After I created my web page, Alfred Blasi, the creator
Recuperation, posted comments about my web page to the
AlfredblasiprotocolFMSCFS yahoo discussion group. Here is my response to his post. The indented lines starting with
“>” are from his post.
> There are published scientific studies that demonstrate that the people with FM and CFS have low levels of> calcium and magnesium at muscular intracellular level. The medical
literature is not as definite about this as you indicate, so it's worthwhile to
look at the published studies. But first, for those people who may not
know, a magnesium deficiency does cause a reduction of magnesium levels in
muscle tissues. Such a condition is actually quite common, and thus may
be present in some people with CFS or fibromyalgia. But a magnesium
deficiency is not specific to either CFS or fibromyalgia, so it is not the root
cause.
Valid methods that test for a magnesium deficiency are either cumbersome or
expensive, so it's not done very often. Here's a study that was done on
random people in a hospital, that shows that magnesium deficiency is fairly
common:
Scand J Clin Lab Invest. 1992 Jun;52(4):245-53.
Magnesium deficiency diagnosed by an intravenous loading test.
"Magnesium deficiency is common but difficult to diagnose and to assess in
clinical practice. The use of a magnesium loading test was therefore evaluated
to diagnose magnesium deficiency in 661 hospitalized patients with medical
conditions assumed to interfere with magnesium uptake and excretion. Thirty
millimoles of magnesium sulphate were administered intravenously during 8 h as
a loading test and related to the urinary excretion in the following 24 h. A
group of 30 patients without any known predisposition for magnesium deficiency
and a group of 27 healthy volunteers served as controls. The mean (with 95%
confidence interval) magnesium retention was 4 (-2-10)% in the control group of
patients and 3 (-2-8)% in healthy subjects. A significantly higher retention
was observed in all the groups of the patients: atrial fibrillation 18
(11-25)%, other arrhythmias 18 (11-24)%, hypertension 27 (20-33)%, coronary
artery disease 25 (20-30)%, congestive heart failure 31 (26-37)%,
cerebrovascular events 38 (24-51)%, gastrointestinal disorders 22 (14-29)%,
diabetes mellitus 16 (9-22)%, and alcoholics 33 (29-36)%."
That study used the magnesium loading test to detect a magnesium
deficiency. The higher the amount of magnesium that is retained, the more
deficient the person is.
Studies on magnesium levels in CFS and fibromyalgia, have an interesting
history in the medical literature. Regarding CFS, one of the earliest
ones is the following:
Lancet. 1991 Mar 30;337(8744):757-60.
Red blood cell magnesium and chronic fatigue syndrome.
"In the case-control study, 20 patients with CFS had lower red cell
magnesium concentrations than did 20 healthy control subjects matched for age,
sex, and social class (difference 0.1 mmol/l, 95% confidence interval [CI] 0.05
to 0.15). In the clinical trial, 32 patients with CFS were randomly allocated
either to intramuscular magnesium sulphate every week for 6 weeks (15 patients)
or to placebo (17). Patients treated with magnesium claimed to have improved
energy levels, better emotional state, and less pain, as judged by changes in
the
This was a triple blind study with patients from random doctors. While
the red blood cell magnesium test that was used in the study, doesn't correlate
with the amount of magnesium in muscles, the study nevertheless appears to be
well done, and thus it would seem to be a pretty significant finding. On
the other hand, here is a later study:
Ann Clin Biochem. 1994 Sep;31 ( Pt 5):459-61.
Normal red cell magnesium concentrations and magnesium loading tests in
patients with chronic fatigue syndrome.
"Red blood cell magnesium concentrations were measured in samples from 89
patients who fulfilled the diagnostic criteria for chronic fatigue syndrome and
the results compared to those found in an age and sex matched group selected
from the normal population. No significant difference was found. Six patients
were further investigated using a magnesium loading test to determine if there
was any evidence of magnesium deficiency associated with this disorder. None
was found. There is therefore no indication for the use of magnesium therapy in
the management of this condition."
Totally different results. Why did this happen? Several
possibilities. Regional populations of patients may have different
contributing factors. It's possible that the first group of patients had
more people with a severe form of magnesium deficiency, which would cause low
RBC magnesium. The patients that were recruited, came from many different
doctors. Using this method, one is more likely to find more people with a
severe deficiency, versus if you took patients from only a few doctors, or from
a limited regional area. Or perhaps there are seasonal effects.
It's also possible that better treated patients may not have the same clinical
symptoms. Or that the control population in the 2nd study was better (or
worse) matched to the patients. But whatever the reason, it's obvious that
studies always have to be repeated, no matter how confident the first study
appears. Even well done studies can be flawed.
Here's a study where a much larger number of people were given the magnesium
loading test:
J Am Coll Nutr. 2000 Jun;19(3):374-82.
Magnesium status and parameters of the oxidant-antioxidant balance in patients
with chronic fatigue: effects of supplementation with magnesium.
"OBJECTIVE: Magnesium deficiency and oxidative stress have both been
identified as pathogenic factors in aging and in several age-related diseases.
The link between these two factors is unclear in humans although, in
experimental animals, severe Mg deficiency has been shown to lead to increased
oxidative stress. METHODS: The relationship between Mg body stores, dietary
intakes and supplements on the one hand and parameters of the
oxidant-antioxidant balance on the other was investigated in human subjects.
RESULTS: The study population consisted of 93 patients with unexplained chronic
fatigue (median age 38 years, 25% male, 16% smokers and 54% with Chronic
Fatigue Syndrome (CFS). Mg deficient patients (47%) had lower total antioxidant
capacity in plasma (p=0.007) which was related to serum albumin. Mg deficient
patients whose Mg body stores did not improve after oral supplementation with
Mg (10 mg/kg/day) had persistently lower blood glutathione levels (p=0.003). In
vitro production of thiobarbituric acid reactive substances (TBARS) by non-HDL
lipoproteins incubated with copper was related to serum cholesterol
(p<0.001) but not to Mg or antioxidants and did not improve after Mg
supplementation. In contrast, velocity of formation of fluorescent products of
peroxidation (slope) correlated with serum vitamin E (p<0.001), which was,
in turn, related to Mg dietary intakes. Both slope and serum vitamin E improved
after Mg supplementation (p<0.001). CONCLUSIONS: These results show that the
lower antioxidant capacity found in moderate Mg deficiency was not due to a
deficit in Mg dietary intakes and was not accompanied by increased lipid susceptibility
to in vitro peroxidation. Nevertheless, Mg supplementation was followed by an
improvement in Mg body stores, in serum vitamin E and its interrelated stage of
lipid peroxidation.
