
   allergy and allergic and environmental stress and 3) reducing the
   infectious load. Immune load is the totality of infectious load
   (yeast, fungal, viral, bacterial) added to the totality of immune
   dysfunction. The status of adrenal, thyroid, energy metabolism, and
   serotonin/dopamine, strongly relates to these factors as well, and
   deficiencies in these systems can produce immune load. Reducing
   infectious load requires addressing foreign organisms which may be
   loading down the system (in addition to the immunodeficiency which
   allows those organisms to persist). For example, patients have
   reported improvements in their health status when bacterial infections
   such as sinusitis and tooth infections are addressed. The infectious
   organisms documented by CFS research relate here as well, and these
   include mycoplasma and Herpes infections. Infectious load may be
   potentially reduced by strengthening the immune system, and this
   includes addressing abnormalities in energy metabolism, adrenal status
   (e.g. DHEA), NK cell and immunoglobulin counts, histamine production
   and environmental load. Treatment which focuses on improving the
   health of the GI tract can also be employed, and addresses such
   problems as intestinal dysbiosis (which is a deficiency in healthy
   bacteria coupled with an excess of unwanted bacteria, yeast, and
   parasites in the gut) and intestinal permeability or leaky gut; the
   last of which can lead to nutritional deficiency and food allergy;
   which can simply increase the immune load. The problem of intestinal
   dysbiosis and leaky gut in FM is something that has been reported by
   clinicians. No scientific research exists which provides any
   quantitative data on these problems in PWFM.

   Immune load can also be reduced by reducing allergic and environmental
   stress, if they exist. Histamine can both suppress the immune system
   and cause wakefulness. A good discussion of the problem of food
   allergy can be found at
   http://www.solgar.com/nutrition_library/healthy_living/food_allergy.ht
   ml and
   http://www.solgar.com/nutrition_library/healthy_living/allergy.html
   Dr. Theron Randolph was the first doctor to publicly note the problem
   of food and chemical sensitivities producing symptoms typical of
   CFIDS. He wrote a book called An Alternative Approach to Allergy and
   recommends a particular diet for reducing food sensitivities and
   reactions to chemicals. Other allergy treatments--besides addressing
   the immune dysfunction directly--are available for reducing allergic
   load, and include antigen therapy and EPD, or Enzyme Potentiated
   Desensitization. A technical discussion of the role of cytokines in
   allergy can be found at:
   http://medic.med.uth.tmc.edu/hcprof/00000770.htm
   In this document the author states that gamma interferon, the
   particular cytokine which Russell noted could cause the low tryptophan
   in FM, plays a role in allergic diseases.

   Chemical sensitivity

   Many PWFM report that they have Multiple Chemical Sensitivities (MCS),
   and so a percentage of patients may be suffering symptoms in response
   to exogenous chemicals in the environment (PWFM have also been
   documented to suffer a lower tolerance to medication[8]). A book which
   pioneered the area of MCS, in addition to Randolph's book, is The EI
   Syndrome by Dr. Sherry Rogers, a clinical ecologist. One of the
   leading scientists in the study of MCS is Dr. Claudia Miller, and she
   wrote a book called Chemical Exposures: Low Levels and High Stakes.
   Dr. Miller is an industrial hygienist who has specialized in the
   problem of chemical injury in the workplace, and she argues that an
   intolerance to chemicals in low doses can cause the symptoms of FM.
   Her focus is on the emergence of chemical sensitivity due to chemical
   exposure, which she calls toxicant-induced loss of tolerance. Dr.
   Miller believes that the Gulf War veterans (a percentage of whom have
   FM) are suffering toxicant-induced chemical intolerance. A discussion
   of Dr. Miller and MCS and her view of Gulf War Syndrome can be found
   at:
   http://www.uthscsa.edu/mission/spring94/featu_6.html

   A good survey of current theories which are sympathetic to MCS can be
   found at:
   http://ehpnet1.niehs.nih.gov/docs/1997/Suppl-2/

   A new source of information for MCS can be found at:
   http://www.mcsrr.org/factsheets/mcsdisorders.html

   Those who suspect that chemical sensitivity may play a role in their
   symptoms can reduce the chemical load which one is exposed to. Both
   Dr. Theron Randolph and Dr. Sherry Rogers go at length to explain what
   this entails. But in short this includes avoiding pesticides and new
   carpet and renovation material, eliminating fragrances and using less
   harsh forms of cleaners and detergents, and avoiding permanent press
   fabrics and dry-cleaned clothing, and avoiding combustion heating such
   as gas and oil. All cosmetics and perfumes applied to the skin are
   absorbed into the bloodstream, so natural alternatives to these
   products are another option to consider. Perfumes and skin care
   products are not currently regulated for content.

