Guaiacum was approved for use as an expectorant by the Food and Drug Administration some 400 years later, in 1952. And 20 years ago the extract was synthesized, pressed into tablets and named 'guaifenesin'.
How Does Guaifenesin Work ?
Guaifenesin works by drawing water into the bronchi – the air passages branching into our lungs. The released water both thins the mucus and lubricates the airway, facilitating the removal of cold, flu and allergy- associated mucus from the chest by coughing and making it easier to breathe.
Guaifenesin is also considered helpful for thinning postnasal drainage from the sinuses and reducing nasal congestion (cfr. : 'The Guaifenesin Story - A centuries-old bark extract used for clearing the airways – Now key to a popular FM symptom-reversal protocol' at : http://www.prohealth.com/library/showarticle.cfm?libid=12081 -) and so may relieve sinus pressure/ headache. As Dr. Sarah Myhill comments : “Whoever designed the human body needs a black mark for putting in sinuses ! They are cavities in the bones of the face with only one entry and exit hole which is easily blocked by catarrh or swollen mucus membranes”. When this occurs, less oxygen can enter the sinuses, promoting bacterial overgrowth and causing sinusitis.
Here again, guaifenesin can help to relieve congestion by increasing the clearance of secretions, helping with the mucus membrane’s natural job of washing away invading viruses, bacteria, pollen and other potential allergens – “the first level of immune defense”.
Guai also enjoys a popular reputation as ‘the opera singer’s friend'. Terming it their ‘wonder drug’ singers have traditionally used guaifenesin to improve the state of their vocal folds in extremes of humidity (very dry or very humid), after flying long distances and during mild allergies, for its ability to promote ‘secondary mucosal secretion’ – the thinner, lubricating mucus that occurs on the vocal folds naturally when they are healthy and well hydrated.
Patients with chronic obstructive pulmonary disease(COPD) may find guaifenesin’s thinning and lubricating action helpful at times when they experience particular difficulty coughing up the thick or sticky mucus that can block their damaged airways.
Similarly, guaifenesin can assist by thinning ‘sticky’ mucus to help expel inhaled particles that can exacerbate asthma symptoms.
Importantly, whether used to ease the congestion of colds, flu or rhinosinusitis or to support healthy vocal folds, guaifenesin works best if one drinks plenty of water, as extra fluids increase the flow of water and mucus.
As with many complex herbal compounds used in traditional medicine, exactly how guaifenesin encourages healthy mucus flow is not yet completely understood. But based on its long history - if taken as instructed on the package or as suggested by a pharmacist or healthcare provider - guai has at most minor side effects and is generally considered safe for use even by youngsters over 12 years of age.
What is the Guifenesin Protocol for fibromyalgia patients ?
Nevertheless, note that Guaifenesin has not been approved by the FDA for this application and should be used as such only with the approval and supervision of a medical doctor familiar with the patient and Protocol.
Excess inorganic phosphate compounds accumulate within the cells of some people rather than being excreted normally, possibly owing to a genetic defect involving a missing enzyme or kidney dysfunction.
It is known that excess phosphate in the cells’ mitochondria impedes their formation of adenosine triphosphate (ATP), the body’s energy source - and that muscle pain after exercise is linked with an inorganic phosphate increase. Also, researchers have reported a 20 percent average reduction in the level of ATP in muscle biopsies taken from people with FM, notes self-described Guaifenesin Protocol beneficiary Devin Starlanyl in her book : 'Fibromyalgia and Chronic Myofascial Pain: A Survival Manual'.
When excess phosphate builds up in the cells, excess calcium – the main buffer for phosphate – builds up too. Excess calcium in the cells tends to stiffen the body’s tissues.
A method of palpating muscles, tendons and ligaments that Dr. St. Amand has described allows a physician to “map” or assess the extent of lesions in the tissues of FM patients, thought to be “contracted cells forming a spastic area caused by an excess of calcium”.
A carefully planned, monitored regime of guaifenesin extract supplementation may help the body eliminate the excess calcium and phosphate compounds, supporting improvement of FM symptoms over time in some individuals.
Dr. St. Amand has reported increases of 60 percent in phosphate excretion and 30 percent in calcium excretion.
What does the Guaifenesin Protocol involve ?
