Interesting article on Gaui - check out the blood thinning properties!

[Guest guest]

Many of us are dealing with coagulation disorders due to our infections. Turns

out, Guai is a blood thinner. Also a pain reliever.

penny

http://f5.grp.fs.com/v1/wCE0REecDMsd-6W-GgQX4YCZhmQ8u_3_I5Cf5dqsU_B_DSy_tJ2\

fHaleJ2gpaiJow4ICfdc3Ly5AsDcIuUo4T4aQ2vjDRwRCww/Mark%20London%20-%20The%20Role%2\

0of%20Guaifenesin%20in%

20Fibromyalgia.htm

The Truths and Myths of the use of Guaifenesin for Fibromyalgia

or

Guaifenesin: One Medicine, Several Effects

by Mark London

Last modified: 10/18/2004 02:46:10

Last modification: Added references to new studies in the Phosphate section.

Recent modifications: Total rewrite of Conclusions.

Please report any links that are not working to mrl@...

In the early 1990s, I belonged to the first fibromyalgia discussion group on the

internet, the FIBROM-L mailing list. We were probably the first people on the

internet to hear about the guaifenesin

treatment. Dr. St. Amand claimed that the drug guaifenesin could treat

fibromyalgia symptoms by removing excess phosphate from the body, which he

believes to be the cause of fibromyalgia. The

removal of the phosphate would supposedly lead to a reversal of all fibromyalgia

symptoms, which would essentially be as close to a cure as possible. Dr. St.

Amand claims that he has successfully

reversed all fibromyalgia symptoms in 90% of his patients. Additionally, Dr.

St. Amand himself claims to have had fibromyalgia, but that he has been pain

free for decades. Given these claims, many

people on the mailing list decided to try it. While some people experienced

positive effects from it, others experienced no effects from it, no matter how

carefully they followed the treatment

plan, which involves taking guaifenesin, and also avoiding products that contain

salicylates. In order to try and understand why some people find benefit from

the treatment, and not for others, I

decided to research guaifenesin, salicylates, and related topics. The following

web page documents what I have found so far, and hopefully will be of some help

to anyone who has an in interest in

the treatment.

But First, a Bit of History...

During the 1990s, Dr. , a recognized expert in the fibromyalgia

field, agreed to do a study on guaifenesin, with Dr. St. Amand being the

technical advisor to the study. The results of

this long term study showed that guaifenesin had no effect on fibromyalgia.

However, the debate did not end. Dr. St. Amand claimed that the patients in the

study must have unknowingly been exposed

to products that contained salicylates, which he believes can block the effects

of guaifenesin. Dr. countered, saying that if there were

sufficient quantities of low levels of

salicylates to block guaifenesin, then this should have caused a decrease in

urinary uric acid. Low levels of salicylates are known to have this effect.

But the lab tests from the study did not

show that this occurred. Thus, Dr. concluded that there was no such

exposure to salicylates.

Dr. went on to say that much of Dr. St. Amand's success with

guaifenesin, could be attributed to the placebo effect. The placebo effect

could be very strong in relation to guaifenesin,

since guaifenesin has been advertised as being able to treat the source cause of

fibromyalgia, and that it can reverse all the symptoms. This would make people

especially hopeful that the treatment

would work. Any beneficial effect that one might see from guaifenesin, would

create a high amount of optimism, since it would mean the drug is working, and

that you are on your way to a recovery.

Additionally, any worsening of fibromyalgia symptoms during the treatment, is

also a good sign, since these symptoms are attributed to guaifenesin's reversal

process, that rids the body

of " metabolic debris " . Thus, even feeling worse, could make a person feel more

optimistic. Plus, many patients are " mapped " , i.e. their bodies are examined

for lumps, and if the lumps decrease in

size, this is also supposedly a sign that the guaifenesin is working by removing

the phosphate deposits from the body. Not to mention, that guaifenesin often

causes a change of smell or color in

the urine. Many people attribute these changes to toxins being released from

the body, when in all likelihood, this is simply due to the fact that the

guaifenesin is metabolized by the liver,

resulting in a form of lactic acid, that is then excreted in the urine. Thus,

there are many possibly ways for a patient to get feedback, that would make them

believe that the treatment is working,

which would thus strengthen any placebo effect. So it's understandable why some

doctors attribute guaifenesin's benefits to the placebo effect.

However, in my own opinion, it's unlikely that the placebo effect could explain

all of the people who have stated that they have benefited from guaifenesin.

And if anyone had bothered to do a

simple search of guaifenesin in the medical literature, they would have found

reasons why guaifenesin can have beneficial effects.

In 1996, before the study was published, I went to a library, and quickly

discovered that guaifenesin has a skeletal muscle relaxant property, a fact that

people in the fibromyalgia community were

not aware of. Surprisingly, anyone could have easily discovered this fact if

they looked up guaifenesin in the Merck Index, a drug handbook, which lists

guaifenesin as having this effect.

Guaifenesin has known neurological effects, but most doctors are unaware of

this, because it is no longer used in humans for this effect. However, it is

used for this effect in veterinary

medicine. And a slightly different form of guaifenesin, guaifenesin carbamate,

is used in humans as a muscle relaxant, and is sold under the name Robaxin.

At the time that I discovered this information, I believed that this was the

reason why it helped some people, so I lost interest in researching it any

further. However, in the summer of 2000, I

became reinvolved in discussing fibromyalgia via the internet, and found that

people were still discussing guaifenesin. Not only that, but many web pages

that were devoted to guaifenesin, contained

false or unproven medical statements, that were being presented as fact. This

prompted me to do a more thorough investigation of guaifenesin and related

substances in the medical literature, and I

found evidence that it's neurological effect is much more complicated than a

simple muscle relaxant effect. It likely also has an analgesic, or pain

relieving capability. Additionally, guaifenesin

may also have the ability to inhibit platelet aggregation, and therefore act as

an anticoagulant. This may also be significant, as all of the uricosuric drugs

that Dr. St. Amand has used for

fibromyalgia, also have this ability.

However, Dr. St. Amand has never considered any other reason for the effects he

has seen from guaifenesin. He believes that the effect of guaifenesin on

fibromyalgia, is related to it's uricosuric

ability. Guaifenesin was selected for treating fibromyalgia by Dr. St. Amand

because it has a uricosuric effect. Uricosuric means that the drug has the

ability to increase uric acid excretion in

urine. He had previously believed that other uricosuric drugs, such as

probenecid, had helped fibromyalgia. But these other drugs often required high

doses to be useful, often leading to side

effects. So he experimented with guaifenesin, and found it to work better than

the previous drugs. Dr. St. Amand believes that it not the excretion of uric

acid that helps fibromyalgia, but that

it's due to the excretion of another substance. He hypothesizes it to be

phosphate.

But no medical evidence has been presented by anyone, that shows that excess

phosphate is the cause of fibromyalgia. Additionally, uricosuric drugs are not

known to increase phosphate excretion,

except in very rare circumstances. If Dr. St. Amand truly believes that

phosphate excretion occurs, why has he not presented evidence of this, not just

to the fibromyalgia community, but to the

rest of the medical community also? Very few drugs are available that mainly

increase phosphate excretion, without causing many side effects. The medical

community would welcome a new option, so

why has this never been done? And if he has done this, why has it been ignored?

And why has he never properly researched the effects of guaifenesin? For

example, he makes mention of the fact that

guaifenesin increases urinary excretion of 5HIAA, a serotonin metabolite. While

indeed guaifenesin does affect 5HIAA urine tests, it doesn't really increase

5HIAA. Instead, one of guaifenesin's

own metabolites interferes with the test, creating a false positive. A more

precise lab test, which is not usually done, is able to distinguish between the

two different metabolites.

Dr. St. Amand also appears to downplay any possible side effects from

guaifenesin. From his web page, he says " Guaifenesin is distinctly more

effective than our previous medications and has no

listed side effects. " Unfortunately, this is not true either, as many web pages

list side effects, including headaches and dizziness. Coincidentally, headaches

and dizziness are symptoms that some

people on guaifenesin initially do experience, yet such symptoms are often

ascribed to the cycling process of reversing fibromyalgia. That is to say, that

Dr. St. Amand believes that guaifenesin is

reversing fibromyalgia by removing phosphate deposits, and this causes cycles in

which fibromyalgia symptoms intensify. However, these symptoms could simply be

side effects from guaifenesin.

People with fibromyalgia often complain that they are very prone to experiencing

side effects from most medicines. This is not surprising, as fibromyalgia is

often described as being a state of

hyperexcitability, or hypersensitivity. Thus, people with fibromyalgia might be

more likely to experience drug side effects. Some of the people who try

guaifenesin, do so because of their

inability to tolerate the side effects of other drugs. And, as will be shown

later, guaifenesin is a drug that has many possible properties. So one could

easily postulate that people with

fibromyalgia, would feel side effects from guaifenesin, that the average person

would either not notice, or would attribute to the condition for which they were

taking guaifenesin (i.e. a cold).

And, of course, these cycling symptoms could simply be fibromyalgia symptoms

that would have occurred anyway, regardless of taking guaifenesin, People with

fibromyalgia often have flare ups of

their symptoms, sometimes due to extraneous factors, but others times seemingly

out of nowhere. Thus, people on the guaifenesin protocol may be wrongly

attributing their worsening of fibromyalgia

symptoms to a reversal process that doesn't exist. And they may avoid seeking

out other treatments, and suffer needlessly, because they believe that these

symptoms represent a good thing. Not to

mention the fact that any phosphate deposits would simply contain phosphorus and

calcium, two of the most abundant and necessary minerals in the body. So one

might wonder why the release of these

minerals would cause any negative symptoms.

Also in doubt, is Dr. St. Amand's claim that hidden salicylates caused the study

on guaifenesin to be flawed. His claim is based on the belief that salicylates

are present in significant amounts in

certain products, especially herbal ones. To quote Dr. St. Amand's web page:

" Natural salicylates are present in barks, but barks also contain glycosides

which are converted by the liver and

intestinal tract to other more potent and long-lasting salicylates. " This

statement implies that salicylates abound in all trees, but that's not true.

The only glycoside that converts to salicylic

acid is salicin. And the only trees that contain salicin are willows and

poplars. And even then, there are some willow species that contain very little

salicin. Besides these trees, there are

only a few other very specific herbs that contain significant amount of

salicylates. So herbs are unlikely to be a major source of hidden salicyates.

The other supposed major source of salicylates, is from topically applied

products, which Dr. St. Amand believes is more potent than those ingested,

because they " deliver salicylates directly into

the blood stream. " However, there is no proof that salicylates can penetrate

through the skin, into the bloodstream, any more efficiently than if the

salicylates were ingested. In fact, as I will

reference later, studies have shown very poor absorption of salicylates from

topical products, even analgesic topicals that contain salicylates specifically

to be absorbed to relieve pain. This

makes sense, considering that the skin is meant to protect the body, while the

intestines are meant to absorb substances.

I will attempt to show, based on all available studies on guaifenesin, that it

has several known effects which may be responsible for claims that it benefits

people with fibromyalgia. I will also

attempt to show that there is no proof that either phosphate retention could be

the cause of fibromyalgia, or that uricosuric drugs can directly cause phosphate

excretion.

Guaifenesin's Effects on the Nervous System

Guaifenesin has a property which is not well known by many people (including

doctors), but is well documented in the medical literature. It is capable of

acting as a skeletal muscle relaxant. It

does this by depressing transmission of nerve impulses in the central nervous

system. The reason that this information is not well documented, is because

guaifenesin was a grandfathered drug, so it

was never subjected to thorough testing, as later drugs had to be. And it is

not used for this property, by traditional doctors, because other drugs with

similar properties, were found to be more

effective.

Guaifenesin's neurological properties first became known in the late 1940s.

During that period, researchers studied the effects of mephenesin, a drug which

is a very close chemical relative of

guaifenesin. Given intravenously to animals, mephenesin was found to have a

ability to induce skeletal muscle paralysis. Researchers continued to study

mephenesin, but they also created and tested

other chemically related compounds, and discovered that mephenesin belongs to a

class of chemicals known as propanediol derivatives, all of which exhibited the

same muscle relaxant effect, to one

degree or another. Mephenesin is 1,2-Propanediol, 3-(2-methylphenoxy)-. One of

other compounds created was 1,2-Propanediol, 3-(2-methoxyphenoxy)-, which is

commonly known today as guaifenesin. At

the time, it was known as guaiacol glyceryl ether. Unfortunately, the muscle

relaxant effect of propanediols only lasts a short time, due to the drugs being

rapidly metabolized. That is to say,

they are converted into other chemicals, and then these resulting " metabolites "

are excreted in the urine. Thus, because of their short effective duration, the

first propanediol drugs that were

created had limited use for humans (the timed release version of guaifenesin was

not created until decades later). However, they could be used in veterinary

medicine, in intravenous anesthetic

preparations for surgery. But another problem was that all of these drugs have

a also hemolytic side effect, i.e. causing cellular destruction of red blood

cells. Guaifenesin, however, has less

hemolytic activity, and it also has greater water solubility, so it became the

preferred drug to use.