In the study's conclusion, it stated that "no association was found
between Mg deficiency on the one side, and Mg dietary intakes, blood
concentrations and the presence of CFS on the other." Magnesium
deficiency occured similarly in both CFS patients, and those people who had
other unexplained fatigue.
Finally, here's a very recent and much different study on CFS, that looked
directly at magnesium levels in muscle cells.
Dyn Med. 2006 Jan 11;5:1.
Increase of free Mg2+ in the skeletal muscle of chronic fatigue syndrome
patients.
"In a previous study we evaluated muscle blood flow and muscle metabolism
in patients diagnosed with chronic fatigue syndrome (CFS). To better understand
muscle metabolism in CFS, we re-evaluated our data to calculate free Magnesium
levels in skeletal muscle. Magnesium is an essential cofactor in a number of
cell processes. A total of 20 CFS patients and 11 controls were evaluated.
Phosphorus magnetic resonance spectroscopy from the medial gastrocnemius muscle
was used to calculate free Mg2+ from the concentrations and chemical shifts of
Pi, PCr, and beta ATP peaks. CFS patients had higher magnesium levels in their
muscles relative to controls (0.47 + 0.07 vs 0.36 + 0.06 mM, P < 0.01),
although there was no difference in the rate of phosphocreatine recovery in
these subjects, as reported earlier. This finding was not associated with
abnormal oxidative metabolism as measured by the rate of recovery of
phosphocreatine after exercise. In summary, calculation of free Mg2+ levels
from previous data showed CFS patients had higher resting free Mg2+ levels
compared to sedentary controls."
Excess free magnesium often implies decreased ATP in cells, as magnesium is
mostly found in cells bound to ATP. A decrease in ATP would lead to
increased free magnesium. However, ATP was not decreased, so it's not clear what
the cause was for the increased free magnesium. Whatever the cause, this
study didn't appear to find a reduced amount of magnesium or ATP in skeletal
muscles in CFS. The increased sensitivity to muscle fatigue in CFS
appears to be due to other parameters.
As for fibromyalgia, here's where that story starts:
Arthritis Rheum 1993; 36(Suppl)
Low tissue levels of magnesium in fibromyalgia.
This study has been quoted on several web pages, even though there isn't even
an online abstract. That's because this wasn't a published study, but was
an abstract presented at a conference. This preliminary study found that
eight women and one man with fibromyalgia were magnesium deficient according to
the magnesium loading test. There was, however, no correlation between
the level of the deficiency and the level of tender point pain.
Nevertheless, the researchers had indicated that they were planning to conduct
a study on fibromyalgia and magnesium supplementation. However, no such
study was ever published. One of the researchers, Dr. Daniel Clauw, has
gone on to publish many other studies on fibromyalgia, and also a few studies
on magnesium that did not involve fibromyalgia. In interviews on
fibromyalgia, he's said that magnesium may help some people.
Several years later, we have the following well-known study:
J Rheumatol. 1995 May;22(5):953-8.
Treatment of fibromyalgia syndrome with Super Malic: a randomized, double
blind, placebo controlled, crossover pilot study.
"OBJECTIVE. To study the efficacy and safety of Super Malic, a proprietary
tablet containing malic acid (200 mg) and magnesium (50 mg), in treatment of
primary fibromyalgia syndrome (FM). METHODS. Twenty-four sequential patients
with primary FM were randomized to a fixed dose (3 tablets bid), placebo
controlled, 4-week/course, pilot trial followed by a 6-month, open label, dose
escalation (up to 6 tablets bid) trial. A 2-week, medication free, washout
period was required before receiving treatment, between blinded courses, and
again before starting open label treatment. The 3 primary outcome variables
were measures of pain and tenderness but functional and psychological measures
were also assessed. RESULTS. No clear treatment effect attributable to Super
Malic was seen in the blinded, fixed low dose trial. With dose escalation and a
longer duration of treatment in the open label trial, significant reductions in
the severity of all 3 primary pain/tenderness measures were obtained without
limiting risks. CONCLUSIONS. These data suggest that Super Malic is safe and
may be beneficial in the treatment of patients with FM. Future
placebo-controlled studies should utilize up to 6 tablets of Super Malic bid
and continue therapy for at least 2 months."
From this abstract, there is no indication that magnesium levels were actually
tested. The supplement that was used, was promoted by the manufacturer as
helping fatigue through the combination of malic acid and magnesium. The
blinded study did not show any benefit. However afterwards, patients were
allowed to increase their dose, and at that point beneficial effects were
seen. This part of the study was not blinded, however, and no blinded
follow-up study on the higher dose was ever done. It also should be noted
that like citrate, malate also has an alkalizing effect. Malate can also
increase urinary citrate. Thus, the effects of magnesium malate are still
very unclear, and if there are any benefits from it, it's not clear which
properties of the supplement would be responsible for them.
Finally, there is the following study in Italian:
Minerva Med. 2000 Jul-Aug;91(7-8):137-40.
[Changes in intracellular calcium and magnesium ions in the physiopathology of
the fybromyalgia syndrome]
"BACKGROUND: Calcium and magnesium ions play a key role in the physiology
of muscular contraction: changes in calcium ions concentration may be involved
in the pathogenesis of fibromyalgia. Since the plasmatic levels of calcium and
magnesium in fibromyalgia patients is always in the normal range, it seemed
interesting to evaluate the intracellular calcium and magnesium concentration.
METHODS: The study was carried out on two groups of subjects: 100 affected by
fibromyalgia and 40 healthy controls. RESULTS: The results obtained show that
in fibromyalgia patients the intracellular calcium and magnesium concentration
seems to be a peculiar characteristics of fibromyalgia patients and may be
potentially responsible for muscular hypertonus. CONCLUSIONS: It is still to be
confirmed the effective role of this anomaly in the pathophysiology of
fibromyalgia and the potential role of drugs active on calcium
homeostatis."
These Italian researchers had published an earlier study, where only
intracellular calcium was tested. Here they also test magnesium.
However, the text of both studies are not available for viewing on the
web. A lot of people assumed from reading the abstract, that they were
testing intracellular muscular levels. However, that would have involved
muscle biopsies, which would have been very expensive if 140 people were
tested. I obtained a copy of the later study, and discovered that they
were testing platelet intracellular levels. Platelet intracellular
magnesium and calcium can be influenced by a host of factors, such as
neurochemical, hormonal, or antioxidant dysfunctions. However, their
levels have no correlation with muscular intracellular levels.