   A recent FM case study lends some support to the notion that FM can be
   environmentally induced. The report tells of a family (and one
   non-relative) which in 1988 developed fibromyalgia upon exposure to
   strong petroleum fumes from a leaky storage tank at a nearby gas
   station. Fibromyalgia and disrupted sleep and associated symptoms were
   diagnosed in all four residents in the house. Within one year of
   relocating away from the site, their fibromyalgia cleared[10].

   There may be several different scenarios in which environmentally
   induced FM develops. In the first scenario, a normally healthy person,
   when exposed to a toxic level of a particular chemical, may develop
   the symptoms of FM. This is basically a systemic response to
   poisoning, and Sick Building Syndrome may be a common instance of
   this. Once the toxic agent is removed, the person's health is
   restored. In the second scenario, a healthy person acquires chemical
   intolerance after a toxic exposure and from that point onward suffers
   FM symptoms upon exposure to lower doses of chemicals which previously
   did not provoke symptoms. A plethora of these cases, especially in
   occupational settings, have been reported, in which a percentage of
   employees complain of chemical intolerance after a toxic exposure in
   the workplace. In the third scenario, the person who is gradually
   developing FM or gradually worsening in health develops a reduction in
   toxicological defense and an increase in chemical susceptibility, and
   this person, due to an increased susceptibility, becomes sensitized
   upon an exposure to chemicals. An example would be the gradual onset
   patient who, upon repainting the house, is exposed to a level of
   chemicals which exceeds that person's toxicological tolerance;
   sensitization/injury then occurs and the person sinks into full FM and
   chemical intolerance. In the fourth scenario, the FM patient suffers a
   general environmental hypersensitivity (light, noise, smell) and
   chemical sensitivity is just one component of this.

   There is new research which shows particular promise in objectively
   documenting both the existence and etiology of MCS, and this is
   research in the subject of neurogenic inflammation[20]. In neurogenic
   inflammation, sensory cells, upon contact with exogenous chemical
   irritants, release neuropeptides which trigger an inflammatory
   response. This is cutting-edge research and may help to explain why
   the adverse response to chemicals in some persons may be upregulated.
   Research has shown that neurogenic inflammation is moderated by an
   enzyme called neutral endopeptidase (NEP), and this research has found
   that, when NEP is absent, sensory cells are more likely to produce
   inflammatory peptides upon contact with chemical irritants (in animal
   studies). Neurogenic inflammation has already been documented in the
   airway in humans and has been postulated as playing a role in Reactive
   Airway Disease, which includes asthma[21,24]. In the next few years we
   can expect to see investigation for biomarkers of neurogenic
   inflammation in patients with chemical sensitivity.

   Neurogenic inflammation has been recently suggested as the cause of
   interstitial cystitis[22]. Interstitial cystitis is a relatively
   uncommon bladder disorder which bears close resemblance to FM[23], and
   shares common symptoms such as allergy, IBS, and widespread pain.

   Substances which are known to inhibit neurogenic inflammation are
   magnesium [17,18,25,26], glucocorticoids [27,28,29], and serotonin
   [30,31]. Cortisol is one of the glucocorticoids produced by the
   adrenal gland. Serotonin deficiency and neurogenic inflammation have
   been implicated as causing migraine. Migraine is a common condition in
   fibromyalgia, and is associated with a constellation of symptoms which
   resembles FM [32]. Migraine is also a common symptom of chemical
   sensitivity. Sumitriptan, a serotonergic drug which relieves migraine,
   has also been found to reduce neurogenic inflammation. Magnesium,
   cortisol, and serotonin have all been found deficient in FM.

   Massage

   Rolfing, a type of massage, has anecdotal support for relieving FM
   symptoms, including brain symptoms. Trager massage, a more gentle
   massage method, has also been reported to be effective, and it can
   also relieve muscle tension and spasm.

   Acupuncture

   A few studies have investigated the use of acupuncture for the
   treatment of FM, and have found it to be effective [13-14]. One study
   was a controlled clinical trial for six sessions over a 3-week period.
   The researchers gave one group electroacupuncture and another group a
   sham procedure. The study found an improvement in sleep quality and a
   reduction in symptoms, including pain, in the treatment group over the
   placebo group.