Researchers continued to study these drugs to find a longer lasting form. In

the 1950s, such a form was created, known as a carbamate. The following paper

documents a study comparing the effects

of mephenesin, guaifenesin, mephenesin carbamate, and guaifenesin carbamate:

Journal of Pharm. Expt. Ther. 1958, 122;239 (Truitt and Little)

This study shows that all these drugs exhibit a comparable muscle relaxant

activity at similar doses. However, guaifenesin carbamate was effective over a

much longer time, so it could be used

effectively in humans as a muscle relaxant. It is now known as methocarbamol or

Robaxin, the latter being the brand name. For the National Library of Medicine

entries on these drugs, see:

http://www.nlm.nih.gov/cgi/mesh/2K/MB_cgi?term=Guaiacol+glyceryl+ether

It has been found that all of these propanediol derivatives act as

central-acting skeletal muscle relaxants by selectively depressing transmission

of nerve impulses at the internuncial neurons of

the spinal cord, brainstem, and subcortical regions of the brain. At low doses

they act to relax hypertonic muscles and to lower response to sensory stimuli,

i.e. pain. Thus, they might be very

useful for people with fibromyalgia. At high enough of a dose, they can cause

temporary muscle paralysis. This is all explained on the following web page:

http://www.vedco.com/products/productpages/FMPro_229.htm

To achieve muscle paralysis, the recommended dose for large animals is 50mg per

pound. Assuming a similar dose rate for humans, for a person weighing 100

pounds, the recommended dose would be

5000mg. Of course, this amount is meant for extreme relaxation to allow for

surgery. A muscle relaxant effect would still be seen at much lower doses.

Patients on guaifenesin for fibromyalgia

take anywhere from 600 to 3600mg per day. Dr. St. Amand's own wife takes as

much as 4800mg per day. So this effect would likely be significant in these

people.

Additionally, in the previously mentioned study that compared Robaxin and

guaifenesin, it was found that the two drugs had comparable muscle relaxant

effects at similar dose levels. Since the

maintenance dose for Robaxin is 1500mg, we can infer that the same level dose of

guaifenesin would also have significant relaxant effects. And in fact, many

people with who take guaifenesin, take a

dose that is close to that amount.

Other propanediol derivate drugs have also been created for their effects on the

nervous system. The first anti-anxiety prescription drug was Meprobamate,

2-Methyl-2-propyl-1,3-propanediol

dicarbamate, commonly known as Equanil or Miltown. It is no longer used,

because the nervous system effect was not specific to anxiety, plus it was also

very addictive. However, several other

propanediols are still in use. Carisoprodol, or soma, is

N-isopropyl-2-methyl-3-propyl-1,3-propanediol dicarbamate. It is a commonly

prescribed muscle relaxant, and is sometimes prescribed for

fibromyalgia. Another propanediol is Felbatol (felbamate),

2-phenyl-1,3-propanediol dicarbamate, an anticonvulsant. It should also be

noted that some people have been found to experience allergic

symptoms from propanediols, and the medical literature warns people not to use

any propanediol drug if they have experienced side effects from any one of them.

This might explain why some people

experience immediate side effects from using guaifenesin.

It is worth noting that guaifenesin's relaxant effect on the nervous system

might be the reason for it's expectorant property. Guaifenesin was being used

as an expectorant, well before propanediols

were discovered, as it can be derived from the bark of the guaiac tree.

However, as shall be shown later, guaifenesin doesn't appear to have a direct

effect on mucus. Instead, it's possible that

it's expectorant ability is actually due to it's muscle relaxant effect. Some

types of expectorants are known to act via a relaxant effect, as the effect

helps to soothe spasms and allow mucus to

flow easier. Two common herbal remedies that are known to act both as relaxants

and expectorants are kava kava and peppermint oil. Some relaxants, like

pepperment oil, are also useful for

digestion problems such as Irritable Bowel Syndrome, so it's not surprising that

some people have reported guaifenesin to be useful for IBS (although IBS is a

multifaceted problem, so relaxants

don't work for everyone.) In any event, this shows how a single property can

have widespread and diverse effects on the body.

Guaifenesin's Analgesic Effect

But guaifenesin's effect on the nervous system is not simply limited to acting

as a muscle relaxant. In the 1970s, mephenesin was found to increase levels of

the amino acid glycine. A later study

in the 1992, showed evidence that mephenesin may be an antagonist of excitatory

amino acids. This could be releavant to fibromyalgia, since studies have shown

that levels of excitatory amino acids

are raised in fibromyalgia, and may be involved in the pain process of

fibromyalgia. And it's also been found that some people with fibromyalgia find

relief of symptoms by avoiding dietary

excitotoxins such as MSG and aspartame, both of which contain excitatory amino

acids. Another study in 1994 on mephenesin went on to hypothesize that this

effect on amino acids may be the reason

for mepehensin's ability to act as a muscle relaxant: " Mephenesin acts mainly by

inhibitting the polysynaptic reflexes in the spinal cord, and these reflexes are

mediated by the intersegmental

network using EAAs as neurotransmitters. " And a study on other EAA antagnoists

have shown them to have muscle relaxant effects. Interestingly, felbamate,

another drug in the propanediol family,

has also been found to a be a broad spectrum antagonist of excitatory amino

acids. Both studies on mephenesin and felbamate indicate that they inhibit NMDA

neuron receptor activity. In fact, it

appears that many propanediol drugs, or for that matter most -diol chemicals,

inhibit NMDA receptors. This is important, because drugs that act as NMDA

inhibitors may be helping in treating

fibromyalgia pain.

Thus, mephenesin, and therefore guaifenesin, may indeed have an ability to lower

fibromyalgia pain levels. While there are few studies regarding this effect,

one study has shown that mephenesin

does have an analgesic effect. Another study on guaifenesin also shows that it

has an analgesic effect.

However, even at low doses, at which guaifenesin doesn't exhibit any of it's own

analgesic or muscle relaxing effect, it still may have neurological properties

that could be useful for

fibromyalgia. One study has shown that guaifenesin at such subeffective doses,

is able to increase the analgesic effect of paracetamol (Tylenol). This might

explain why some people immediately see

effects from even the lowest dose of guaifenesin, as it might be increasing the

effectiveness of analgesic medicine that patients are already taking. And this

effect appears not to be specific to

any single analgesic. Veterinary web pages claim that guaifenesin potentiates

the effect of other anesthesia medicines. Plus, guaifenesin is believed to have

an additive effect on narcotics. And

finally, guaifenesin is being used transdermally, in combination with other pain

killers, to relieve localized pain: " Guaifenesin appears to provide benefit as

an adjunctive treatment, of painful

spasticity. For the patient population described herein, amitriptyline appeared

to offer limited pain relief when administered transdermally. It appears that

combining gabapentin with doxepin may

offer some additional benefit. The addition of guaifenesin to doxepin may be of

particular value when painful spasticity is present. " Doxepin is a tricyclic

antidepressant.

As an aside, neurontin at low doses is able to potentiate the anaglesic property

of opioids such as morphine. This potentiating property is likely due to an

antagonistic effect on excitatory amino

acids. Increased levels of EAAs are known to cause tolerance and the loss of

antinociceptive response to morphine, and neurontin has been shown to reduce

morphine tolerance. While guaifenesin has

not been tested for a potentiating effect on morphine, Robaxin (guaifenesin

carbamate (methocarbamabol) is known to potentiate morphine. Thus, perhaps

guaifenesin's ability to potentiate the effect

of pain killers, is also due to an EAA antagonistic effect

Given the possibly unique mode of action of guaifenesin, i.e. an anti-excitatory

amino acid effect, it might explain why some people with fibromyalgia have

noticed an effect from it, while others

have not. Many drugs used for fibromyalgia have varying success between

patient.s. Studies have shown neurochemical differences in the spinal fluid of

fibromyalgia patients. Some have high levels

of excitatory amino acids, while others do not, so there is a lot of variability

between patients. Plus, the neurological effects of guaifenesin might explain

why the original study on guaifenesin

didn't show any results. The patients in the study might have already been

taking analgesics at doses high enough that they wouldn't see any additional

effect by taking guaifenesin. Many people

who take guaifenesin, often do so because either they haven't found any meds

that have worked for them, or they can't tolerate the side effects from such

meds. In other words, the guaifenesin study

might have not accurately reflected the population who have found the most

benefit from taking guaifenesin.

As an aside, probenecid, the drug previously used by Dr. St. Amand, may also

indirectly antagonize the effects of excitatory amino acids. Probenecid is an

" anion transport inhibitor " , meaning it

can affect the transport of certain acids. Probenecid has been studied with

regard to kynurenic acid, a naturally occurring EAA antagonist. In studies,

it's been found that probenecid can affect

kynurenic acid, and in one study on rats, it was found to increase the level of

kynurenic in the brain by a factor of 2.5. And in other studies, kynurenic acid

has been found to have analgesic

effects.

Unfortunately, propanediol drugs often have hemolytic side effects, which is why

they are not being used to treat pain. For example, the propanediol drug

felbamate, was definitely found to be able

to reduce neuropathic pain. But research on it was discontinued, when

significant hemolytic side effects were discovered. Guaifenesin has much lower

hemolytic side effects. However it is

metabolized quickly from the body, so it was not considered to be useful.

However, most of the research on guaifenesin was done well before a timed

release version of guaifenesin was created, which

would significantly prolong the levels of guaifenesin in the body.

Additionally, the rate of metabolism of guaifenesin appears to have a wide range

of variance between people. A study in MEDLINE

shows that the half-life of guaifenesin in healthy subjects varied from 1.36 to

5.25 hours. This quoted maximum is much much higher than the average half-life

which is usually reported for

guaifenesin in the literature. It could be that some people have a slower

metabolic rate, and that this could account for why some people with

fibromyalgia find it useful, while others do not, and

why the effective dose varies widely between people.

By the way, guaifenesin is a centuries old remedy, as Dr. St. Amand himself

notes. He points out that extracts of the guaiac tree, have a long history of

being used for rheumatism. I assume that

he mentions this, as a possible proof that it can treat fibromyalgia. However

the specific history, isthat in the 1500s, explorers to the new world of North

America became aware of the guaiac tree,

due to the fact that they were looking for remedies to treat untreatable

diseases, such as syphilis. Basically, they were looking for a way to make

money. They discovered that the local natives

were using extracts of the guaiac tree for medicinal properties, and so they

tested it on syphilis. The extracts were able to treat the back pain related to

syphilis, so they believed that it could

therefore treat syphilis. Thus, for a long time, it was more well known for

treating syphilis, than rheumatism. The fact that guaifenesin has a history of

treating various ailments, supports the

theory that it has a more general analgesic effect, rather than a specific

effect that only treats fibromyalgia. So it's no wonder that people such as

Penniston, a chiropractor who designed

the GuaiLife form of guaifenesin, markets it for a very wide range of pain

conditions, such as pelvic pain, Ehlers-Danlos Syndrome and restless leg

syndrome, among others.

As an aside, if one believes that salicylates can block the effects of

guaifenesin, one wonders how guaifenesin was useful at all in the past as a

herbal remedy. Because in those days, extracts of

the guaiac tree were created from the bark of the tree. And the bark of the

tree surely should contain salicylates, according to Dr. St. Amand's theory that

salicylates are abundant in trees and

herbs. And even if salicylates aren't present in the guaiac bark, then they

very likely are present in other herbal remedies, that patients in those days

would have been taking for their pain

condition. Surely some of those impure herbal remedies, would have also

contained salicylates. In fact, herbal web pages specifically mention that it's

ok to combine guaiac extracts with other

herbs that contain salicylates:

http://www.nevdgp.org.au/geninf/ArthritisF/management/herbal.htm

http://www.holistic-online.com/Herbal-Med/_Herbs/h244.htm

Additionally, no herbal web page makes any mention that guaiac extracts make a

person feel worse before they get better.

Uricosuric Drugs and Phosphate Excretion

Dr. St. Amand believes that the increased phosphate excretion is the reason for

guaifenesin's benefit, and that by reducing excess phosphate in the body one can

totally reverse fibromyalgia. While

I believe guaifenesin to have some benefit, there is no evidence that it can

reverse fibromyalgia, nor is there any evidence that phosphate is the cause of

fibromyalgia. In addition, there is no

evidence that uricosuric drugs can increase urinary phosphate excretion.