Interestingly, two of the researchers listed on that study, took part in a
later study:
Pain. 2002 Dec;100(3):259-69.
Reactivity to superficial and deep stimuli in patients with chronic
musculoskeletal pain.
"Fibromyalgia is a syndrome of unknown origin which displays interesting
aspects of chronic pain, including deep pain and hyperalgesia to deep and
superficial stimuli. It is agreed that there are no distinctive muscle changes
that can define fibromyalgia in terms of specific muscle pathology while
several lines of evidence suggest that the pain experience of fibromyalgia
patients is partly the result of disordered sensory processing at the central
level. Indeed, with respect to control subjects, fibromyalgia patients display
lowered thresholds for experimentally induced heat pain, pressure pain and
lowered pain threshold and pain tolerance to electrical stimuli."
These researchers obviously believe that fibromyalgia is not simply a muscle
pain condition, but that pain processing is disrupted in a general manner, as
displayed by the fact that peripheral pain thresholds are lowered in the
fibromyalgia.
By the way, here's another study which was conducted by these same Italian
researchers:
Minerva Med. 1999 Jan-Feb;90(1-2):39-43.
A new approach to the treatment of fibromyalgia syndrome. The use of Telo
Cypro.
"The aim of this study was to evaluate the effect of a pure copper wire
sheet ("Telo Cypro") used as bedsheet, on sleep quality as well as
spontaneous and provoked pain. METHODS: The study was double-blind, with two
parallel groups, versus placebo. Forty patients with fibromyalgia were
enrolled, thirty-eight females and two males, with a mean age of 48.8 years and
without any current pharmacological treatment. RESULTS: The results obtained
show how the use of "Telo Cypro" is extremely beneficial in subjects
with fibromyalgia, in reducing painful symptomatology at the tender point level
and improving sleep quality, with a positive effect on the patients'
cenesthesia at awakening. CONCLUSIONS: In conclusion, the use of "Telo
Cypro" can be a valid help in the treatment of fibromyalgia."
This is just one of many published studies on unconventional treatments for
fibromyalgia, that supposedly show positive effects. The problem is that
none of these studies ever bother to compare their efficacy with other
treatments. Lots of things can help fibromyalgia. Everybody with
fibromyalgia that I've ever met, are all taking a different combination of
remedies and treatments. This wide variety of remedies, seems to confirm
that it is a generalized chronic pain problem, that can have many different
contributing factors.
> In my case, I am convinced that it has been sufficient to recover me totally;> thus, I have been several years without symptoms.> Something similar happens to many people anywhere in the world. I believe that this> ion combination can help a lot of people who suffers from muscular affectation,> independently of their diagnosed disease.
Most researchers
don't believe that fibromyalgia is mainly a muscular disease. To most researchers, fibromyalgia is a
chronic pain problem. Muscle pain may initiate or aggravate
fibromyalgia pain, but researchers don’t believe it’s the sole
cause. People with fibromyalgia
experience pain dysfunctions that aren’t present in other muscle pain
problems. Here is a description of
fibromyalgia from a recent article on fibromyalgia, that I particularly like:
"Fibromyalgia (FM) pain is frequent in the general population but its
pathogenesis is only poorly understood. Many recent studies have emphasized the
role of central nervous system pain processing abnormalities in FM, including
central sensitization and inadequate pain inhibition. However, increasing
evidence points towards peripheral tissues as relevant contributors of painful
impulse input that might either initiate or maintain central sensitization, or
both. It is well known that persistent or intense nociception can lead to
neuroplastic changes in the spinal cord and brain, resulting in central
sensitization and pain. This mechanism represents a hallmark of FM and many
other chronic pain syndromes, including irritable bowel syndrome,
temporomandibular disorder, migraine, and low back pain. Importantly, after
central sensitization has been established only minimal nociceptive input is
required for the maintenance of the chronic pain state. Additional factors,
including pain related negative affect and poor sleep have been shown to
significantly contribute to clinical FM pain. Better understanding of these
mechanisms and their relationship to central sensitization and clinical pain
will provide new approaches for the prevention and treatment of FM and other
chronic pain syndromes."
This description explains why people with different conditions and symptoms can
all have fibromyalgia. Anything that causes pain, can initiate
fibromyalgia. The nervous system is transformed, resulting in a
centralized chronic pain state, such that even much lower amounts of pain will
continue to maintain the condition. Other factors that increase pain
sensitivity, such as a sleep disorder, will further maintain the condition.
If you have only a single source of pain, such as a mineral imbalance causing
muscle pain, then if you treat that single source, perhaps this might cause the
fibromyalgia to resolve. Of course, you would first have to diagnose that
source. If someone was told that they had fibromyalgia, they would be
given medicines to treat the pain, which would not help a mineral
imbalance. Such an imbalance will continue to get worse.
On the other hand, for people like myself, who have a host of different
problems, some of which are not fully treatable, then the fibromyalgia will be
maintained, as it will continue to have sources of pain that will constantly
aggravate it.
This theory of fibromyalgia also explains why so many widely different
treatments are claimed to help fibromyalgia. Treating any source of pain
will reduce fibromyalgia symptoms. Such treatments will be of most help
to people who have the specific problem that the treatment is designed to
treat. If one doesn't have that specific problem, then that treatment is
unlikely to help. Muscle problems can obviously be a source of
pain. But a remedy that simply improves muscle functioning is not likely
going to treat the elevated centralized pain in fibromyalgia.
This elevated pain is demonstrated in the following study. Hypertonic
saline (high salt water) was injected into resting muscles that initially had
no pain. Saline causes pain by directly stimulating muscle nociceptors
(neurons). But in people with fibromyalgia, the pain lasted longer, and
was felt in a larger area. It was concluded that in fibromyalgia, the
central nervous system was in a higher excitable state.
J Rheumatol. 1998 Jan;25(1):152-5.
Hyperexcitability in fibromyalgia.
"We tested whether muscular hyperalgesia can exist in a muscle without
spontaneous pain, which could indicate a generalized hyperexcitability of the
nociceptive system in patients with FM. METHODS: Twelve women with FM and 12
age matched female controls participated in this blind study. Patients had no
spontaneous pain in the anterior tibial (AT) muscle. The pressure pain
threshold was tested on the AT muscle. The pain threshold to electrical single
and repeated stimulations of the skin and of the right AT muscle was assessed.