Basically, it includes :
Adjusting or “titrating” the guaifenesin dosage to the individual’s needs, based on response over time.
Strict avoidance of the salicylates in aspirin and other similar pain-relief products, plus a long list of personal care products including plant derivatives such as aloe or mint that are applied to and absorbed through the skin; and many plant extracts taken by mouth. These can completely block the action of the guaifenesin. Salicylate-containing foods are not a problem, as the digestive process neutralizes their effect.
And strict adherence to a low carbohydrate diet, if the individual is hypoglycemic.
The Protocol also commonly delivers a significant physical impact in the early weeks, including a worsening of the individual’s worst FM symptoms and frequently headaches, burning on urination and/or strong-smelling perspiration and urine. These are not considered side effects, but rather “the signs and symptoms of the toxins and wastes being released by the guaifenesin” - and therefore an indication that the Protocol is working.
So far the Guaifenesin Protocol has not been demonstrated effective in a controlled clinical trial or approved by the FDA for support of Fibromyalgia symptoms. An early one-year trial completed at the University of Oregon in June 1995 by Dr. Robert Bennett concluded that “patients in the placebo group compared with patients in the guaifenesin group appeared to improve equally, a finding that suggested a placebo effect,” says Dr. St. Amand. But “it is our belief that this study was flawed, due to our own lack of knowledge,” he explains.
Though Dr. Bennett’s patients were warned to avoid aspirin and aspirin-containing compounds, it wasn’t until after the study was completed that Dr. St. Amand came to understand the immense number of personal products and ingested plant extracts that, even in minute quantities, could reverse patients’ progress. Also, in reviewing the patients’ wellness questionnaires, he noted that the study had not screened for hypoglycemic individuals, who therefore were not treated with the necessary diet. As a result, he contends, “the study was doomed for lack of knowledge of these pitfalls”.
What is the status of research ?
Currently, one of the stated goals of Dr. St. Amand’s not-for-profit Fibromyalgia Treatment Center is to provide supporting research for the Guaifenesin Protocol.
He is now engaged in a three-year investigation with The City of Hope that involves a cohort of his FM patients (an "Immunological and Genetic Analysis of Autoinflammatory Genes in Fibromyalgia"). By mid-2008 the research had identified abnormal elevations in a cluster of inflammatory cytokines that appear highly predictive of Fibromyalgia, two of which drop to normal in patients taking guaifenesin (cfr. 'Dr. St. Amand Comments on First Report from City of Hope Fibromyalgia Research' at : http://www.prohealth.com/library/showarticle.cfm?id=8940&t=CFIDS_FM -. And in November 2008 Dr. St. Amand issued a call to patients he has diagnosed with FM, to widen the sample of DNA used in the investigation.
In the meantime, the scores of physicians who employ the Guaifenesin Protocol – as well as many of the individuals, like Devin Starlanyl, who have adopted it – provide personal testimonials indicating that this regime supported significant improvements in their Fibromyalgia symptoms.
A virus linked to chronic fatigue syndrome - Dr. Nancy Klimas interviews
A virus linked to chronic fatigue syndrome
The New York Times, October 15, 2009
Denise Grady, a science writer for The New York Times, recently explored the link between a recently discovered virus called XMRV and chronic fatigue syndrome, in “Is a Virus the Cause of Fatigue Syndrome ?” (cfr. : http://www.nytimes.com/2009/10/13/health/13fatigue.html?_r=1&ref=health -). On the Consults blog, scientists and doctors from the International Association for Chronic Fatigue Syndrome, a society of 500 biomedical and behavioral professionals, took readers’ questions on chronic fatigue syndrome.
Here, Dr. Nancy G. Klimas, who serves on the board of directors of the organization, answers questions on the recently discovered retrovirus and clinical care of chronic fatigue syndrome. Dr. Klimas is a director of the department of immunology of the University of Miami School of Medicine and director of research for clinical AIDS/H.I.V. research at the Miami Veterans Affairs Medical Center. Also read Fred Friedberg’s responses to behavior-related questions in “Behavioral Treatments for Chronic Fatigue Syndrome” (cfr. : http://consults.blogs.nytimes.com/2009/10/13/behavioral-treatments-for-chronic-fatigue-syndrome/ -).
Is chronic fatigue syndrome contagious ?