Previous to using guaifenesin for fibromyalgia, Dr. St. Amand used other

uricosuric drugs, such as anturane and probenecid. Both are used for gout, due

to their ability to increase urinary uric

acid. However, neither is known to be able to enhance phosphate excretion. The

medical literature appears to have no references to any studies which tests

anturane for this ability. However,

there are several studies which have tested for this effect in probenecid.

Probenecid is believed to increase urinary uric acid by reducing the amount that

is reabsorbed via the kidneys back into the serum. The section of the kidneys

where this occurs is known as the

proximal tubule. Probenecid is secreted into the proximal tubule via a process

known as renal tubular secretion, which only occurs for certain weak acids. One

of those acids includes salicylates.

Since this process has a limited capacity, acids compete with each other for

secretion. If salicylate levels are too high, they block probenecid from being

secreted.

Once in the proximal tubule fluid, probenecid is believed to act as an anion

transport inhibitor, which is to say it prevents the kidneys from reabsorbing

negatively charged substances, including

such acids as uric acid. The following study extensively tested the effects of

probenecid on urinary electrolytes, and did not find any increased excretion of

urinary phosphate.

Can Med Assoc J. 1970 Sep 12;103(5):473-83 AUTHORS: DA, Yendt ER (No

abstract available in MEDLINE)

Additionally, other studies have confirmed that probenecid does not increase

urinary phosphate excretion, such as the following:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=8\

09224 & dopt=Abstract

In that study, the action of probenecid was monitored in connection with

Didronel, a drug used for osteoporosis. Didronel has a known side effect of

increasing serum phosphate levels, an effect

which lasts from 2-4 weeks after discontinuing the drug. Probenecid was tested

to see if it would cause any increase in phosphate excretion, which it did not.

Interestingly, Dr. St. Amand actually

recommends Didronel for osteoporosis for his patients, and it does not appear to

cause any worsening of fibromyalgia symptoms, even in people who exhibit a rise

in phosphate levels. This casts doubt

on the phosphate theory, since a rise in serum phosphate levels should offset

the effect of guaifenesin, but it does not.

It's not surprising that uricosuric agents cannot affect phosphate excretion.

The process in the proximal tubule of the kidneys, where most of the phosphate

reabsorption occurs, is highly

controlled and specific to phosphate. In that area of the kidneys, there exist

" type II sodium-phosphate cotransporters " , which control phosphate reabsorption,

and they are very specific for

phosphate. They are controlled by several mediators of phosphate homeostasis

(eg, parathyroid hormone [PTH], dopamine, dietary phosphate). If a drug could

simply affect phosphate excretion, and

not other minerals, then that would be of remarkable help for many

hyperphosphate disorders. Right now, the way to treat such disorders, is via a

low phosphate diet, combined with using phosphate

binders that block the absorption of dietary phosphate. In severe case,

diuretics are also used. However, these methods are not always very successful,

or can create side effects. A drug that

could remove only phosphate, without affecting other minerals, and without the

need to change one's diet, would be a great discovery.

As for Dr. St. Amand's urine tests on his patients, which he claims show

increased phosphate excretion, it should be noted that many drugs initially

cause side effects that gradually disappear.

Thus, long terminal studies are the only reliable tests. This is especially

true of phosphate excretion which is very much dependent on hormonal levels. If

a drug has the ability to disrupt

mineral excretion, it can take many days and sometimes weeks, before the body is

able to compensate for the disruption, and bring mineral excretion back to

normal. For example, prednisone initially

causes increased phosphate excretion, but the effect disappears after long term

use.

The reason for any possible initial increase in mineral excretion, that is seen

from guaifenesin, might be due to the fact that guafenesin is metabolized by the

liver into an acid, which is then

excreted into the urine. In theory, this could increase urinary acidity, and

increased urinary acidity has been associated with increased calcium excretion.

This might explain why Dr. 's

study showed a small but significant increase in urinary calcium. However, when

initially starting guaifenesin, there might be large increases in mineral

excretion, until the body adapts to the

changes. For example, high protein diets that increase urinary acidity, can

initially increase mineral excretion, especially calcium However, a recent long

term study on such a diet, has shown

that such effects disappear after several weeks. Thus, only long term studies

show the true effects.

No Evidence that Excess Phosphate Can Cause Fibromyalgia Symptoms

Phosphorus, commonly referred to as phosphate, is one of the most common and

most necessary minerals in the body. Phosphate is used everywhere, from the

building of bones, to balancing the body's

PH, and most important, for providing energy to run the body, via the formation

of ATP. However, since phosphate is so common in the foods we eat, a phosphate

deficiency is rare. And so is an

excess of phosphate.

This is because the kidneys are the main factor in regulating proper phosphate

levels in the body. And the kidneys are well able to excrete very large amounts

of excess phosphate, up to several

times the amount normally found in one's diet. Kidney functioning must fail by

at least 50%, before they lose their ability to excrete the amount of excess

phosphate that is ingested.

There are several factors that influence the rate of phosphate excretion by the

kidneys. The main influence is the parathyroid glands, as they controls

excretion rates via the production of

parathyroid hormones, or PTH. Thus, phosphate problems mainly occur due to

either kidney or parathyroid problems.

If phosphate excretion is too low, phosphate serum levels rise, resulting in the

condition known as hyperphosphatemia This is normally due to either kidney

failure, parathyroid deficiency

(hypoparathyroidism), or due to the body not reacting properly to parathyroid

hormone. The Merck Manual pages that relate to this condition are found here:

http://www.merck.com/pubs/mmanual/section2/chapter12/12e.htm

http://www.merck.com/pubs/mmanual/section2/chapter12/12d.htm

Such a condition is easily detected via a blood test. Initially, this condition

is symptomless. The main symptoms occur due to the excess phosphate combining

with calcium. This causes a calcium

deficiency, which is the main source of symptoms in hyperphosphatemia. However,

if phosphate levels are high enough, metastatic calcification occurs. This

causes calcium phosphate to accumulate in

soft tissues, resulting in deposits in the heart, lungs, blood vessels, kidneys,

brain, eyes, peri-articular tissues, and skin. But no such condition has been

found in fibromyalgia, so there is no

direct proof that excess phosphate is present in fibromyalgia. And even if it

did exist, the effects of excess phosphate would be first seen in tissues other

than the muscles, as studies show that

muscle cells appear to be somewhat protected from serum phosphate levels

changes. This is one of the possible reasons why hyperphosphatemia first

causes deposits to initially occur in soft

tissues, but not in muscles.

If excess phosphate really was the cause of fibromyalgia, then everyone with

hyperphosphatemia should develop fibromyalgia. In fact, since all children,

adolescents, and postmenopausal women have

elevated serum phosphate levels, then all of them should also develop

fibromyalgia. But this is not the case.

Nevertheless, Dr. St. Amand believes that uricosuric drugs help fibromyalgia,

because of their supposed effect on phosphate excretion. Dr. St. Amand

conducted a few urinary tests on some of his

patients, and found that both urinary calcium and phosphate levels were raised.

Since phosphate levels were raised the most, Dr. St. Amand believes it is this

effect that helps to treat

fibromyalgia. The following quote is taken from his web page:

http://www.guaidoc.com/

" My theory, simplistically stated, is that minimal phosphate retention year

after year is leading to gradual excesses. An elevated phosphate in the blood is

not tolerated since it would depress

calcium levels. The parathyroid glands will not allow this and phosphate must be

spread evenly not only in body fluids but also within cells. "

If this statement is true, then either serum calcium levels should be depressed

in people with fibromyalgia, or parathyroid levels should elevated. However,

neither condition has been noted in

fibromyalgia. Additionally, an increase of PTH not only increases serum calcium

levels, but also decreases phosphate levels, by increasing urinary phosphate

excretion.

But the body has yet another method for reducing elevated serum phosphate. It

does this by decreasing levels of vitamin D. Vitamin D regulates the amount of

phosphate absorption in the

intestines. The decreased levels of vitamin D results in less phosphate being

absorbed, and thus lowers the serum phosphate.

Thus, there are several ways for the body to reduce serum phosphate levels, in

order to avoid phosphate from being deposited in cells. Only in cases where

phosphate serum levels are very

significantly elevated, would PTH not be able to compensate. If that was so,

the condition would again be easily noted via symptoms and lab tests.

Dr. St. Amand has stated that " Phosphates readily enter cells " . It is true that

most phosphate is contained in the cells. Intracellular phosphate levels are

much higher than extracellular levels.

However, because of this concentration difference, phosphate cannot easily enter

cells on it's own. An active process is necessary to push the phosphate into

cells. One of the major ways in which

this is accomplished, is via a mechanism known as sodium-phosphate

cotransporters, which are present in all cells. On the other hand, phosphate

can readily exit cells via a passive process. This

is because there is much less phosphate outside of the cells, and thus phosphate

can ready exit cells without much resistance. This process is believed to be

dependent on the amount of phosphate in

the cells.

Thus, there are several methods available to cells, that can be used to control

their intracellular levels of phosphate. And in fact, these processes are

constantly at work, exchanging inorganic

phosphate between the intracellular and extracellular space. In muscles, which

have high energy needs, and which therefore contain large amounts of phosphate,

the intracellular inorganic phosphate

is totally removed and replaced within a couple of hours, even when the muscles

are at rest. And because phosphate is so necessary for proper muscle

functioning, the level of intracellular

phosphate is especially well controlled in muscles. For example, studies have

shown that when intracellular phosphate levels increase in muscles, due to

physical activity, phosphate is released at

a greater rate, and it's uptake into cells is reduced. Thus, these two

processes can used by cells to avoid excessively high levels of phosphate.

Additionally, the concentration and electrical

difference between the intracellular and extracellular space is especially high

in muscles, making it particularly hard for phosphate to enter muscle cells on

their own. Thus, these factors help to

explain why muscles don't appear to be significantly affected by elevated serum

phosphate levels, even at levels seen in hyperphosphatemia.

Dr. St. Amand also believes that the excess phosphate combines with calcium in

cells to form calcium phosphate deposits in cells. However, one study has shown

that intracellular calcium levels in

fibromyalgia is actually decreased.

Dr. St. Amand believes that the calcium phosphate deposits in cells is the cause

of lower levels of ATP, which is found in fibromyalgia. ATP is a key chemical

that the body creates for storing

energy. However, studies have shown no relationship to the level of ATP and

actual fibromyalgia symptoms. And there have been no published studies which

have found that excess phosphate is

associated with ATP depletion, or for that matter, any fibromyalgia symptoms.

But there are studies which show that ATP deficiencies are found in people with

phosphate deficiencies, which is not

surprising, since ATP requires phosphate. In fact, one study has found that

some people with chronic fatigue syndrome have phosphate diabetes, a condition

caused by kidneys excreting too much

phosphate.

If deposits in cells is the cause of fibromyalgia, then fibromyalgia should

develop slowly, as the deposits slowly grow. And the disease should be

progressive, i.e. the deposits would continue to

keep growing, as in conditions such as hyperphosphatemia. This would then cause

symptoms to constantly get worse. However, fibromyalgia is not believed to be a

progessive disease, and many people

with fibromyalgia develop it in a very short period. And if fibromyalgia was a

truly a disease caused by ATP depletion from these deposits, then fibromyalgia

symptoms and other ATP depletion

symptoms, should overlap. For example, ATP depletion can cause muscle problems

such as rhabdomyolysis. However, no such conditions are observed in

fibromyalgia.

Some people have pointed to studies which show that fibromyalgic muscles contain

low levels of ATP and high levels of inorganic phosphate as being proof of the

phosphate theory. However, these same

abnormalities have been known for a while, and are quite common in other

conditions. For example, studies have shown that similar muscle conditions

occur due to hormonal disorders, such as a

hypothyroidism. Insulin resistance, another condition commonly found in

conjunction with fibromyalgia, is also known to decrease ATP levels in muscles.

In fact, reduced levels of ATP in muscles, can occur in the average person, due

to experiencing exercise that causes muscle fatigue. Basically, what happens is

that ATP utilization exceeds the

oxidative capacity of the muscles, leading to a build up of inorganic phosphate.