Pain was evoked in the left AT muscle by infusion of sterile hypertonic saline
(5.7%, 2.8 ml over 480 s).z' "RESULTS: Pressure pain thresholds were lower
(p < 0.02) in patients with FM compared to controls. Thresholds for pain
evoked by electrical stimulation at the skin were not significantly different
in the 2 groups. The pain threshold to repeated intramuscular stimulation was
significantly (p = 0.02) lower for the patients with FM compared to the control
group, indicating that the temporal nociceptive summation was more pronounced
in patients with FM. This is an indication of central sensitization
(hyperexcitability). Infusion of hypertonic saline evoked muscle pain with a
longer duration (p = 0.01) in patients with FM, and referred pain that spread
to a larger area (p = 0.002) than in controls. This is an indication of central
hyperexcitability. CONCLUSION: There is a state of central hyperexcitability in
the nociceptive system in FM. This hyperexcitability can be revealed by
excitation of intramuscular nociceptors in a muscle with no spontaneous
pain."
Muscles without
any apparent prior pain, showed higher amounts of pain in fibromyalgia
patients, compared to normal paitents, when subjected to hypertonic saline
solution injections. Such solutions are
believed to directly stimulate muscle nociceptors (sensory neurons), without
causing inflammation or injury. Thus,
this higher pain perception, demonstrates that the nervous system is in a state
of hyperalgesia. This means that low
level sources of muscle pain, may be able to aggravate and sustain this
hyperactive state. And fibromyalgia pain
can perpetuates itself in several ways.
For example, pain interferes with sleep, and disrupted sleep increases
the level of pain. Fibromyalgia pain can
also lead to the formation of myofacial trigger points, which becomes an
independent source of pain. This is why
fibromyalgia is hard to treat in most people.
> The calculations of Mark London are based on 4 daily sachets of recuperat-ion.> It concludes that they are little amount of magnesium and calcium.> All the calculations are based on the %RDA. This is correct.> In London > I do not consider in anyway the amount of these ions but the proportion among them. Oral ingestion of
small amounts of common minerals by themselves, that are already present in
large quantities in the body, have yet to be shown in the medical literature as
having significant effects on skeletal muscles, no matter what ratio they are
given in. On the other hand, Recuperation does contain a significant
quantity of sodium citrate. Sodium citrate has been studied for several
decades as a way to increase athletic performance. This is mainly
believed to be due to it's ability to cause alkalosis. One effect of
alkalosis is to remove the buildup of potassium inside of muscles which is
pumped out of cells during exercise. This potassium plays a role in the
fatigue of muscles. However, the amount of sodium citrate used in these
studies was much higher than what Recuperation contains, and muscle fatigue is
not the same as fibromyalgia pain. On the other hand, alkalosis is known
to increase the uptake of minerals into cells, including magnesium, and this
effect might be relevant at lower doses of sodium citrate. For example,
alkalization of the urine increases magnesium and calcium retention in the
kidneys. There might also be other possible effects on the vascular
system, as alkalosis increases magnesium uptake in vascular smooth
muscles. While the small amount of magnesium in Recuperation is not
significant in relation to the amounts in skeletal muscles, it could be
significant in relation to the concentrations in the bloodstream.
Finally, I've listed other possible effects from the sodium itself on my web
page, and even one packet of Recuperation has a decent amount of sodium.
Another reason to believe that sodium citrate is the key ingredient, is due to
the fact that no study has shown that magnesium supplementation has helped
athletic performance.
Even if the ratio of the ingredients in Recuperation is optimum for some
people, that doesn't mean it's optimum for everybody. People absorb and
excrete minerals at different rates. For example, one's vitamin D level
would affect the percentage of ingested calcium that is absorbed. Each of
the minerals in Recuperation are absorbed using different known
processes. Sodium, potassium, and calcium, are mainly absorbed in the
upper small intestine, all via their own mechanisms. Magnesium is mainly
absorbed in the lower small intestine, and thus is absorbed at a slower
rate. The absorption rate of magnesium in mineral water has been found to
be similar to absorption rate of magnesium in food, so there is no reason to
believe that magnesium gets absorbed any faster from Recuperation.
Minerals are also reabsorbed in different areas of the kidneys, which affects
the retention of minerals. Thus, given all these different processes,
it's obvious that the minerals in Recuperation become disassociated once they
are ingested. And if digested food happens to be present in the intestine
when one takes Recuperation, then the absorption of minerals from that food
(especially magnesium) will be entering the serum at the same as the minerals
that are derived from Recuperation. It takes about 3 hours for all food
to pass out of the small intestine. So unless you take Recuperation at
least 3 hours after you eat, the ratio of minerals entering the serum will
vary, depending on the meal you ate. Another effect from food will be
insulin levels, as insulin is a major control of potassium transport into muscle
cells. Insulin will affect the level of potassium absorbed by the
muscles.
Besides which,
even if the minerals were all absorbed at the same rate for everyone, once the
minerals are absorbed by the body,they merge with the minerals that exist in
the body, so the original ratio vanishes.
The new ratio is the ratio of the minerals from Recuperation combined
with the much larger amounts already in skeletal muscles. Small ingested amounts of calcium and
magnesium are not going to affect the ratio of minerals that already exists in
the muscles.
And the mineral
content in muscle cells is constantly being exchanged, with minerals flowing in
and out in response to food, physical activity, ph changes, hormonal changes,
and neurochemical changes. Only sodium citrate is at a high enough level
that could have some effect on this situation. It's the only ingredient
which is not already present in large doses in the body. It's the only
ingredient that may be able to affect hormones, due to the effects of sodium on
the kidneys. It's the only ingredient that may affect ph levels, due to
the citrate.
> In fact, I believe that one or two sachets daily is the optimal quantity at the beginning.> In this group, there are people who have begun with just half a sachet or even less per day.> Later on, each person can adapt the dose to her/his needs.
This fact even
strengthens my argument. One packet
contains 15mg of magnesium. A 50% absorption rate for magnesium is
common, so that's means 7.5mg of magnesium is absorbed. This is then distributed to soft tissues and
muscles. In a typical 70 kg adult,
muscles will contain about 6500mg,and soft tissue about 4600mg. So let's say 4mg of the 7.5mg goes into the
muscles. We're thus talking about .1%
additional magnesium, which is almost a homeopathic dose. How could such a small change be a factor
with regard to muscle functioning? In
fact, if you don't have a real magnesium deficiency, studies have shown that
magnesium supplementation doesn'tincrease the magnesium storage in
muscles. And if you are really magnesium
deficient, you would need to take many packets of Recuperation a day to reverse
the deficiency. And depending on the
level of the magnesium deficiency, it can sometimes take months of high oral supplementation to
fully restore magnesium stores in
muscles.
