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 Nottingham health profile. 12 of the 15 treated patients said that they had benefited from treatment, and in 7 patients energy score improved from the maximum to the minimum. By contrast, 3 of the 17 patients on placebo said that they felt better (difference 62%, 95% CI 35 to 90), and 1 patient had a better energy score. Red cell magnesium returned to normal in all patients on magnesium but in only 1 patient on placebo. The findings show that magnesium may have a role in CFS."

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's explanation, there is a big failure.
> 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 - 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