   Pain

   Before addressing the problem of pain, it is important to note that
   there are different kinds of pain. That is, the FM community is in my
   opinion reporting a whole amalgam of pain problems, and these include:
   1) centralized pain amplification, 2) Myofascial Pain Syndrome (MPS),
   3) nerve impingement, 4) muscle spasm, and 5) tender points and
   diffuse muscle aching. I state this with the full observation that
   fibromyalgia is formerly defined as a problem of 11 tender points.

   Pharmacological relief of pain is an obvious option and will not be
   covered here.

   The first alternative approach to pain relief assumes that the pain is
   just one of the many symptoms of the disordered state, and so pursuing
   any FM treatment which improves health status might potentially
   relieve pain. Examples would include improving sleep, improving energy
   metabolism, reducing immune load, etc. Since serotonin is known to
   play a role in pain sensitivity, treatments which enhance serotonin
   are another option to consider. However, what role serotonin
   deficiency might play in the pain sensitivity of FM has not been
   established.

   A second approach is to directly address regional problems in the
   musculoskeletal system which might exist, and these are mainly
   Myofascial Pain Syndrome, nerve impingement, and muscle spasm. These
   regional problems often develop from the illness itself, but
   addressing them directly might provide more immediate relief. Massage,
   physical therapy (e.g. stretching exercises) and osteopathic and
   chiropractic manipulation are treatments which can potentially relieve
   these problems, albeit temporarily.

   Specific treatments have been developed for Myofascial Pain Syndrome
   (MPS), such as that devised by Dr. Janet Travell, the pioneer who
   first recognized this syndrome and identified an exhaustive array of
   trigger point locations throughout the muscle system. These treatments
   include temperature-change-and-stretch, trigger point injections, and
   acupressure. There are therapists who specialize in this technique and
   they are called Myofascial therapists. It should be noted, however,
   that massage is reported by many patients to be as effective or more
   effective than Dr. Travell's technique.

   Muscle spasm seems to vary in intensity, in which there can be varying
   degrees of muscle tension and pain. The spasm can be local or general,
   chronic or acute. MPS also includes muscle tension as part of the
   dysfunction it defines, but in MPS pain is often referred to some
   location distant from the trigger point. The pain experience of muscle
   spasm if quite different than MPS.

   Nerve entrapment problems are also causing pain in the FM population,
   but unfortunately these in my view are not being given sufficient
   medical attention, either due to the difficulty in diagnosing such
   problems or simply medical oversight. These entrapment problems may
   exist independently of the abnormalities of FM, they may result from
   the abnormalities of FM, or they may be causing abnormalities. The
   critical region of entrapment is the spine, particularly the cervical
   spine (neck). The thoracic outlet and brachial plexus (nerve bundle
   going to the arm) are common impingement areas as well.

   In the first case, the patient may have CFIDS plus a co-existing nerve
   impingement problem which is unrelated to the disease, but the patient
   has been diagnosed with fibromyalgia since pain is one of the
   presenting complaints.

   In the second case, the patient may suffer pain and other symptoms
   (e.g. due to the stress response, disrupted sleep, etc.) from the
   impingement itself. A recent study found that people with neck
   injuries are 13 times more likely to develop fibromyalgia than people
   with lower extremity injuries [9]. At a 1997 symposium on
   fibromyalgia, Dr. Michael Rosner of the University of Alabama reported
   diagnosing problems of cervical stenosis (compression in the spinal
   cord in neck area) in a sample of FM and CFS patients. This diagnosis
   was made by an MRI and neurological exam. Surgical relief of the
   compression brought about symptom improvement in roughly 75% of the
   patients.

   In the last case, the patient may suffer nerve impingement as a result
   of FM itself, i.e. from the muscle tightness or muscle dysfunction as
   it is called. Muscle dysfunction is a common abnormality in FM and
   commonly produces problems such as TMJ. Changes in musculoskeletal
   arrangement due to muscle dysfunction can then cause nerve entrapment
   problems. At this time, however, no statistics exist on nerve
   impingement problems in the population. But in my own case, I suffered
   three sites of nerve impingement due to the muscle dysfunction of FM:
   two in the thoracic outlet (Thoracic Outlet Syndrome) and one in the
   cervical spine. The nerve impingement in the cervical spine was caused
   by swelling of an intervertebral joint due to the chronic tension in
   the attached muscle. It should be noted that nerve impingement can
   also cause Myofascial Pain Syndrome in areas affected by the nerve.