However, even if
you did take a high amount of magnesium, it's still no guarantee that this will
increase magnesium in tissues. In the
previously mentioned study on magnesium in patients with fatigue, magnesium
supplements were given to those patients who had a magnesium deficiency. While some patient's magnesium stores
increased due to the supplementation, others did not. This would explain why some people don't
notice any effect from oral magnesium supplementation. One might need other methods to increase
magnesium absorption, such as altering ph levels that affects magnesium
transport into cells.
> The amount of sodium could be a problem, but as it has been confirmed in early studies> that this formula because its composition is eliminated very quick, in some minutes, from body. Since sodium
citrate doesn't increase blood pressure as sodium chloride can, there is less
to worry about.
Excess sodium and potassium is excreted relatively quickly in the urine.
However, even here, there is much variability. Elevated water intake can
increase urinary sodium excretion rates. And dietary protein can also
increase excretion rates. On the other hand, insulin has the opposite
effect. Thus, a high protein diet can increase sodium excretion rates,
while a high carbohydrate diet that elevates insulin, may decrease the
rates. Eating after taking Recuperation, will thus have an effect on
retention of the ingested sodium. Thus, these are even more variables
that affect the absorption and retention of the ingredients in Recuperation,
casting more doubt in the idea that there can be an ideal ratio for everyone.
I am unclear what the original reason was for including sodium in
Recuperation. Lack of sodium is definitely not an issue with people on
the standard American diet. And there is no evidence of extra sodium loss
in people with fibromyalgia. Studies show that a high salt diet only
results in a small increase in serum sodium, and no study has shown an increase
any intracellular sodium, except in people that are salt sensitive. Even during exercise, sodium loss is not a
major problem, expect under high sweat inducing conditions (see: Am J Clin
Nutr. 2000 Aug;72(2 Suppl):564S-72S.
“Fluid and electrolyte supplementation for exercise heat
stress.”) Salt from sweat is
reabsorbed by sweat glands, so there is not much sodium loss under normal
sweating conditions. One of the main reasons for salt being added to
sports drinks like Gatorade, is actually to give it enough flavor to encourage
drinking of more liquid. Perhaps one of the benefits of Recuperation is
to encourage more water drinking.
The main reason that I'm aware of, as to why some people with fibromyalgia or
CFS take sodium, is to increase blood volume, which is an effect that occurs
seperately from the other minerals in Recuperation. The other effects of
sodium which I've mentioned on my web page, are also all separate effects.
Given a normal diet, the body is more likely to lack magnesium, calcium,
potassium, and sodium, in that order. But their amounts in relation to
their need is in reverse order in Recuperation, i.e. more sodium than potassium
than calcium than magnesium. Thus, I theorize that the positive effects
of taking extra sodium are likely due to some indirect effect, i.e. not from
the sodium itself, but from the body's response to increased intake, such as ph
change, hormonal changes, etc.
I suspect that
sodium's ability to lower sympathetic nervous system activity and increase
blood flow, may be the most significant effect of sodium for fibromyalgia. Increased sympathetic activity is associated
with both myofacial trigger points and fibromyalgia. In fibromyalgia, decreased blood flow has
been observed in muscles, and this may be due to elevated norepinephrine levels
that is the result of increased sympathetic activity. Studies show that blocking this sympathetic
activity, reduces pain in fibromyalgia, and this may be due to an increase in
blood flow:
Pain. 1988 May;33(2):161-7.
Regional
sympathetic blockade in primary fibromyalgia.
“Twenty-eight
patients with primary fibromyalgia participated in the study. Eight patients
received a stellate ganglion blockade with bupivacaine, and 14 days later an
intravenous regional sympathetic blockade with guanethidine. The remaining
patients served as controls and were randomly allocated to receive either a
sham (placebo) injection with physiologic saline superficial to the stellate
ganglion (n = 10) or bupivacaine intramuscularly (n = 10). The efficiency of
the stellate ganglion blockade was evaluated by measuring skin blood flow
(using a laser Doppler flowmeter), skin temperature, and skin conductance
responses ('sympathogalvanic reflex'). Trigger and tender points (TePs) were
counted, and rest pain in the arm, shoulder and neck evaluated at intervals up
to 4 h after the injection. The guanethidine blockade was evaluated 24 h after
the injection by counting TePs and by assessment of rest pain in the hand and
forearm. The results indicate that a complete sympathetic blockade, produced by
a stellate ganglion blockade, markedly reduced the number of TePs and produced
a marked decrease in rest pain. The guanethidine blockade reduced the number of
TePs, but had no effect on rest pain. The reduction in pain and TePs produced
by a sympathetic blockade may be due to an improvement in microcirculation.
Sympathetic activity may, in some patients, contribute to the pathogenesis of
primary fibromyalgia.”
Researchers have
lately been considering that abnormal input to the muscle neurons, may be an
important factor in the maintenance of the central pain state in fibromyalgia.
Increased sympathetic activity could be resposnsible for that abnormal input,
as it may chronically sensitize the muscle neurons: Anyone interested in this theory, should read
the following excellent article by Charles J. Vierck Jr., Ph.D., former
director of the Center for Neurobiological Sciences in the University of
Florida’s McKnight Brain Institute, who has been conducting studies on
fibromyalgia pain during the last 5 years:
Pain. 2006 Jul 12
Mechanisms
underlying development of spatially distributed chronic pain (fibromyalgia).
“Chronic
fibromyalgia (FM) pain is prevalent (estimated as high as 13%), predominantly
affects women, and is associated with a variety of focal pain conditions.
Ongoing FM pain is referred to deep tissues and is described as widespread but
usually is maximally located within a restricted region such as the shoulders.
Palpation of deep tissues reveals an enhanced nociceptive sensitivity that is
not restricted to regions of clinical pain. Similarly, psychophysical testing
reveals allodynia and hyperalgesia for cutaneous stimulation at locations
beyond regions of clinical pain referral. The combination of widely distributed
clinical pain and generalized hypersensitivity is highly disabling, but no
satisfactory treatment is regularly prescribed. A thorough understanding of
mechanisms will likely be required to develop and document adequate therapies.