Inorganic phosphate is formed due to the usage of ATP, and is then reused to

synthesize new ATP. But when the

oxidative capacity is exceeded, ATP synthesis can't match usage, and inorganic

phosphate levels rise. Studies have shown that people with fibromyalgia have

lower than normal oxidative capacity in

muscles. But studies also show that untrained muscles have lowered oxidative

capacity, and higher levels of inorganic phosphate, when compared to trained

muscles. Thus, considering that many

people with fibromyalgia have reduced physical activity, due to the pain, it's

very likely that untrained muscles is a major reason why lowered oxidative

capacity exists. Numerous studies by

Finnish researchers, have shown that strength excercising by fibromyalgia

patients, results in similar levels of increased muscle strength, when compared

to normal people. This should not be the

case, if fibromyalgia muscles contained significant cell abnormalities. It's

because of this and other findings, that many people have thus come to the

conclusion that fibromyalgia studies on

muscles do not show any conditions which are the primary cause of fibromyalgia,

and that fibromyalgia is not related to any muscle disorder.

So there presently is no proof to support the phosphate theory, nor is there any

proof that ATP depletion could cause all the immune, hormonal, and brain

disfunctions which have been found in

fibromyalgia, or for that matter chronic fatigue syndrome, which Dr. St. Amand

believes is the same disease as fibromyalgia. This is the reason why, that

although ATP levels were found to be

abnormal as far back as the early 1990s, present day research is not focused on

that as being the primary cause of fibromyalgia or chronic fatigue syndrome

symptoms.

But even if we accept this theory, we must also believe that guaifenesin can

lower the serum phosphate level to the point where it would cause phosphate to

be released by the cells into the serum

and be excreted. Such an effect would have to be quite significant, in order to

create a large enough gradient between the blood and the cells to make the

phosphate want to move into the blood.

And it has to be large enough to allow the released phosphate to be excreted,

rather than simply being reabsorbed by other cells. Such a significant effect

would be easily noticed in lab tests.

And in fact, such a test should probably be used as a parameter for how much

guaifenesin is needed, in order to make sure that phosphate isn't being lowered

too much. Phosphate blood and urine

levels are usually extremely constant, and assuming one is taking a timed

release version of guaifenesin to achieve a steady decrease of phosphate, a

blood test should be quite reliable. However,

such tests have not been published, nor are they being used for verifying the

dose of the drug. Increasing excretion of minerals can theoretically lead to

many health problems. Yet, Dr. St. Amand

only uses symptoms as his guide for doses. In fact, his treatment protocol

expects that you will initially feel worse when taking guaifenesin, which makes

one wonder how one is supposed to know if

one is feeling bad or good effects, without a proper lab test.

Dr. St. Amand himself has said his theory is purely theoretical, and that

perhaps guaifenesin is changing the excretion level of some other anion. His

main reason for originally believing in the

phosphate theory was due to what he had observed in his patients, such things as

weaknesses in teeth and nails, which he believed was due to calcium deposits

resulting from the high level of

phosphate. However, weak and abnormal bone formations can be due to a phosphate

diabetes, which we have previously described. And it can also be due to a much

more common problem, which is a

magnesium deficiency. Bones are not only formed from calcium and phosphate, but

also from magnesium. Without magnesium, the resulting formations will be soft.

Teeth will have soft enamel, nails

will be brittle, symptoms which match Dr. St. Amand's observations.

Magnesium is extremely necessary for proper ATP synthesis, because ATP is stored

in the body as a combination of magnesium and ATP, which is known as MgATP. ATP

requires magnesium in order to be

stable. Without magnesium, ATP would easily break down into other components,

ADP and inorganic phosphate.

Magnesium deficiency is very common in the general US population. Not only is

our daily intake low, but we eat a diet which increases the demand for

magnesium. And unfortunately, urinary magnesium

loss can be increased by many factors, both physical and emotional. Magnesium

loss increases in the presence of certain hormones. Stress can greatly increase

magnesium loss. Even loud noises can

extra magnesium loss. One article on the web goes so far as to say that that

almost everyone is the United States is at least marginally deficient in

magnesium. So there is an excellent chance

that a person with fibromyalgia has a magnesium deficiency. But since people

with fibromyalgia often have high levels of stress, and a disrupted hormonal

system, they are more likely to be

candidates for magnesium deficiency. Plus, sleep deprivation has been shown to

cause lower magnesium levels:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=9\

068914 & dopt=Abstract

Magnesium is known to regulate or inhibit many nerve receptors, such as NMDA or

5-HT3, which have been considered as sources of certain types of fibromyalgia

pain. Neurontin, for example, is used

because of it's ability to regulate NMDA. Since magnesium also blocks NMDA

receptors, studies have used intravenous magnesium therapy to try and treat

similar types of neuropathic pain:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

0687324 & dopt=Abstract

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=9\

785788 & dopt=Abstract

And it's because of magnesium's ability to regulate nerve functions that other

fibromyalgia symptoms occur. Migraine headaches, mitral valve prolapse, and

Raynaud's phenomenon, all problems

commonly found in people with fibromyalgia, are also problems that have been

associated with a magnesium deficiency. Without enough magnesium, nerves fire

too easily from even minor stimuli.

Noises will sound excessively loud, lights will seem too bright, emotional

reactions will be exaggerated, and the brain will be too stimulated to sleep,

all symptoms commonly found in fibromyalgia.

And if the oversensitivity to light and noise reminds you of someone suffering

from a hangover, they are one and the same problem, as alcohol is known for

decreasing magnesium levels, and magnesium

supplementation has been found to relieve hangover symptoms.

A magnesium deficiency also increases levels of substance P, a chemical which

has been implicated as being responsible for increased pain levels in FMS.

Several studies, such as the following, show

this:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

384353 & dopt=Abstract

Unfortunately, magnesium deficiency is not easily detected, as serum levels do

not reflect the levels of magnesium in tissues. This is the reason why it is so

overlooked and ignored, both by

doctors and by studies. And unfortunately, oral magnesium supplementation can

be difficult because of absorption problems. Digestion and diet play a key role

in absorption. People with

fibromyalgia often have conditions like Irritable Bowel System, gluten

intolerance, or other problems that might limit absorption. Phosphate can bind

to magnesium in the gut, creating magnesium

phosphate, an insoluble salt that can't be utilized. Many forms of oral

magnesium supplements are hard to assimilate. The most common, magnesium oxide

and citrate, happen to be the worst to

assimilate, which is why both have a strong laxative effect. If you suffer from

that effect when you take magnesium, it is often not because you are taking too

much, but because you are not

assimilating it well. And it may take long term use of supplements before

magnesium levels are raised in all the tissues, and for damaged cell functions

to be restored.

Therefore, the symptoms which Dr. St. Amand has attributed to an excess of

phosphate, would more likely be due to a magnesium deficiency.

Can Guaifenesin increase vitamin D?

Up until recently, doctors only associated a vitamin D deficiency with weak

bones, and they believed that a vitamin D deficiency in young people was rare in

countries like the US. However, both of

these beliefs have been proven false. Not only does it occur in young people,

but sometimes a vitamin D deficiency can manifest itself mainly as pain.

Initial symptoms in adults can often appear

as vague musculoskeletal pains, muscle weakness, and fatigue, symptoms commonly

found in fibromyalgia. Also, studies on the muscles of vitamin D deficient

patients, show a reduction of ATP levels,

similar to that of fibromyalgia patients.

In some cases, the deficiency leads to myopathy, with quite severe muscle

weakness, especially affecting the legs and ability to walk. On the other hand,

sometimes the symptoms are less severe, in

which case it could be easily overlooked in fibromyalgia patients. In fact,

several small studies have shown that at least 40% of patients with fibromyalgia

have a vitamin D deficiency.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=12810939

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=11708429

And while some blood tests can possibly indicate a vitamin D deficiency, often a

deficiency can exist without any other biochemical changes. Thus, the only

definite way to tell if you have this

problem, is by testing vitamin D levels. Unfortunately, very few doctors do

this. So It's quite possible that some people who have fibromyalgia, might also

have a vitamin D deficiency. Or perhaps

they never had fibromyalgia to begin with. In the following study from Canada,

only 12% of patients referred to rheumatologists with the diagnosis of

fibromyalgia, actually had fibromyalgia:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=12595620

In any event, if you do have a vitamin D deficiency, supplementation with

vitamin D, would obviously be the most direct method of treating it. However,

besides sunshine, there are other methods

that naturally cause the body to increase it's own production of vitamin D. One

particularly well known way is to decrease serum phosphate levels. The body

compensates for this, by increasing the

production of vitamin D. It does this, because vitamin D has the ability to

increase the intestinal absorption of phosphate, and this would then lead to

restored serum phosphate levels. If

guaifenesin can truly increase phosphate excretion, then in theory, this would

result in an increase in vitamin D.

However, there is little proof that uricosuric drugs can directly increase

phosphate excretion. However, there is some proof that they can increase

calcium excretion. For example, an excess of

guaifenesin has been shown to cause kidney stones. This indicates that

insoluble calcium crystals are being formed in the urine, preventing the body

from reabsorbing the calcium. This could still

be happening at lower doses, but simply not at a rate high enough to produce

stones. This may explain why the study on guaifienesin showed an

increase in calcium excretion. And a study on

probenecid, the uricosuric drug previously used for fibromyalgia, shows that it

has the ability to increase calcium excretion.

An increase in calcium excretion, causes a rise in the production of parathyroid

hormones, or PTH. PTH causes several things to happen in the kidneys. It

causes an increase in calcium absorption,

thus offsetting the loss of calcium. Plus, it causes the kidneys to increase

production of the active form of vitamin D, which has the ability to increase

intestinal absorption of calcium. But it

also causes a decrease in phosphate absorption in the kidneys. And, as seen

above, a decrease of phosphate by itself, causes an increase in vitamin D

production. Thus, a reduction of calcium could

increase vitamin D production in 2 different ways.

But whichever situation is present with guaifenesin, either could possibly be

causing an increase in vitamin D levels. Furthermore, it's also known that uric

acid in the serum, can decrease levels

of vitamin D.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=8286711

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=9500573

Thus, decreasing serum uric acid, in combination with reducing phosphate, may be

working together to raise vitamin D levels. This would explain why Dr. St.

Amand uses uricosuric drugs to treat

fibromyalgia, yet does not use the traditional methods to reduce phosphate

levels.

While a reduction of phosphate can lead to increased vitamin D production, there

are factors which would prevent or reduce this effect. For example, a magnesium

deficiency can decrease PTH's

ability to increase vitamin D production. In fact, it's possible that this is

the reason why some people require more guaifenesin than others. I.e., those

with a lower magnesium status, would

require a greater amount of guaifenesin, in order to raise PTH levels enough to

produce the same amount of vitamin D.

On the other hand, vitamin D itself is a factor in controlling the amount of

magnesium that is excreted by the kidneys: Thus, an increase in vitamin D could

increase magnesium levels, further

benefitting fibromyalgia symptoms.

Additionally, a vitamin D deficiency can also lead to increased sulfate

excretion, as vitamin D is a factor in regulating sulfate reabsorption in the

kidneys:

In any event, while vitamin D may have an influence on sulfate and other

minerals, it also has many other effects. It appears to have immunological

effects, and low levels of vitamin D appear to be

associated with certain types of cancers and autoimmune diseases. In some of

these cases, vitamin D supplementation may be of help. For example, vitamin D

may have an influence on certain cases of

autoimmune thyroiditis:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=1783101

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=12039697

And even in simple forms of hypothyroidism, it has been found that vitamin D

levels are often low.

Other autoimmune diseases, which commonly overlap fibromyalgia, also have an

association with vitamin D. For example, people with either lupus or sjogren's

often have lower than normal serum

vitamin D. And low levels of vitamin D are associated with a higher risk of

developing diseases such as type 1 diabetes, rheumatoid arthritis, and multiple

sclerosis.

And vitamin D appears to have both indirect and direct effects on the nervous

system. For example, vitamin D may have a role in reducing the production of

inflammatory cytokines and nitric oxide

(NO) substances which are factors in the development of pain and other types of

neurological diseases. And vitamin D was also shown to have a direct

neuroprotective effect. Such research, however,

is still in it's infancy, so how significant these effects are is still unknown.

In any event, even if you are already taking a vitamin D supplement, it might

still not be enough. Some doctors believe that if you do not get enough

sunshine, that you may need as much as 1000IU

of vitamin D per day, rather than the RDA dose of 400IU, in order to achieve

normal serum levels.

Additionally, if you have an intestinal absorption problem, such as celiac, you

may not be absorbing all of the vitamin D supplement.

And if you think that drinking milk is a good way of getting vitamin D, think

again. Supplemented milk is actually a poor source, since it's been shown that

the amount of vitamin D in milk is

highly variable. That is why the following study showed no difference in the

vitamin D levels of adults who drank milk, versus those those that didn't:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

2034416 & dopt=Abstract

On the hand, taking vitamin D supplements did make a difference.