I’ve had C.F.I.D.S. for 25 years. If it is a virus, is it contagious ? How is it transmitted ? Now I worry about passing it on to others. Thank you. Nona
Dr. Klimas responds :
In general, retroviruses are not spread by air or droplet but are transmitted sexually, vertically (mother to fetus) and by blood transfusion. From what we have learned about other retroviruses, it is clear that the amount of virus matters and people with low amounts of circulating virus are not as infectious as people with high levels of virus in the blood. With XMRV, the retrovirus recently found in many patients with chronic fatigue syndrome, we do not have enough information to judge how infectious it might be.
Whenever the possibility of sexual transmission comes up, people worry that they are in some way responsible for infecting sexual partners. While this is possible, it is important to remember that many infections can come from exposures between great-great-grandparents and maintained for generations as latent infections or as infections from early experiences of any sexual partner in a chain of partners. We know that it is very unusual for both partners to develop chronic fatigue syndrome or C.F.S. And while mother-to-child C.F.S. can happen, it is unusual.
It is clear that there are a number of factors that increase the risk for C.F.S. : genetics, immune function, severity of inciting infection — to name a few. Just being exposed to or even infected with, a virus does not mean that a person will become ill. We don’t even know if infection with the XMRV virus actually causes illness or if it one of several associated reactivated viruses (like HHV-6, EBV and enterovirus).
It important not to take these new findings about the XMRV virus as anything more than an exciting new development. We need confirmatory studies, then studies to see if the virus is contributing to the cause of illness persistence and symptoms. The good news is that if XMRV is linked to C.F.S., there are many antiviral drugs that have already been safety tested in H.I.V. that may inhibit viral replication. So those studies could be designed very rapidly
Is there a blood test for the C.F.S. virus ?
Is there a specific test, blood or other, to determine whether a person is infected with the XMRV virus ? Beau Brincefield
Dr. Klimas responds :
The test for XMRV that has been reported is currently used only in research settings. The research director of the Whittemore Peterson Institute, which was involved in the recent findings, was quoted as saying they were developing a commercial assay that they expected to be available “within weeks”. Several other commercial laboratories are also developing assays.
Some important points : First, antibody tests mean you have been exposed to a virus and do not tell you actually have an active infection. Second, a technique known as P.C.R. assays measures something called “viral load” and the assay is designed to measure either active replicating virus or latent (inactive) virus. Either measure would be helpful with this new virus, but we don’t have access to them except in research settings.
Another way to see if you are infected is with viral cultures. The recent study published in Science used both cultures and P.C.R. Assays.
Exercise and chronic fatigue syndrome
I used to be very active and used to love playing sports. Then I was hit with some sort of infection. Eventually, after going to different doctors and health professionals, I was finally diagnosed with C.F.S.
I’m finding it easier to cope now. I try to have rest periods during the day. I would love to play sports again, but I just so feel so ill after I try and my muscles feel so sore. Have you any advice ? Should I push through and go back to playing sports ? I’m finding it tough enough as it is keeping up with college and the normal walking you have to do. I don’t want to drop out of college. Pat.
Dr. Klimas responds :
Most C.F.S. patients do better if they break up their exercise into short segments, take brief rest periods and then try again. Certainly pushing through can cause “crashes” and relapses that can last days, even weeks. So I tell my patients the five-minute rule : five minutes of exercise, then five minutes lying flat, then five more minutes — increasing their exercise by five-minute increments.
If you can already tolerate more exercise than this, then try going that far, taking a break, then trying another round. Also, C.F.S. patients tolerate flexibility and resistance exercise (stretching and weight training) better than aerobics. Because C.F.S. patients are prone to blood pressure drops while exercising, they usually tolerate aerobic training best while in a flat position — swimming, recumbent bicycling, that sort of thing.
Can I volunteer for a study ?
I’d like to second Post No. 25 and ask when and how one could volunteer to be part of a drug trial ? Please help us. Sally.
Dr. Klimas responds :
There are drug trials and other studies under way all around the United States and the globe looking at this illness and its possible treatments. Investigators at the Whittemore Peterson Institute and elsewhere are already planning antiviral trails based on this exciting research development. I would watch three Web sites in particular — the International Association for CFS/ME - http://www.iacfsme.org/ -, the CFIDS Association of America - http://www.cfids.org/ - and the Whittemore Peterson Institute for Neuro-Immune Disease - http://www.wpinstitute.org/ - for more developments.