The generalized hypersensitivity associated with FM has focused considerable
interest on central (CNS) mechanisms for the disorder. These include central
sensitization, central disinhibition and a dysfunctional
hypothalamic-pituitary-adrenal (HPA) axis. However, the central effects
associated with FM can be produced by a peripheral source of pain. Chronic
nociceptive input induces central sensitization, magnifying pain, and it
activates the HPA and the sympathetic nervous system. Chronic sympathetic activation
indirectly sensitizes peripheral nociceptors and sets up a vicious cycle. Thus,
it appears that central mechanisms of FM pain are dependent on abnormal
peripheral input(s) for development and maintenance of this condition. A
substantial literature defines peripheral-CNS-peripheral interactions that are
integral to FM pain. These reciprocal actions and related phenomena of
relevance to FM pain are reviewed here, leading to suggestions for testing of
therapeutic approaches.”
Different factors
can increase sympathetic activity.
Stress is the most common one, and of course pain would itself be a
source of stress. Sleep disturbances can
also affect sympathetic activity, as activity increases during REM sleep, but
much less in other types of sleep (such as slow wave sleep, which is often
deficient in fibromyalgia). And it's
interesting to note that many of the drugs given for fibromyalgia (such as
elavil, pregabalin, and xyrem) all have the ability to decrease REM sleep. Yet another factor is inflammatory
cytokines. Studies have shown that IL-8
levels coorelate with fibromyalgia pain , and IL-8 is able to stimulate
sympathetic activity. IL-8 can be
elevated due to a number of reasons, one of which is infections. Thus, in theory, an injury or infection or
stress, that occurs for a long enough period of time, could increase
sympathetic activity, leading to decreased muscle blood flow, resulting in
muscle pain and eventually fibromyalgia.
Some studies
indicate that sodium can lower
sympathetic ctivity and increase blood flow.
The positive effects of sodium on non-salt sensitive people, have not
nearly been studied as well as the negative effects that occur on salt
sensitive people, which is why these positive effects are not well known. I postulate that these effects from
sodium’s might be the reason for any positive effects from Recuperation.
Ironically,
Recuperation may not be the only treatment that believes sodium works in one
way, whereas it might be working in a different way. A popular alternative
treatment for Lyme disease is one that combines salt with vitamin C. The
reason for the salt is based on the fact that high salt concentrations can kill
certain types of bacteria. The problem with this theory is that salt
intake does not necessarily correlate with increased sodium concentrations in
the body. And no study that I could find has ever shown
a direct positive effect of a high salt diet on infections. Thus, if
this treatment does help, it's likely via indirect effects of sodium intake,
possibly via some of the ones that I've presented.
> It is certain that my first diagnosis was Fibromyalgia and Ankylosing Spondilitys. Fibromyalgia was confirmed in every > hospital and doctor by which I was.. Ankylosing Spondilitys was discarded at the second hospital where I was. Evidently, it was> an error by my diagnosis since Ankylosing Spondilitys is irreversible and I am perfectly well restored.
Actually no,
people with this condition can go into remission. This is not only
recognized by the medical literature, but there are also many stories on the
web of it happening to people, due to different reasons. There's even a
book by someone who claims that a diet can cause it to go into remission.
Other people have gone into remission via other methods (lasting many
years). What's interesting is the similarity between this condition and
fibromyalgia. I.e. people with Ankylosing Spondylitis complain of sleep
problems, fatigue, digestion problems, infections, allergies, etc. Any
type of hronic pain can lead to other problems, due to the interconnections
between the nervous system, and the hormonal and immune systems.
Ankylosing Spondylitis can be just as bad or worse than fibromyalgia.
However, cases of remission do exist, via totally different methods.
Unfortunately, most people do not achieve full remission, even using these same
methods. Thus, the fact that someone has achieved remission in a disease,
doesn't mean that they have found a cure for everybody, or even a significant
number of people. It just means they happened to find something that
works for them.
> The reason of this bad diagnose was my back's muscular contraction, but the same doctors who made> this diagnosis denied it some months later. However, you did
have symptoms that were not fibromyalgia symptoms, as you say on your web page
"Oddly, my symptoms of ankylosing spondylitis have also let up, of which I
don’t have any traces." Therefore, this implies you did have
some problem other than fibromyalgia. Whatever that problem was, it could
have been the primary problem, with fibromyalgia being secondary. And of
course, a mineral deficiency is a possibility, since you were cured by taking
minerals. I've known people who said that they cured their fibromyalgia
with vitamins, but they were actually curing secondary fibromyalgia.
Maybe your remedy treated the "symptoms of ankylosing spondylitis",
and the fibromyalgia also went away because of that.
The majority of people with primary fibromyalgia do respond somewhat to at
least one of the treatments you tried. They may not always experience a
huge amount of relief, but at least they see some benefit. The fact that
you as a young person, without any other diagnosed health condition, were not
helped by any of these treatments, and continued to get worse, indicates to me
that you likely had some other undiagnosed problem (either that, or you had
poor doctors). I've known many people in the same situation, i.e. that
they were told they had fibromyalgia, but were not being helped by
treatments. Most of these people eventually discovered they had some
other condition, such as lyme disease, hypothyroidism, and myofascial pain
disorder, to name just a few.
I question any diagnosis of fibromyalgia, because so many bad diagnoses have
been made, especially in the 1990s when you were diagnosed. Even now,
most doctors don't recognize a magnesium deficiency. How many people have
had a magnesium loading test? Many people with lyme disease were first
mistakenly diagnosed with fibromyalgia. I've known people who were told
for years that they had fibromyalgia, but then eventually discovered they had
lyme disease. Celiac disease is also often overlooked, as when it occurs
in adults, sometimes it's main symptoms can be pain.
Back pain is a major symptom of ankylosing spondylitis. Treating back
pain with alkaline producing minerals is an idea that other people have had:
J Trace Elem Med Biol. 2001;15(2-3):179-83.
Supplementation with alkaline minerals reduces symptoms in patients with
chronic low back pain.