In any event, whether guaifenesin could really increase vitamin D production is

unknown However, what is definitely known, is that a vitamin D deficiency is

much more common than previously

realized. Therefore, it's a real possibility that some people with fibromyalgia

have a vitamin D deficiency, and people should be getting tested, if there is

any possibility that a deficiency

exists.

What Your Doctor Never Told You About Salicylates

Dr. St. Amand, and many patients on guaifenesin, believe that salicylates block

guaifenesin's effects. The theory is that the effects of uricosuric drugs are

blocked by salicylates, due to their

interaction in the kidneys. Dr. St. Amand believes that the reason that Dr.

's study did not show any effects from guaifenesin, was that the patients

were exposed to hidden sources or

salicylates that they weren't aware of, such as those that might be contained in

cosmetics and lotions. Dr. St. Amand believes that sunscreen lotions can be a

significant source of salicylates, yet

a lab test has shown that less than 1% of the salicylates over a 48 hour period

are absorbed from these lotions. The form of salicylate in sunscreens is

usually octyl salicylate, because it is

water resistant, and thus is not very easily absorbed compared to other forms of

salicylates.

But even in cases of analgesic topicals, where the salicylates aren't hidden

ingredients, and where the salicylates are meant to be absorbed by the skin,

most of is still not absorbed in the blood

stream. In a study on an topical analgesic containing methyl salicylate, one of

the more active forms of salicylates, only 22% of the salicylates were recovered

in the urine.

But even if hidden sources of salicylates do introduce low levels of

salicylates, there is no process in the kidneys that would allow a very small

amount of salicylates to block a very large amount

of guaifenesin. To give you an idea of how small we're talking about, Dr. St.

Amand has stated that he's had patients who have had their guaifenesin blocked

by " Listerine twenty seconds in the

mouth once a day " . Listerine contains approximately 0.060% methyl salicylate.

In comparison, Listerine contains over 22% ethanol, which is more likely to a

source of side effects, since ethanol is

toxic if swallowed.

The fact is, that on every web page that describes the guaifenesin treatment, no

one accurately describes the kidney functions that relate to salicylates, uric

acid, and uricosuric agents. This

process is important to understand, because one of Dr. 's main arguments

against significant amounts of salicylates being present in the study, is based

on this process, and what would occur

if such salicylates were present.

In the kidneys, there is a section called the proximal tubule. The fluid in the

kidneys pass through there, and this is where much of the useful components of

the fluid is reabsorbed, and

eventually sent back to the bloodstream. This process is known as tubular

reabsorption.

There is also a different process, known as tubular secretion. Weak acids, such

as uric acid, are secreted into the tubule. This is the body's way of quickly

getting rid of these acids. However,

only a limited amount of acid can be secreted at any given time. If enough of

one acid is present, it will saturate the process, and this will block the

secretion of other acids. This is how a

lower amount of one acid, is able to block the secretion of larger amounts of

another acid, resulting in less of the other acid being excreted into the urine.

This is why low doses of

salicylates,are able to block excretion of uric acid.

Probenecid, being a weak acid, is also secreted using tubular secretion. This

is why salicylates can also block probenecid. However, the amount has to be

quite large to do this, definitely not

small hidden amounts. This is why people who take uricosuric drugs, are not

told that they need to avoid small sources of salicylates. On the other hand,

Dr. St. Amand believes that small amounts

can block guaifenesin.

As an aside, it should be point out that guaifenesin itself is not secreted into

the kidneys. Guaifenesin is not an acid, but is slightly basic. However,

guaifenesin is almost totally metabolized

by the liver, and the metabolites are excreted in the urine. Guaifenesin's

major metabolite is beta-(2-methoxyphenoxy) lactic acid. Lactic acid is similar

in strength to uric acid, and competes

with uric acid for tubular secretion. And the medical literature states that

lactic acidosis, a buildup of lactic acid in the body, can be caused by taking

salicylates. Thus, it's likely that

guaifenesin's lactic acid metabolite is handled by tubular secretion.

However, as previously noted, it still takes a fair amount of salicylates to

block a uricosuric drug, such as probenecid. Even if guaifenesin is weaker than

probenecid, we still know that

guaifenesin can block uric acid, and uric acid itself isn't that weak. It still

takes a fair amount of salicylates to block uric acid, so we can deduce that we

need a similar amount of salicylates

to block guaifenesin. This amount is very unlikely to occur without taking

medicine that contains salicylates. Many studies in the 1990s have been done to

study the amount of urinary salicylates

that exist in people not taking salicylate medication, and they all have shown

extremely low amounts of urinary salicylates:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=9110565

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=8901795

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=12944546

Additionally, studies from the 1990s have shown that the salicylate content in

foods, herbs, and spices, is much lower than was found in previous studies.

Unfortunately, many web pages which

discuss salicylates, only refer to the earlier studies, and thus distort the

true level of salicylates.

However, even if a person was somehow exposed to a hidden amount of salicylates,

an amount large enough to block guaifenesin, then these same salicylates should

also be large enough to block uric

acid. This would then result in lower urinary uric acid levels.

It is this fact that Dr. uses as one his reasons why the patients in the

guaifenesin study, were not exposed to enough salicylates to block guaifenesin.

Had they been so, they should have

had lower than normal urinary uric acid levels. However, 24 hour urinary tests,

before and during their guaifenesin treatment, were always about 500mg. The

normal range is 250-750mg, so they were

just about average.

Now, if the patients were not exposed to salicylates, and the guaifenesin wasn't

blocked, shouldn't their urinary uric acid increase, due to the uricosuric

effect of guaifenesin? Not necessarily

so. Uricosuric drugs have to reach a threshold dose before they are able to

block enough reabsorption of the uric acid in the proximal tubule, in order to

create a uricosuric effect.

What is the effective dose of guaifenesin necessary to exhibit the uricosuric

effect? Unfortunately, the only study that were conducted on this effect, was

done so decades ago, and only used pure

guaifenesin, rather than the sustained release form that was used in the

study:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=4\

617771 & dopt=Abstract

In that study, people were given 600mg doses every 2 hours for 6 hours, for a

total of 1800mg. The uricosuric effect was noticable, but not deemed high

enough to be of clinical use. At a much

lower dose, i.e. 600mg sustained release over 12 hours, which was the dose used

by the guaifenesin study, there might be little or no uricosuric effect.

However, what the guaifenesin study did show, was a noticable increase in

calcium excretion in the guaifenesin group vs. the placebo. See:

http://www.myalgia.com/guaif2.htm

This may be significant, because there have been cases of people developing

kidney stones after taking large quantities of cought medicine containing

guaifenesin:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

0414721 & dopt=Abstract

Analysis of the kidney stones found an insoluble salt of the guaifenesin

metabolite combined with calcium. If anyone does experience mineral excretion

from taking guaifenesin, it might be due to

the formation of such insoluble salts. Additionally, guaifenesin is metabolized

into acids, which are excreted in the urine. This would increase the raise the

acid level of the urine, and

increased acidity is associated with increased calcium excretion.

In any event, there is little proof that salicylates in small amounts can

totally block guaifenesin in the kidneys. On the other hand, there is the

possibility that people with fibromyalgia are

being directly affected by salicylates, and that any benefits from avoiding

salicylates might have nothing to do with guaifenesin. In large enough doses,

salicylates significantly inhibit oxidative

phosphorylation, the process that creates ATP. ATP is source of energy for the

body, and ATP levels has been shown to be low in people with fibromyalgia.

Whether people are exposed to high enough

levels for this effect to be noticed is unknown.

However, even small amounts of salicylates are believed to be capable of causing

problems in some people. This condition is known as salicylate sensitivity.

Sensitivity and side effects from

salicylates have long been claimed by many people to be able to affect many

different health problems. While many of these claims lack proper studies, a

well documented sensitivity is known to

exist in people with asthma and chronic sinusitis. Aspirin sensitive asthma is

not only a reality, but it affects a very significant amount of people with

asthma, especially those who also have

allergies. This is significant, since many people with fibromyalgia also have

asthma, sinus problems, and allergies. One of the main reasons for aspirin

sensitivity, is that salicylates cause an

increase in a class of chemical known as leukotrienes. Leukotrienes are known

to cause inflammation, vasoconstriction, and pain. People who are senstivity to

salicylates, may either produce more

leukotrienes, or are sensitive to their effects, and that could be why some

people feel better when they avoid salicylates. People with asthma, who are

aspirin sensitive, are often helped by taking

drugs like Singulair, which block some of the effects of leukotrienes.

Aspirin sensitivity may also be related to aspirin's effect on platelets.

Aspirin is usually known to reduce platelet activity. However, when aspirin is

introduced to platelets from aspirin

sensitive asthmatics, the platelets become more activated. This appears to be

due to aspirin's ability to inhibit cyclooxygenase. In these people, salicylate

sensivity could therefore be adversely

affecting people with fibromyalgia, and blocking the anticoagulant effect of

guaifenesin, which will be discussed later.

Salicylate sensitivity has also been associated with low levels of

glutathione-peroxidase activity. This may be significant, as some people

believe that chronic fatigue syndrome is partially due to

low levels of glutathione, and many people with fibromyalgia also have CFS.

Some people with CFS have found that taking whey supplements help them, and whey

contains amino acids that increase

glutathione production. Therefore, perhaps low glutathione levels might make

some people with fibromyalgia likely to be sensitive to salicylates, and

avoiding them would help to alleviate

fibromyalgia symptoms.

By the way, even if people with asthma and sinus problems aren't aspirin

sensitive, they might be helped on the guaifenesin protocol from the well known

expectorant effect of guaifenesin. Relieving

congestion would not only improve sleep, but would also help to avoid

infections, both effects which could help to relieve fibromyalgia symptoms.

Salicylates can also block Vitamin K. This may be important for some people

with fibromyalgia, as easy bruising is a common symptom in some people with

fibromyalgia, and a vitamin K deficiency

could cause this. However, Vitamin K does much more than this. It is also a

significant antioxidant, controls insulin release, and is important in

protecting osteoporosis. Additionally, vitamin K

reduces IL-6, an inflammatory cytokine, which some people theorize places a role

in creating fibromyalgia pain. Vitamin K deficiencies have also been linked to

mitral valve prolapse and

hypermobility, both conditions which also commonly overlap in some people with

fibromyalgia. Therefore, reducing salicylates may be helping some people with

fibromyalgia by increasing levels of

vitamin K.

Perhaps even more important, salicylates are known to cause hypoglycemia in some

people. This is important, since many people with fibromyalgia that Dr. St.

Amand treats, also have hypoglycemia,

and their fibromyalgia symptoms are often greatly affected, simply by going on a

hypoglycemic diet. Additionally, Dr. St. Amand has said he has treated many

children with fibromyalgia, and children

are more likely to experience hypoglycemia due to salicylates, than adults.

In any event, avoiding salicylates can have a wide range of effects on the body,

and therefore it's impossible to tell what is the result of avoiding

salicylates, without proper lab tests or

studies. Additionally, perhaps avoiding salicylates, causes people to avoid

other substances that might be affecting them. This leads into our next

section.

Salicylates, Phenols, Thyroid, and Sulfur

Many herbs and supplements, which contain significant amounts of salicylates,

also contain high amounts of a family of substances known as phenols.

Salicylates are related to phenols, as salicylic

acid is a phenolic acid. If one adheres to a salicylate free regimen, one will

likely reduce one's intake of phenols, and phenols themselves have their own

effects. This might explain why certain

supplements, such as quercetin and peppermint oil, which are high in phenols,

yet are not known to contain salicylates, are on the list of supplements to

avoid by Dr. St. Amand. Either it's poor

research on his part, or he has seen people have reactions to these supplements.

One of the most commonly known phenols in foods are flavonoids, and several lab

studies have shown that flavonoids do have anti-thyroid effects This is

important, because hypothyroid disorders can

often lead to fibromyalgia, and normalizing thyroid levels other helps to treat

or resolve fibromyalgia symptoms Soy flavonoids has been best studied, with

regard to this effect While this

property may not have a direct effect on thyroid levels in the average person,

there is a concern that it may be a significant effect for people who have other

contributing factors that would lead

to a thyroid problem, such as low levels of iodine, or high level of thyroid

antibodies.

Also, this effect has only been studied on the original flavonoids themselves.

But once ingested, flavonoids do not always stay in their original form.

Flavonoids are mostly metabolized via a

process known as sulfation, where they are combined with sulfur. This results

in phenolic metabolites, which may not have any anti-thyroid effects. So any

such effects, would be dependent on how

quickly the phenols are metabolized by sulfation. The rate of sulfation is

dependent on several factors, one of them being the availability of inorganic

sulfate. A low level of sulfur, would lead

to a lower rate of sulfation, leading to increased levels of phenols in the

body. And as shall be seen in a minute, there are many factors in fibromyalgia

that could lead to low sulfur levels.