   Thoracic Outlet Syndrome (TOS) is a neurovascular entrapment syndrome
   in which both nerves and blood vessels leading to the arms and hands
   can become pinched due to a narrowing in the upper part of the chest.
   A common symptom of TOS is pain, numbness, and/or circulation loss to
   the arm/hand/fingers when sleeping on one's side. TOS can also
   masquerade as Carpal Tunnel Syndrome (CTS). The compression in the
   thoracic outlet, which causes the symptoms of TOS, can be caused by
   postural strain and/or muscle dysfunction, but muscle dysfunction is
   the distinguishing factor in FM. Standard non-surgical treatment for
   TOS is physical therapy, and provides a set of exercises to open up
   the compressed areas and to stretch the pectoralis and scalene
   muscles. With this treatment, patients who suffer TOS secondary to
   muscle dysfunction are required to manage their condition. They must
   continually stretch the neck and pectoralis muscles to prevent a
   relapse into muscle tension and compression.

   Relying on physical therapy to deal with the problems of muscle
   dysfunction is in my own experience a somewhat crude approach. Often
   the muscles will return to spasm 1-2 hours after performing the
   stretching exercises. A more appropriate therapy is to address the
   muscle dysfunction directly, either with muscle relaxants (a
   non-pharmacological relaxant is GABA) or by addressing the very
   biochemical abnormalities documented in PWFM which are known to cause
   muscle dysfunction, namely magnesium deficiency and ATP deficiency.
   Both magnesium alone and the magnesium/malic acid combination has
   received anecdotal support from PWFM in successfully clearing the
   tension.

   TOS can set up the patient for further muscle, tendon, and nerve
   impingement problems in the arms and hands (such as Carpal Tunnel
   Syndrome) upon repetitive stress. This is due to the circulatory
   impairment caused by the vascular entrapment. Raynaud's Syndrome
   suffered by PWFM may play a role as well.

   One or more of the above pain problems may co-exist. For example, the
   coexistence of tender points and myofascial pain syndrome is common.
   Likewise, nerve impingement often includes painful trigger points in
   the affected areas.

   Magnesium

   A 1994 study found PWFM low in magnesium [16]. A magnesium deficiency
   can cause many of the symptoms of FM, including fatigue, sleep
   disorders, mood disorders, and muscle dysfunction. A description of
   the problem of magnesium deficiency can be found at:
   http://www.healthy.net/library/articles/schacter/magnesim.n.htm

   In his book From Fatigued to Fantastic, Dr. Teitalbaum states that
   magnesium supplementation may require 8-10 months in order to fully
   replace the deficit.

   Integrative/comprehensive treatment

   The strategy of comprehensive treatment is to get your whole body back
   into working order. Rather than blindly dispense a treatment which has
   been found to reduce symptoms, instead the doctor seeks to identify
   and address all the factors which are contributing to the ill health
   of the patient. Treatment is multifactorial and variable, and is
   custom-tailored to the patient based upon a patient history, physical
   examination, and laboratory findings. Nutritional and hormone
   deficiencies may be corrected. Stresses such as intestinal dysbiosis,
   persistent infection, and allergy may also be addressed. Doctors who
   specialize in this area are usually naturalpaths or into nutritional
   or orthomolecular medicine. They are often M.D.s but do not have to
   be. Orthomolecular medicine is the specialty of treating disease by
   restoring optimum amounts of substances which are normally present in
   the body.

   The diversity of findings (including clinical observation) in FM lend
   support to this comprehensive approach. We have evidence and clinical
   testimony, often with competing and narrow foci, that fibromyalgia can
   be caused by disrupted sleep, infection, allergy, chemical exposure,
   mitochondrial insufficiency, and neck injury. Some of these theories
   have more support than others. But they may all be true. If
   fibromyalgia is indeed a common systemic manifestation of a diversity
   of potential causes (which in many patients may co-exist), then the
   comprehensive approach may be especially apt, since the comprehensive
   approach insists that the physician clinically investigate or address
   the unique totality of problems which exist in the patient.
   Unfortunately, little or no research has been undertaken to study the
   effectiveness of this approach.