"The cause of low back pain is heterogeneous, it has been hypothesised
that a latent chronic acidosis might contribute to these symptoms. It was
tested whether a supplementation with alkaline minerals would influence
symptoms in patients with low back pain symptoms. In an open prospective study
82 patients with chronic low back pain received daily 30 g of a lactose based
alkaline multimineral supplement (Basica) over a period of 4 weeks in addition
to their usual medication. Pain symptoms were quantified with the "Arhus
low back pain rating scale" (ARS). Mean ARS dropped highly significant by
49% from 41 to 21 points after 4 weeks supplemention. In 76 out of 82 patients
a reduction in ARS was achieved by the supplementation. Total blood buffering
capacity was significantly increased from 77.69 +/- 6.79 to 80.16 +/- 5.24
mmol/L (mean +/- SEM, n = 82, p < 0.001) and also blood pH rose from 7.456
+/- 0.007 to 7.470 +/- 0.007 (mean +/- SEM, n = 75, p < 0.05). Only
intracellular magnesium increased by 11% while other intracellular minerals
were not significantly changed in sublingual tissue as measured with the
EXA-test. Plasma concentrations of potassium, calcium, iron, copper, and zinc
were within the normal range and not significantly influenced by the
supplementation. Plasma magnesium was slightly reduced after the supplemenation
(-3%, p < 0.05). The results show that a disturbed acid-base balance may
contribute to the symptoms of low back pain. The simple and safe addition of an
alkaline multimineral preparate was able to reduce the pain symptoms in these
patients with chronic low back pain."
People who conduct such studies believe that low grade chronic metabolic acidosis
exists in a lot of people, and that even slight changes in blood ph can signify
a problem.
Granted though, this was not a double blind study, and people weren't screened
for a magnesium deficiency beforehand. In fact, I hope the studies on
Recuperation, eliminate, or at least identify, people who were magnesium deficient,
by using a magnesium loading test. This would help to make sure that the
remedy simply isn't treating a magnesium deficiency.
It's possible that Recuperation may also be treating myofascial pain instead of
fibromyalgia pain. Almost everyone with any type of chronic pain
condition, has myofascial trigger points. If these are not proper
treated, then they would continue to aggravates fibromyalgia, and prevent it
from being treated. One possible way that Recuperation might be able to
treat trigger points is via alkalization, as the following study shows that
myofascial trigger points are associated with an acidic environment:
J Appl Physiol. 2005 Nov;99(5):1977-84.
An in vivo microanalytical technique for measuring the local biochemical milieu
of human skeletal muscle.
"In our study, subjects with active MTrPs [myofascial trigger points] and
greater pain levels (i.e., pressure sensitivities) had lower pH levels in the
vicinity of their MTrPs. A positive correlation has previously been shown between
pain and local acidity. In a rat model, repeated injections of acidic saline
into one gastrocnemius muscle produced bilateral, long-lasting mechanical
hypersensitivity (i.e., hyperalgesia) of the paw. The hyperalgesia was reversed
by spinally administered µ- or {partial}-opioid receptor agonists or
N-methyl-D-aspartate (NMDA) or non-NMDA ionotropic glutamate receptor
antagonists. This model clearly demonstrates secondary mechanical hyperalgesia
that is maintained by neuroplastic changes in the CNS. Furthermore, the
persistent mechanical hyperalgesia was not caused by muscle tissue damage and
was not maintained by continued nociceptive input from the site of injury.
Therefore, an acidic milieu alone (without muscle damage) is sufficient to
cause profound changes in the properties of nociceptors, axons, and dorsal horn
neurons (i.e., the pain matrix). Mechanical hyperalgesia is a hallmark of a
MTrP. An acidic pH is well known to stimulate the production of bradykinin
during local ischemia and inflammation and may explain the cause of pain in
patients with an active MTrP."
Or perhaps the sodium itself has benefits for trigger points. Sodium can
reduce angiotensin II and insulin resistance. Insulin resistance is
associated with higher levels of TNF-alpha in skeletal muscles, and TNF-alpha
may play a role in trigger points, as the above study pointed out:
"We found significantly elevated levels of TNF-{alpha} and IL-1{beta} in
subjects with active MTrPs. In a rat model, TNF-{alpha} produces a time- and
dose-dependent muscle hyperalgesia within several hours after injection into
the gastrocnemius or biceps brachii. This hyperalgesia was completely reversed
by systemic treatment with the nonopioid analgesic metamizol. Furthermore,
TNF-{alpha} did not cause histopathological tissue damage or motor dysfunction.
One day after injection of TNF-{alpha}, elevated levels of CGRP, nerve growth
factor (NGF), and PGE2 were found in the muscle. Therefore, TNF-{alpha} and
other proinflammatory cytokines such as IL-1{beta} may play a role in the
development of muscle hyperalgesia, and the targeting of pro-inflammatory
cytokines might be beneficial for the treatment of muscle pain syndromes."
People with secondary fibromyalgia, i.e. where another condition such as
myofascial pain is the primary problem, may actually have a different pain
profile, and thus may respond to different treatments. The following study
shows one such difference:
Pain. 2000 Aug;87(2):201-11.
Changes in the concentrations of amino acids in the cerebrospinal fluid that
correlate with pain in patients with fibromyalgia: implications for nitric
oxide pathways.
"We found that the mean concentrations of most amino acids in the CSF did
not differ amongst groups of subjects with primary FMS (PFMS), fibromyalgia
associated with other conditions (SFMS), other painful conditions not
exhibiting fibromyalgia (OTHER) or age-matched, healthy normal controls (HNC).
However, in SFMS patients, individual measures of pain intensity, determined
using an examination-based measure of pain intensity, the tender point index
(TPI), covaried with their respective concentrations of glutamine and
asparagine, metabolites of glutamate and aspartate, respectively. This suggests
that re-uptake and biotransformation mask pain-related increases in EAAs.
Individual concentrations of glycine and taurine also correlated with their
respective TPI values in patients with PFMS. While taurine is affected by a
variety of excitatory manipulations, glycine is an inhibitory transmitter as
well as a positive modulator of the N-methyl-D-asparate (NMDA) receptor. In
both PFMS and SFMS patients, TPI covaried with arginine, the precursor to
nitric oxide (NO), whose concentrations, in turn, correlated with those of
citrulline, a byproduct of NO synthesis."
Such differences may explain why one treatment for fibromyalgia may work for
and people, but not for others. It may explain why you didn't respond to
normal fibromyalgia treatments, but responded extremely well to your remedy.
> Since the best way to see the effect of a compound of this type is with people whose muscles are easily> measured the first investigations with Recuperat-ion have been done, as expected, it with elite sportsmen. > The results were: Diminution of lactate in blood after a prolonged exercise.> Recovery of an optimal hydration and ATP levels. Such results
would be of great interest if someone
was trying to increase exercise performance, and reduce fatigue and pain which
is caused by the delayed onset of muscle soreness, which occurs many hours
after exercise. But this has nothing to do with the type of pain that
people with fibromyalgia experience, which normal people don't. One such
difference is demonstrated in the following study:
Pain. 2005 Nov;118(1-2):176-84.
Isometric exercise has opposite effects on central pain mechanisms in
fibromyalgia patients compared to normal controls.