On the other hand, lab studies show that phenolic acids, which are related to

phenols, also have an effect on thyroid levels. Salicylic acid, being a

phenolic acid, may therefore have a similar

effect. And in fact, studies have shown that 2 forms of salicylate medicines,

given to humans, have the ability to lower serum thyroid levels. In those

studies, it was found that salicylates

compete in the serum with thyroid hormones, for binding to serum protein. This

directly affects thyroid levels. Supplements and other organic sources, that

contain salicylates, may cause this

effect. This could be true, even if the amount of salicylates is small. This is

because, other similar acting phenolic acids, are often found together with

salicylates, and together they may cause a

significant effect.

Since the sulfation process requires sulfur, a high rate of sulfation could, in

theory, contribute to a lack of sulfur. And a lack of sulfur can lead to

symptoms that are commonly present in

fibromyalgia, such as joint problems, skin disorders, and immune disfunctions.

Sulfur baths and spas are an age old remedy for such problems, and in fact one

study has shown sulfur baths to have a

positive effect on fibromyalgia. Plus, many people with fibromyalgia take

supplements that contain high amounts of sulfate, such as whey, MSM, SAMe, and

glucosamine sulfate. Several researchers

have expressed the belief that the benefits from such supplements, may actually

be from the sulfate itself:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=11436179

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=12623294

But while phenols themselves may not significantly lower sulfur levels, there

are factors that might be present in some people, that have the ability to lower

sulfur levels, by increasing urinary

sulfate excretion Vitamin D, T3 thyroid hormone, and growth hormones, are all

substances which are found low in some people with fibromyalgia, and a lack of

any of them can result in increased

urinary sulfate excretion.

Additionally, although salicylates themselves do not appreciably require sulfur

to be metabolized, one lab study has shown that salicylic acid can increase

urinary sulfate excretion. Unfortunately,

this effect has not been studied humans, to see how significant it is.

Sulfur is necessary for many processes in the body, so that a lack of it is

likely to have some effect on fibromyalgia. In fact, since sulfur is especially

well known for providing proper

connective tissue health, it's possible that the lumps which Dr. St. Amand feels

in fibromyalgia patients, could actually be a disorder related to a lack of

sulfur.

There are other possible clues that sulfur could be a problem in fibromyalgia.

Many people with fibromyalgia find benefits from hypoglycemic or low

carbohydrate diets, which are high in protein.

While there are a number of possible reasons for this, perhaps one reason is

because of the increased levels of sulfates derived from the amino acids. In

particular, sulfate is mainly derived from

the amino acid cysteine. However, this process depends on the cysteine

dioxygenase enzyme, and in some individuals, the activity of this enzyme is

decreased. Of particular note to people with

fibromyalgia, is that autoimmune or inflammatory conditions, such as rheumatoid

arthritis and lupus, can cause decreased activity of this enzyme, and thus

decreased sulfate levels. This appears to

be due to the fact that certain cytokines directly influences the enzyme's

activity. Cytokines are inflammatory substances which are elevated in RA and

lupus and other autoimmune conditions,

conditions often found in combination with fibromyalgia. People who have such

problems, might require other means to raise their sulfur levels.

Additionally, tylenol is one of the well known drugs that is metabolized by

sulfation, and it definitely has been found to lower serum sulfate levels.

Since many people with fibromyalgia are either

taking tylenol, or drugs that contain tylenol such as ultracet and vicodin,

these people may need extra sulfate. Guaifenesin's analgesic effects may help

people to decrease the use of pain killers

containing tylenol, and thus may indirectly be helping sulfur levels.

Salicylates, Benzoates, and Hypoglycemia

Phenols aren't the only ingredients which are commonly found in combination with

salicylates. There are others that may be able to reduce the effectiveness of

the guaifenesin treatment. Several

clues indicate this might be happening. People who are salicylate sensitive,

must also avoid foods that contain significant amounts of salicylates. However,

patients on the guaifenesin treatment,

are told that no special diet is required, as " the liver adds glycine to the

small amount of salicylates contained in food plants, and this process prevents

guaifenesin from blocking. " Instead,

they are only told to avoid supplements and topical sources of salicylates. The

theory is that supplements contain higher amounts of salicylates than food,

which would then overwhelm the liver.

Or, in the case of topicals, the salicylates would directly enter the

bloodstream, and be more likely to bypass the liver. But even if these sources

introduce more salicylates to the body, the

liver should still be able to properly metabolize them. A study using a single

dose of 600mg of aspirin, has shown that the majority of the salicylate was

metabolized into the glycine conjugate,

salicyluric acid. Only at higher doses, is the glycine metabolic process

saturated, at which point substantial amounts of other forms of salicylates will

appear.

But more importantly, it's salicyluric acid, the form of salicylate combined

with glycine, and not other forms of salicylates (such as salicylic acid), that

is mainly excreted by the kidneys. For

example, the following quote is from a study where different forms of

salicylates were tested, to see if any of them might renally compete with a

carboxylate drug:

Renal elimination plays a minor role in the elimination of salicylic acid

(<16%), and hence the potential for competing with the carboxylate via the renal

tubular secretory pathway is low. In

contrast, renal excretion plays a significant role in the elimination of

salicyluric acid (~60%).

So this seems to be totally at odds with Dr. St Amand's claim that salicyluric

acid, the form of salicylate that is conjugated with glycine is less likely to

cause blocking effects than other

forms. Because it is that form of salicylate that is more likely to be the one

that would compete with guaifenesin. So what's the real story here? Is this

another case of misinformation?

Perhaps, but perhaps not. One alternative explanation for why salicylates in

foods are not a problem, is that the amount of salicylates is simply too low to

be a problem.

On the other hand, as I previously noted, studies on the major form of

salicylate in lotions, i.e. octyl salicylate, have shown that very little of it

is absorbed through the skin. So how is it

that some people claim that salicylates in these products can block

guaifenesin's effects, yet salicylates in food are not able to do so? One

answer is found by looking at the other ingredients

that are found in such lotions..

In topical sources, you will often find additives that contain benozic acid.

Benzoate compounds are extremely common in topical products, oral products such

as toothpaste, and also processed foods

(jams, juices, non yeast bakery products), and sodas. They are used as both

preservatives and aromatics. But benzoates can be absorbed through the skin.

And benzoates are metabolized by the same

glycination process that salicylates are, which is why they can end up competing

with each other for glycine conjugation, which lowers their rates of

metabolization. This would then prolong the

time that salicylates would be circulating in the body.

Alternatively, people could be reacting directly to the benzoates. Sensitivity

to benzoates has been reported by people who have salicylate sensitivity. In

fact, there have even been cases where

benzoates by themselves have been reported to cause symptoms such as joint pain,

headaches, and concentration problems.

While it's claimed that benzoates are natural substances, they actually are only

found in a few select foods that we eat, mainly fruit, such as plums, prunes,

and cranberries. On the other hand,

other fruits contain quinic acid, an acid which is metabolized into benzoic

acid. The most well known fruit that contains a significant amount of quinic

acid, is the coffee bean. Quinic acid is

the 2nd most plentiful acid in coffee, after caffeic acid, of course. And

substantial amounts of the metabolites of benzoic acid, have been found in the

urine of coffee drinkers, indicating that

significant conversion of quinic acid is occurring.

Additionally, cinnamic acids are also converted to benzoic acids. Cinnamic acid

and it's derivates, are found in some processed foods. But they are especially

common in topicals and aromatic

products.

People on guaifenesin are told to avoid flavonoid supplements, as they are

believed to contain salicylates. However, such substances also appear to

contain both benzoic and cinnamic derivatives:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=11996210

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=10589442

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=10752646

And just as the salicylate metabolites are subjected to tubular secretion in the

kidneys, so are the benzoate metabolites, i.e. hippuric acid and it's

derivatives. In fact, probenecid itself

contains benzoic acid, being that it's chemical name is

p-[Dipropylsulfamoyl]benzoic acid. And even more interesting, salicylic acid is

2-Hydroxybenzoic acid! So it's surprising that no one has

considered that benzoates might be also be problematic. If one believes that

salicylates can block the effects of guaifenesin at the kidneys, one could

easily theorize that benzoates have a similar

effect.

But it's also quite possible that any adverse effects caused by these chemcials,

could be solely due to the fact that they share the same path of metabolization

in the liver, rather than any effects

they might have on the kidneys. Both of these chemicals can decrease the

available amount of glycine in the liver. Glycine is an important amino acid,

with regard to carbohydrate metabolism, as it

regulates gluconeogenesis in the liver, one the processes which controls blood

glucose levels. A reduction of glycine can lead to inhibited carbohydrate

metabolism and hypoglycemia. Perhaps this

is why, as previously mentioned, there have been cases of salicylates causing

hypoglycemic symptoms.

In addition, one study has shown that hypoglycemic effects from salicylates,

could possibly be due to salicyl Coa. Salicyl Coa is the intermediate form of

salicylate, which salicylates are first

transformed into, before they are conjugated with glycine. With insufficient

glycine, there would then be an excess of salicylyl Coa, which could be the

reason for the disrupted carbohydrate

metabolism.

These possible hypoglycemic effects could be significant, considering that Dr.

St. Amand has claimed that a large percentage of people with fibromyalgia have

some form of hypoglycemia, and that

these people can't successfully be treated with guaifenesin, unless the

hypoglycemia is also untreated. But the hypoglycemia could be due to the

effects of salicylates and benzoates. These

chemicals could be the reason why some people have hypoglycemia, while others

don't, or why some people are very sensitive to salicylates, while others are

not. It may not be a coincidence that Dr.

St. Amand states that salicylates and hypoglycemia are the 2 main reasons why

the guaifenesin treatment may fail. They may, in fact, be one and the same

problem.

But I don't think it's likely that people are being exposed to high enough

levels of salicylates, for hypoglycemia to solely occur due to them. I suspect

it's more likely that it's a combination of

salicylates, and other chemicals, such as benzoate compounds. Benzoates are not

just found in foods and topical sources, but in many other products we are

exposed to. And beyond that, there are

many petrochemicals, such as xlyene, tolunene, and other benzenes, that many of

us are exposed to on a daily basis, without us knowing it, that are also

processed by glycination. Which is why some

people have theorized that these chemicals are a significant reason why so many

people have a problem in metabolizing carbohydrates. An overload of such

chemicals would deplete glycine, and allow

such chemicals to circulate longer in the body, causing other adverse effects.

And the lack of glycine could also lead to low oxidation levels, a condition

which has been proposed as a trigger for

fibromyalgia, given that some people with fibromyalgia have low levels of

antioxidants.

If you avoid products that contain salicylate additives, you are likely to also

avoid some benzoate additives. I.e., many salicylate free products are also

fragrance free, which means that aromatic

benozate compounds may also be removed And if you go on a hypoglycemic diet,

you will also lower the amount of natural benzoic and quinic acids that you

ingest. Is this just a coincidence, or a

meaningful observation?

It could be, that the benefit of avoiding salicylates, may have nothing to do

with a possible interaction between salicylates and guaifenesin. Instead, the

benefit could be due to the reduction of

detrimental effects, which are directly being caused by salicylates and similar

substances.

Avoiding salicylates and other possible chemicals and substances, taking

guaifenesin, and going on Dr. St. Amand's hypoglycemic (or other healthy) diet,

may have a combined effect which could be

significant, and which could lead to beneficial effects on fibromyalgia, but in

a different way than Dr. St. Amand theorizes. It may have nothing to do with

any effects on the kidneys.

Guaifenesin's Anticoagulant Effect

Guaifenesin has another effect that might be useful for some people with

fibromyalgia. It has a known anticoagulant effect, And interestingly, both of

the previous uricosuric drugs that Dr. St.

Amand used for fibromyalgia, i.e. anturane and probenecid, also have an

anticoagulant effect. This effect is relevant, because it has been found that

some people with CFS/FMS have hypercoagulant

activity, and initial studies have shown some success with using heparin and

other anticoagulant drugs. The anticoagulant effect was first noticed in 1994

by a Dr. Couvaras, an infertility

doctor, who began using heparin for fertility problems, and discovered that it

helped many symptoms of his patients who also had CFS and fibromyalgia. Perhaps

not so coincidentally, guaifenesin is

also known to have the ability to increase fertility (originally it was thought

that this effect from guaifenesin was due to thinning of cervical mucus. But

guaifenesin has not been found to have a

direct effect on thinning mucus, but instead simply stimulates mucus glands to

allow more mucus to flow, possibly by irritating gastric linings. This effect

is not likely to occur in the cervix,

because little if any guaifenesin could appear there. Plus, it's the thinning

of the mucus which is important, not increased mucus flow. Thinning mucus

occurs due to a raise in estrogen levels,

and coincidentally estrogen inhibits platetlet aggregation.)