   Dietary/behavioral

   A diet in fresh produce and whole grains, with rotation of foods, can
   increase the nutrient level and also reduce allergic stress. Sources
   of healthy fatty acids such as Omega-3 and Omega-6 fatty acids, e.g.
   flax seed oil and various fish, may also be helpful. A food-combining
   rule given by nutritionists is the following: Either eat: 1) protein
   with vegetables, or 2) starch with vegetables, but NOT protein,
   starch, and vegetables together. Lastly, eat fruit ALONE, and wait at
   least 30 min after the fruit before eating anything else. Fruit is the
   most easily digested food, and contains many enzymes. This
   food-combining practice improves digestion and potentially improves
   nutrient availability.

   Mineral deficiencies may also play a role in FM. Particular minerals
   to address are calcium, magnesium, and potassium. Trace minerals are
   another option to consider, and these will include minerals such as
   copper, selenium, and molybdenum. People may wish instead to consider
   juicing fresh fruits and/or vegetables, as a means for getting
   vitamins and minerals in a bioavailable form. Celery, for example, has
   lots of potassium. Good sources of magnesium are the dark green
   vegetables. It should be noted, however, that the magnesium deficiency
   in FM may not be due to a deficiency in dietary intake.

   Amino acids are also important, and PWFM may wish to consider taking
   an amino acid complex, which contains all the essential amino acids.
   This is taken on an empty stomach. Many amino acids have a significant
   role in brain function. Deficiencies in amino acids have been found in
   PWFM.

   If widespread nutritional deficiency appears to be a problem, one can
   investigate possible root causes. One example is pancreatic
   insufficiency causing a deficiency in digestive enzymes. The
   pancreatic digestive enzymes are protease (for protein), amylase (for
   carbohydrates), and lipase (for fats). A standard supplement called
   Pancreatin is available which contains these three enzymes. Some PWFM
   have reported benefits from this. Another cause of nutritional
   deficiency is an inflamed bowel, and the problems of immune
   dysfunction,
   food allergy and intestinal dysbiosis relate here as well.

   Many PWFM suffer carbohydrate intolerance, and this may be the result
   of the low cortisol and/or abnormal glycolysis (carbohydrate
   metabolism to produce ATP) which has been documented in FM. Many PWFM
   report that they feel better if they increase the proportion of
   protein in their diet.

   The serotonin, dopamine, and norepinephrine deficiencies suffered by
   PWFM can cause addictive cravings. The various "addictants", caffeine
   or chocolate or sugar or tobacco, etc., provide rapid neurotransmitter
   boosts which can temporarily give the patient a relief of symptoms.
   But the behavior may, in the long term, worsen the neurotransmitter
   deficiencies. The addictive compulsivity is also likely a symptom of
   neurotransmitter deficiency. Anti-depressants and serotonin and
   dopamine agonists have to date shown effectiveness in curbing
   compulsivity, thus lending credence that addictive compulsivity is
   rooted in neurochemical imbalances.

   Simple carbohydrates can provide a rapid serotonin boost, but several
   hours later can result in a serotonin crash, prompting another fix.
   Complex carbohydrates, OTOH, promote a more stable glucose supply and
   more stable serotonin level, including high fiber.

   Exercise also impacts neurotransmitter levels. Exercise increases
   serotonin levels, and can also increase the amount of time spent in
   stage 4 sleep, potentially increasing the amount of GH produced. The
   amount of exercise a PWFM can tolerate depends entirely on his/her own
   unique condition. If a person feels worse after exercise, then the
   amount was excessive. The amount of exertion must be tailored so that
   the person feels better, not worse, after exercise. A suggested
   approach is to begin exercising at a low level and increase the amount
   as tolerance and endurance improves. Increasing the exercise rate as
   endurance improves will bring about aerobic exercise, which is the
   kind which may be the most therapeutic.

   Since stresses on the body are additive, PWFM may improve by
   successively _subtracting_ those stresses and _feeding_ the body what
   it needs. The strategy is: reduce the stress, feed the body. If food
   allergy is a problem, a restricted, rotation diet can reduce the
   stress. Addictive stresses can be reduced by addressing the
   neurotransmitter deficiency, either by direct or indirect means.
   Caffeine, which temporarily enhances energy and brain function but
   also drains the body of nutrients like calcium and B1, is one typical
   addictant to address. Sugar drains the body of nutrients also.

   Disclaimer

   All the above treatments discussed in this document should be
   considered experimental. Studies on efficacy and safety have not been
   done, and furthermore such studies are not likely to appear in the
   near future. None of the content in this documented should be
   construed as medical advice, and the author assumes no responsibility
   for therapeutic consequences.

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   Steve Emerson semerson@teleport.com