"Aerobic exercise has been shown to activate endogenous opioid and
adrenergic systems and attenuate experimental pain in normal control subjects
(NC). In contrast, fibromyalgia (FM) subjects' experimental pain ratings
increase after aerobic exercise, suggestive of abnormal pain modulation. In
order to determine whether central or peripheral mechanisms are predominantly
involved in the abnormal pain modulation of FM patients, the effects of
handgrip exercise on thermal (cutaneous) and mechanical (somatic) experimental
pain was tested in local as well as remote body areas of FM and NC
subjects." "This isometric exercise resulted in substantially decreased
thermal pain ratings and increased mechanical thresholds in local as well as
remote body areas in NC. Opposite effects were detected in FM patients. Thus,
sustained local muscular contraction induced widespread pain inhibitory effects
in NC. In contrast, the widespread hyperalgesic effects of exercise on FM
patients clearly indicate altered central pain mechanisms. However, whether
these exercise effects of FM patients result from abnormal descending
inhibition or excessive activation of muscle nociceptive afferents needs to be
addressed in future studies."
This study is describing pain which occurs in fibromyalgia within minutes of
exercise, which doesn't occur in normal people. The muscle's normal
ability to reduce pain in response to exercise, is missing in
fibromyalgia. Hyperalgesia of the nervous system is occurring.
Normal people don't have this dysfunctional behavior, and therefore what helps
normal people is often not applicable to fibromyalgia.
> Studies with ill people are presently running on and will be finished in some months.> These studies aim to analyze the following variables:> Criteria FM diagnosis. Criteria CFS diagnosis Many studies have
shown that a variety of remedies help fibromyalgia and CFS, so that having a
positive study doesn't always mean the remedy cures fibromyalgia. The
important question to me would be how does a treatment work, and how does it
compare with other treatments? How does Recuperation compare to taking
plain sodium citrate, or sodium citrate with potassium, or magnesium
supplementation? How are the patients diets? Are they high in
protein or carbohydrates? Are they taking any minerals supplements
already? Are they deficient in magnesium or calcium? Have they been
given a magnesium loading test? Was there any change in magnesium
retention before and after Recuperation? Was serum ionized magnesium or
calcium changed? Was urinary PH changed? Etc. In other words,
instead of determining if a supplement can help fibromyalgia, it would be more
important to find out why it helps, and who it would help the most.
Remedies for fibromyalgia are big business. The product O24 is an example
of that. It is a topical pain relieving remedy. It is being
marketed as a patented formula containing various herbs and oils. But if
you look at the ingredients, the only ingredient listed as an active ingredient
is camphor. Camphor is a very common ingredient in topical pain
relievers. O24 was tested in a double-blind study on fibromyalgia patients
and was found to be effective. However, they never bothered to study how
well it works compared to camphor by itself. In fact, no camphor remedy
has ever been tested on fibromyalgia before. This company thus saw a
vacuum, and moved in. Chain drug stores in the US, such as CVS, have
begun stocking it, marketed specifically for fibromyalgia.
> Finally, independently of the results of the current, the fact is that I am absolutely without> symptoms and many people report a health improvement from several parts of the world. Is it chance? There are
actually quite a few people on the web who have claimed that they have
reversed, cured, or put in remission their fibromyalgia. They have done it
using various treatments. Given that there are so many cures for
fibromyalgia, why aren't more people getting cured of it? It's because
everybody with fibromyalgia is different. In studies on medicines for
fibromyalgia, there are always some people who respond to the medicine, and
some who don't. Everybody has different genes, and different health
conditions to deal with. The people that I know of who are coping the
best with fibromyalgia. are people who have spent a long time finding the
treatments and remedies work for them. This is what you did. You
experimented until you found the right remedy that works for you. There
is no reason to believe it is an optimum remedy for other people, because we
are all different.
As an aside, in searching the web, I found that several people have
independently claimed to have reversed their fibromyalgia, through eating a raw
food diet. And interestingly, one of the main reasons why the raw food
diet is supposed to be beneficial, is due to it's alkalizing effect.
> I believe that it is not possible that my personal experience influences them mentally.> It must have a scientific explanation for it.
Perhaps you
haven't read much about the placebo effect with regard to pain relief.
The placebo effect in pain relief is not imagined, but often involves real
chemical effects, and can be quite strong. For example, the placebo
effect can cause the release of opioid substances and dopamine in the body,
which have real pain relieving effects. This and other effects have been
proven in many studies. For example, pain relief due to placebos have
been reversed by a drug that antagonizes the actions of opioids, showing that
placebos can cause the release of opioids. And pain relieving placebo effects definitely
can occur in people with fibromyalgia:
Pain,Volume 99, Issues 1-2 , September 2002, Pages 49-59
Enhanced temporal summation of second pain and its central modulation in
fibromyalgia patients.
"Hypoalgesic effects of saline placebo and fentanyl on windup were at
least as large in FMS as compared to NC subjects." "The larger
effects of fentanyl and placebo on temporal summation of heat tap-evoked pain
in FMS patients as compared to NC subjects suggests that FMS patients may in
fact have an enhanced sensitivity to exogenous and/or endogenous opioids.
Enhanced sensitivity to opioids could result from several possible factors,
including increased sensitivity of opioid receptors or enhancement of factors
that contribute to placebo hyopoalgesia, which was greater for FMS subjects.
For example, it is possible that FMS patients had larger desires for pain
reduction, greater expectations of pain reduction, and consequently a larger
placebo contribution to effects of fentanyl for FMS subjects."
Such placebo effects explains why in some studies on fibromyalgia, that people
who are given placebos, will sometimes report that their pain was reduced by
over 50%.
And the placebo effect could be even stronger, when someone is given a remedy
such as Recuperation, which is not just an average remedy, but one that is
supposed to cure them:
Pain. 2002 Apr;96(3):393-402.
The contribution of suggestibility and expectation to placebo analgesia
phenomenon in an experimental setting.
"The pairing of placebo administration with painful stimulation was
sufficient to produce a generalized placebo analgesic effect. However, verbal
expectancy for drug efficacy and individual differences in suggestibility were
found to contribute significantly to the magnitude of placebo analgesia. The highest
placebo effect was shown by the most pronounced reductions in pain ratings in
highly suggestible subjects who received suggestions presumed to elicit high
expectancy for drug efficacy."
We are not necessarily suggesting that Recuperation is simply a placebo.
However, the pain relieving affects of any remedy, may be increased by the
placebo effect, if the person's expectations are raised.
Mark