There are several reasons given as to possibly why anticoagulants have helped

some people. But there is one specific effect that might be very relevant for

fibromyalgia. In a recent study on

fibromyalgia, it's been found that some fibromyalgia symptoms coorelate with

lower levels of serum serotonin and higher levels of plasma serotonin. See:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

1203736 & dopt=Abstract

But platelet activation, which causes platelet aggregation, also causes the

release of serotonin, resulting in high plasma serotonin In addition, only in

the last few years has it been recognized

that serotonin influences many other problems, such as migraines, hypoglycemia,

asthma, Raynaud's, and IBS, all conditions which are associated with

fibromyalgia. Some of these conditions are

exacerbated due to serotonin's ability to cause constriction. However, Dr.

Couvaras has said that migraines, irritable bowel syndrome, and pelvic pain, all

went away when he put his patients on

heparin. Interestingly, Dr. St. Amand has also claimed that guaifenesin is able

to treat many different conditions. An imbalance of serotonin in the blood

could be the link that connects all these

conditions.

Hypoglycemia is one of the more interesting conditions related to serotonin, as

it is especially common in fibromyalgia. It is so common, that Dr. St. Amand

himself regularly prescribes a diet for

hypoglycemia to many of his patients, and it is often an integral part of his

treatment in combination with guaifenesin.

However, hypoglycemia can be influenced by a serotonin release, as serotonin has

been shown to increase insulin levels. Not only that, but platelet aggregation

sensitivity is increased due to

hypoglycemia. Thus, this is one possible explanation of why hypoglycemia is so

common. (As an aside, so many people have remarked how helpful the diet is, that

anyone considering going on the

guaifenesin protocol and the diet, might want to first try the diet alone, in

order to be able to tell which effects are occurring from diet, and which

effects are from the guaifenesin.)

Other commonly seen conditions also have a serotonin link. For example, plasma

serotinin in celiac patients has been found to be elevated. Problems associated

with blood pressure, such as Neurally

Mediated Hypotension, are also influenced by serotonin.

In addition, platelet activity causes a release of other substances that might

be affecting fibromyalgia. For example, ATP is also released, and this might be

the cause of reduced levels of ATP

found in red blood cells of people with fibromyalgia.

Both of the previous uricosuric drugs used by Dr. St. Amand, anturane and

probenecid, also affect platelet activity. Anturane (sulphinpyrazone) is well

known for having antiplatelet activity.

Probenecid's effect is a bit different. It's able to block a number of

different aggregating agents. And it's main effect may be due to it's ability to

inactivate thrombin, which is the cause of

platelet activation which leads to the secretion of serotonin from the serum to

the plasma. See the following studies:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=8\

865538 & dopt=Abstract

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=2\

3532 & dopt=Abstract

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=2\

474820 & dopt=Abstract

But what's more, is that an anticoagulant effect might be the reason for the

increased phosphate excretion. The clue to this possibility is a recent report

of a patient being treated with

probenecid for calcinosis:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

1361202 & dopt=Abstract

According to most studies, probenecid does not cause phosphate excretion in

either non-gout or gout patients. However, there are several reports in the

medical literature of it occurring. But they

are so rare, that whenever a case occurs, it's reported in a medical journal.

In the above report, the patient had Juvenile Dermatomyositis which led to

calcinosis, a condition where calcium is

abnormally deposited around bones, causing severely limited mobility. The

patient also had hyperphosphatemia, and probenecid was able to reverse this

condition by increasing phosphate excretion,

and this led to reversing the calcinosis.

However, it's possible that the hyperphosphatemia seen in this patient was due

to a drug that she was taking, which was Cyclosporin A. This drug is known to

cause platelet aggregation and high

plasma serotonin levels:

http://www.sums.ac.ir/~ijms/9834/fardaee9834.html

This paper mentions that impaired renal functioning and reduced renal plasma

flow also occur with this drug. The impaired renal functioning could lead to

phosphate retention. If an anticoagulant

could improve renal flow, then theoretically this could cause increased

phosphate excretion.

And there is possible proof that the phosphate excretion from probenecid is due

to an effect other than the uricosuric effect. Here is a study of an earlier

case of probenecid being successfully

used for calcinosis:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=9\

360503 & dopt=Abstract

In that case, phoshate excretion occurred even without a significant increase in

uric acid excretion. In other words, the two effects might be unrelated.

This would also explain the puzzle of why uricosuric drugs produce increased

uric acid excretion in normal people, yet phosphate excretion does not occur.

They are two separate effects, and the

phosphate excretion would only occur in people who had impaired platelet

functioning.

But it should be pointed out that not all anticoagulants affect the impaired

renal functioning which is caused by platelet aggregation. This is not

surprising, as there are several different

pathways involved in platelet aggregation Thus, different drugs inhibit

aggregation in different ways. In the following study, renal impairment was

induced by endotoxin, a platelet growth factor

which causes aggregation. In high enough doses, endotoxin is able to cause

reduced phosphate excretion. Heparin had no effect on the renal impairment,

while aspirin was able to restore proper

renal functioning:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

667536 & dopt=Abstract

Heparin is strictly an anticoagulant, while aspirin is an antiplatelet drug.

This study theorized that only antiplatelet drugs could reverse the renal

impairment caused by platelet aggregation, but

perhaps the real reason is how the kidneys handle the drugs. Drugs such as

uricosuric drugs and salicylates are actively secreted into the kidneys. Thus,

uricosuric drugs might be the only

anticoagulant drugs that are able to reverse all the affects of platelet

aggregation.

What is causing the platelet aggregation? There are many possible reasons. A

magnesium deficiency can be the cause. Another interesting possibility is that

low levels of certain antioxidants

factors, glutathione and thiols, can also be the cause. This is interesting

because some people with fibromyalgia and CFS appear to have this condition, and

people have found benefit from taking

supplements that increase glutathione, such as special forms of whey. Elevated

blood homocysteine levels is also a possible cause. This can be due to a B12

deficiency, and many people with CFS and

fibromyalgia find benefit from taking B12 shots. Homocysteine levels are also

increased in hypothyroidism, and hypothyroidism is commonly found in

fibromyalgia patients. Estrogen may be a factor

in women, since it's known to inhibit platelet aggregation. Fibromyalgia is

more likely to occur in older women, when estrogen levels are decreasing. One

study showed lowered basal levels of

estrogen in women with fibromyalgia. Another study showed that fibromyalgia

symptoms were worse during part of the cycle with the lowest level of estrogen.

Certain infections, such as candida, can

increase platelet activity, as platetets secrete toxins against infections.

Lyme disease might also increase platelet aggregation.

It's quite possible that a number of factors can be increasing platelet

aggregation. This is true in other conditions, such as diabetes, where platelet

aggregation exists, and different treatments

have been found to be useful, One treatment of specific interest is the use of

amino acids which have been found to be low in diabetes. Taurine and arginine

have been successfully used to reduce

platelet aggregation. Since amino acid levels have been found to abnormal in

both fibromyalgia and CFS, this is another possible factor.

However, even if platelet aggregation or coagulation problems exist in people

with fibromyalgia, this would not necessarily mean that the problem is worse

enough to impair renal functioning. If

that was the case, then decreased phosphate excretion would be noted in patients

with fibromyalgia. Not only is this not true, but people with fibromyalgia have

found benefit from guaifenesin

without observing any increased phosphate excretion.

If platelet activity is a factor in fibromyalgia, then how is it that other

drugs and supplements for fibromyalgia are also effective, yet they don't have

any effect on platelet activity? The

answer is that coincidentally (or perhaps not), most other drugs and supplements

for fibromyalgia do inhibit platelet aggregation. All of the following have

some affect on platelet activity: Some

antidepressants, especially tricyclics, benzodiazepines such as xanax and

valium, antihistamines such as benadryl, anesthetics such as procaine,

supplements such as MSM, ginko, pycnogenol,

quercetin, and bromelain, magnesium, B12 (homocysteine increases platelet

aggregation), whey (treats glutathione deficiency, which causes platelet

aggregation), some amino acids such as taurine and

arginine, and relaxin (presently experimentally used for fibromyalgia). Thus,

like guaifenesin, all of these substances are recommended for use for

fibromyalgia, but they also have some ability to

inhibit platelet aggregation

In fact, one could hypothesize that some of the people in the guaifenesin study,

who did not see any benefit from guaifenesin, might have already been taking a

supplement or medicine that inhibited

platelet activation, and thus were not affected by the addition of guaifenesin.

This hypothesis gains further strength from the fact that Dr. St. Amand

recommends to people to avoid most

supplements, because he feels they are not necessary, so that his own patients

would be less likely to be exposed to such remedies. Additionally, many of the

supplements that inhibit platelet

activation, may contain traces of salicylates, so they are avoided by people

taking guaifenesin. The fact that both guaifenesin and many salicylate

containing supplements are able to inhibit

platelet aggregation is not simply a coincidence. Both guaifenesin and many of

these supplements are derived from the skins and barks of plants, so they are

likely to have similar effects.

However, guaifenesin is now artifically produced, rather than being naturally

derived, so it doesn't have the traces of salicylates that the other supplements

might have.

Regardless of whether the anticoagulant theory is correct, people should be

aware of this effect from guaifenesin, as many other drugs and supplements also

have anticoagulant effects. The

combination of several such drugs could causes side effects. Too much of an

anti-platelet effect can destroy platelets, resulting in a much larger release

of serotonin and histamine. Also, if

guaifenesin doesn't help your platelet aggregation problem, it could be that you

need a different type of anticoagulant, as platelet activation is caused by

several different effects. Additionally,

guaifenesin's effect is dependent on how long it stays in the blood stream.

However, guaifenesin is rapidly metabolized and removed from the blood, so that

it doesn't necessarily make for the best

anticoagulant drug. And it also has other effects which are not found in other

anticoagulants.

So what are the lumps that Dr. St. Amand claims to find in his patients?

One of the main diagnostic tools which Dr. St. Amand uses to determine if a

patient is correctly responding to guaifenesin, is by examining lumps which he

detects on a patient. He maps the body for

such lumps. While the definition of fibromyalgia includes the presence of

tender points in the body, these points are not necessarily lumpy. Plus, Dr.

St. Amand finds many more lumps than the

number of known tender points. They literally are all over the body, not just

on muscles, but also on tendons and ligaments. Such lumps are not described by

any other fibromyalgia researcher, and

are not a part of the description of fibromyalgia. It's perplexing that Dr. St.

Amands finds these " lesions " (as he often refers to them), while no other

fibromyalgia researcher has found any such

abnormalities that are specific to fibromyalgia.

Some fibromyalgia researchers used to wonder if perhaps there were major

abnormalities in the muscles that could be the reason for the pain. However, no

major differences could be found that would

be responsible for the pain. Therefore, they no longer believe that the primary

cause of fibromyalgia originates from the muscles themselves, but in the

neurological and immune system. Any

abnormalities found in muscles and tissues surrounding them are believed to be

secondary effects. Thus, any changes in the muscles do not necessarily reflect

whether the primary cause of

fibromyalgia is being treated.

And as an aside, even by Dr. St. Amand's own theory, he believes that these

lumps are secondary to the source of fibromyalgia pain. Because he doesn't

actually believe that the lumps are " phosphate

deposits " . This might surprise the many people who use guaifenesin, and who

talk about such deposits. He believes that the excess phosphate is actually

stored in all the cells of the body. The

lumps are simply areas where excess calcium has been dragged into cells by the

excess phosphate, causing constriction of the tissues. They aren't even

necessarily painful. Dr. St. Amand only uses

them as gauge to determine if the phosphate is " clearing " . They by themselves

aren't the source of fibromyalgia pain. And anecdotally, I've spoken with

people who have taken guaifenesin for over a

year, and had all their lumps reduced, creating a clear map, yet their level of

fibromyalgia pain was still quite high.

But this doesn't quite make sense. Because areas of constriction, means areas

of lower blood flow, and Dr. St. Amand has often said that tissues with lower

blood flow, should clear more slowly.

Phosphate in the other areas of the body, i.e. brain and the immune system,

where the true source of fibromyalgia pain comes from, should actually clear

first. The lumps should be the last areas

to clear.

So what exactly are these lumps? Could they be myofascial trigger points or

knots in the muscles? Possibly. However, Dr. St. Amand has stated he does not

feel for areas which are painful or

tender, but which are swollen to the touch. Thus, if they are swollen, another

possible explaination is that they are related to edema, or water retention.

Edema is a very common side effect of

many pain killers and antidepressants. Edema can also be caused by an excess of

anything that causes vasodilation, which then leads to capillary permeability.

Abnormally high levels of cortisol

are known to cause this, and studies have shown higher that levels are increased

in some people with fibromyalgia. Other substances such as serotonin and

histamine can also cause vasodilation.

These substances are released when blood platelets are activated. Thus, the

antiplatelet effect of guaifenesin might be responsible for reducing such lumps.

And it's interesting to note that the

study that looked at guaifenesin's analgesic properties, also looked looked at

possible anti-inflammatory effects. In comparison with aspirin, guaifenesin was

found to affect certain inflammation

effects, but not all of them. One of those effects happened to be a reduction

in edema lesions. The fact that guaifenesin didn't act as a full

anti-inflammatory, could lead one to speculate that

the effect was not a true anti-inflammatory one, but that it was a different

effect that was at work, such as the antiplatelet effect.

Is Guaifenesin Safe?

No study has ever been done on long term use of guaifenesin. It was an old drug

that was grandfathered in, and thus avoided the normal tests that are done for

new drugs. There have been no study

to determine whether it is a carcinogenic Dr. St. Amand claims that it's been

used long term by patients with asthma and emphysema, but this is false.

Patients with these conditions are actually

warned against using guaifenesin for coughs, unless they are productive coughs,

so they are not for long term use.

If guaifenesin really could increase excretion of phosphate, this could be a

problem, as phosphate is necessary for proper bone formation. This is

especially true in children and adolescents, whose

serum phosphate levels are significantly higher than adults. This effect is

most likely due to increased growth hormone levels, which is known to increase

phosphate reabsorption in the kidneys.

The elevated phosphated is believed to be an important factor for bone

mineralization. Inappropriately decreasing phosphate levels, could therefore

affect bone growth. But as I've noted, there is

little evidence that guaifenesin can affect phosphate levels.

And, as an aside, if every growing child retains phosphate, so much so that

serum levels are increased (i.e. that there are not enough places to put the

phosphate, so that it stays in the

bloodstream), one wonders why that effect doesn't cause fibromyalgia in every

child. Because that retention effect is obviously much more significant than

the retention which Dr. St. Amand claims

to occur in fibromyalgia, as no noticable rise is seen in serum phosphate in

fibromyalgia patients.

In any event, while there is no proof of increased urinary phosphate due to

guaifenesin, it's possible that guaifenesin may be able to increase calcium

excretion. The study showed an

increase in urinary calcium without a corresponding increase in urinary

phosphate. Dr. St. Amand himself has said he's seen an increase in urinary

calcium, and that he believes that this from

deposits being removed by guaifenesin, but there is no proof of this. However,

taking calcium supplements while on guaifenesin would, however, easily offset

this problem.

However, if guaifenesin can significantly lower serum uric acid, there is the

possibility this may be harmful to some people. Guaifenesin has the capability

of lowering serum uric acid by

increasing urinary uric acid excretion. While it's always been known that high

uric acid levels can be harmful, only recently has it been found that low uric

acid levels may also be harmful. This

came about on the discovery that people with Multiple Sclerosis almost never

have high levels of uric acid. It has since been found that uric acid can

counteract the effects of peroxynitrite, a

potent oxidant which is created from nitric oxide. High nitric oxide levels may

not only play a role in the developement of MS, but also in many other diseases,

inflammation diseases such as

arthritis, and brain disorder diseases such as Parkinsons and Alzheimers. A

similar role for nitric oxide has been proposed for both CFS and fibromyalgia:

If serum uric acid levels drop too low, it

is possible that this could trigger other diseases to occur. And since these

diseases take years to develop, it would not be easy to notice this is

occurring. Thus, it would seem prudent for anyone

taking large doses of guaifenesin to have their uric acid levels checked.

Guaifenesin users often avoid sources of salicylates, many of which also include

substances such as phenols. Both phenols and salicylic acid inhibit the

sulfation of toxins. While the sulfation

process is meant to be detoxifying, unfortunately it has the opposite effect on

many present day toxins, creating substances that are even more toxic. This

effect is believed to play a significant

in some forms of cancer. Patients on the guaifenesin might well be advised to

seek out sources of phenols that don't contain salicylic acid.

Conclusions

Guaifenesin is not a simple drug, and fibromyalgia is not a simple disease.

Because of this, it's possible that there are a number of reasons why

guaifenesin might help someone with fibromyalgia.

I've presented several alternative reasons, that are based on what is known

about fibromyalgia and guaifenesin from the medical literature. On the other

hand, the medical literature contains little

support for the phosphate theory. In order for the phosphate theory to be

valid, not only would it contradict what is known about fibromyalgia and

guaifenesin, but it would also contradict what is

known about phosphate metabolism, kidney functioning, and the effects of

uricosuric drugs, not to mention the dubious claims regarding salicylates.

All of this is probably is why present day fibromyalgia researchers have

basically ignored Dr. St. Amand's phosphate theory. Is Dr. St. Amand correct,

and the rest of world's researchers wrong?

Fibromyalgia is a syndrome of symptoms. It often is triggered by a wide range

of other health problems, i.e. a sleep disorder, hypothyroidism, lyme disease,

chronic myofascial pain, to name just a

few. In many cases, fibromyalgia is secondary to these other problems, and

treating these primary problems can often significantly relieve the

fibromyalgia. Unfortunately, some problems often go

undiagnosed for years and decades. For example, lyme disease, which causes

fibromyalgia symptoms in many people, has gone undiagnosed in many people, due

to inadequate lab tests. Many people who

were told that they didn't have lyme disease, have later discovered that they

actually had it.

Hypothyroidism is another condition which can be a primary reason for

fibromyalgia. It too has been undiagnosed in many people, due to a previously

large normal range for the TSH lab test. The

normal range for TSH has only recently been narrowed, so that people who

previously believed they didn't have a thyroid problem, are now being diagnosed

with hypothyroidism. And even the present

TSH normal range, is still viewed by some people as being too wide.

Other hormonal imbalances, such as a deficiency of either progesterone or

testosterone, can play a major role in fibromyalgia symptoms. Progesterone not

only has hormonal effects, but also has many

neurological ones. A progesterone deficiency can lead to symptoms commonly

found in fibromyalgia, such as disturbed sleep and migraines. The effect that

causes migraines, may be related to a

release of substance P, a neurotrasmitter that is involved in the pain process,

and known to be elevated in fibromyalgia. Studies show that progesterone can

reduce levels of substance P.

Progesterone also appears to be able to relieve pain, via an effect on NMDA

neuron receptors, receptors that play a role in pain perception.

Low levels of testosterone, both in men and women, can also play a role in

chronic pain. Testosterone may be the reason why many more women have chronic

pain problems, such as fibromyalgia, than

men. A study has shown that testosterone is significantly lower in some groups

of women with fibromyalgia. And another study has shwn that low testosterone

can lead to low levels of ATP in

muscles. Additionally, there is ongoing research to develop a testerone patch

to help treat fibromyalgia patients that have low testosterone.

And, as an aside, one of the reasons why some people with fibromyalgia can't

tolerate narcotics, may be because opioids are known to suppress hormones such

as testosterone, progesterone, and growth

hormones.

What these examples show, is that there are many conditions that can be the

primary cause of fibromyalgia symptoms. However, even when fibromyalgia is the

primary problem, other conditions may

still be present as secondary problems, affecting the severity of the

fibromyalgia symptoms.. And fibromyalgia in itself can cause other problems

which take a life on their own, such as chronic

myofascial pain. It's basically hard to find someone with fibromyalgia, who

doesn't have at least one other health problem that affects their fibromyalgia

symptoms. And it's these other

conditions, which make fibromyalgia much harder to treat.

Thus, given the variety of symptoms and health problems that can occur in people

with fibromyalgia, it is extremely unlikely that a single remedy can treat all

the symptoms that a person is likely

to suffer with this syndrome. Because of this, it's common for fibromyalgia

patients to use a wide range of different remedies and treatments.. In fact, in

a survey of 1200 fibromyalgia patients,

no one medicine was being by more than 20% of the patients. It's almost

impossible to find two people with fibromyalgia, who are taking the same

combination of remedies and supplements.

And unfortunately, it can sometimes take a very long time for people to discover

a set of remedies and treatments that can help their fibromyalgia. It is often

a frustrating and stressful search.

Here is a good site for reading about new and alternate treatments and remedies

for fibromyalgia:

http://www.immunesupport.com/

In fact, the actual act of deciding on a treatment plan that one believes in,

and stopping the seemingly endless search for remedies, can by itself be very

beneficial to a patient. For example, in

one small study, it was found that people who recovered from fibromyalgia, did

so regardless of the specific treatment The study showed that " resistance to

the unpleasantness of the sick role and

the stigmatization associated with the uncertain nature of the FM diagnosis

promoted recovery. " So it's no wonder that many people are attracted to a

therapy that claims to be able to treat the

root cause of fibromyalgia, and to be able to reverse all the symptoms. There

is no need to try out different medicines and supplements. And all of the

treatment instructions are readily available

in books and on the web, and are straight forward enough that almost anyone can

easily follow them.

And once on the guaifenesin treatment, many people tend to stay on it for months

and years, even if they only experience a limited benefit from it. They do so,

because of the promise that if you

stay on it long enough, you will achieve a full clearing of all phosphate

deposits. People are also told that it can take years to clear the deep

phosphate deposits that supposedly exist in the

deeper tendons and ligaments. Dr. St. Amand has been quoted as saying " Tendons

and ligaments are often the last to clear so always expect aches and pains of

considerable duration in those

regions. " Thus, according to the treatment, it's possibly to be on guaifenesin

for years, but still continue to experience pain. This logic therefore gives

people a reason to stay on the treatment

plan for many years, even if their pain levels have not significantly decreased.

Fortunately, there is no evidence that these deep deposits exist. Because in

conditions such as hyperphosphatemia,

where such deposits definitely do occur, there is a high incidence of

spontaneous rupture of tendons and ligaments. This phenomena is not seen if

fibromyalgia patients.

The guaifenesin treatment also has major psychological benefits. The main one

being the ability to picture one's pains in a more optimistic positive light.

One's normal response to pain is to

reduce activity, as pain is usually a signal to the body that an injury has

occurred. Unfortunately, inactivity leads to unconditioned muscles, which is a

major problem in many people with

fibromyalgia. Constant pain and inactivity can then lead to other problems,

such as myofascial pain. Gentle exercies and stretching can be beneficial to

both problems. If one is assured that pain

is not indicative of an injury, one is more likely to keep active. While on the

guaifenesin treatment, pain can be attributed to the reversal process, and is

thus thought to be a good sign. Pain

is less frightening. Combining this outlook, with increased physical activity,

and a possible neurological effect on pain and muscles, could lead to a

significant improvement of fibromyalgia.

Thus, while the phosphate theory is just a theory, there are benefits from

believing in it. On the other hand, it can also lead to unintentional harm.

The obvious one being that it may prevent

people from looking at other remedies and treatments that might help them, and

it might prevent from looking at the possibility that they have an undiagnosed

condition. And paradoxically, the

phosphate theory may actually deter some people from trying guaifenesin. Some

of the people who do not find any benefit from guaifenesin, end up becoming

angry that the treatment didn't work for

them. This happens because most people end up devoting a very long time to

trying to make it work, due to the fact that it's advertised as being the best

remedy for fibromyalgia. Many end up

believing that they have been deceived about the true success rate from

guaifenesin, and discourage others from trying it. In the end, there is no

reason to deceive people by continuing to

advertise a theory. I believe that guaifenesin's benefits should stand on it's

own, just like any other remedy. Although it's understandable why Dr. St. Amand

continues to talk about his phosphate

theory. It's hard to give up on a theory that one has been trying to prove for

40 years.

Personal Comments

I am not a doctor. But, given the resources of the internet, it is now possible

for anyone to do their own research and find out the real facts for themselves.

Sites like

http://www.ncbi.nlm.nih.gov/PubMed/ allow anyone to discover more facts than

probably their own doctors know. While I had to visit medical libraries to find

the older journal articles on probenecid

and guaifenesin, most of the useful articles can be found online, either as

abstracts or in complete text. Hopefully the presence of such tools will make

it possible for medical advances to

increase at a more rapid pace, and for medical mistakes to be reduced.

Copyright © 2001

Contents of this article are the property of Mark R. London, MRL@...

Contents can be forwarded to other people and posted on the internet, as long as

it is forwarded in full. Contents

cannot be used in any way in any other media, without permission of the author.

Mark London MRL@...