Was a C.F.S. virus discovered years ago ?
Back in the early 1990s, Dr. Elaine DeFreitas at the Wistar Institute in Philadelphia discovered a novel human retrovirus (very closely related to HTLV 2, with Spuma-viruslike aspects) in C.F.I.D.S. patients. This was subsequently confirmed by two other prominent researchers (and a commercial laboratory).
Dr. DeFreitas was almost done sequencing its genes and published a meticulous paper in a top journal. Then the Centers for Disease Control and Prevention and the National Institutes of Health intentionally destroyed her reputation because it did not mesh with their vigorous assertions that C.F.I.D.S. was psychoneurosis. No one else has followed this up for fear that their career might likewise be destroyed. This was all detailed in the amazing book “Osler’s Web”.
Is this the same virus as the “novel” XMRV ? Justin Reilly.
Dr. Klimas responds :
Dr. DeFreitas was doing exciting work and should be congratulated for her early results suggesting retroviral infection in C.F.S. Since that time, technology has advanced in a dramatic way, giving investigators new tools to search for viruses that were yet to be identified in 1990-92, including the XMRV virus.
New antiviral drugs have also been developed that could potentially be effective in controlling this sort of infection. We also have a much stronger understanding of these drugs’ toxicity and safe use.
I congratulate the Whittemore Peterson Institute researchers for their diligent work. I am also very happy for Elaine today. I would also ask patients to be patient a little bit longer so that researchers can devise and perform the sort of clinical trials that will let us know if this virus is the linchpin in continued illness.
Links between H.I.V. and XRMV ?
I found the comparison to H.I.V. (all because it happens to be another retrovirus) to be alarmist, unnecessary and at worst, the kind of sensualist factoid reporting that’s more typical of a tabloid ! From what I gather... the link between the two is weak and general at best.
What angers me is that the comparison to H.I.V. is completely out of context; there are many retroviruses that are not known to cause any pathologies at all – comparing it to the one that is most well known and feared is simplistic and quite simply wrong. We should not forget that retroviruses have been common through out human history and while some do not cause disease at all, most are nowhere near as extreme as H.I.V.
To compare the virus to H.I.V. is to create undue alarm and suffering to people who are already dealing with a difficult disease. Not only is the comparison useless outside its context, it does nothing to provide useful information to the reader.
I ask that you think of the moral consequences of your sloppy comparison — the horror and anguish of those that might have thought that it might be as debilitating as H.I.V., as well as the dread of the thought of potentially passing it on to another person. David.
Dr. Klimas responds :
You make a good point. This is one study, the results needs to be validated, then the next study will look at treatment options. And you are right, some retroviruses are seemingly benign, whereas others are pathogens.
But I hope you are not saying that C.F.S. patients are not as ill as H.I.V. patients. My H.I.V. patients for the most part are hale and hearty thanks to three decades of intense and excellent research and billions of dollars invested. Many of my C.F.S. patients, on the other hand, are terribly ill and unable to work or participate in the care of their families.
I split my clinical time between the two illnesses and I can tell you if I had to choose between the two illnesses (in 2009) I would rather have H.I.V. But C.F.S., which impacts a million people in the United States alone, has had a small fraction of the research dollars directed towards it.
Despite these limitations, there has been considerable effort to understand the cause and develop effective treatments. The Whittemore Peterson Institute should be congratulated for its outstanding work, performed in a brand new center paid for with private donations, state money and N.I.H. collaboration. Creative research and creative financing !
Is sleep a factor in chronic fatigue syndrome ?
Do you think sleep could be a factor in C.F.S. ? Have you heard of Xyrem being used to facilitate Stage 4, deep sleep ? Most everyone with fibro and/or C.F.S. report of not being able to sleep deeply — to have restorative sleep. We are all anxiously waiting for help in this lifetime. So many years have been lost to these illnesses. Abot Bensussen.
Dr. Klimas responds :
There is a clinical trial under way to study the effects of Xyrem, a medication used to treat sleep disorders like narcolepsy, in fibromyalgia. Certainly, getting restorative sleep is a good thing and slow wave sleep is key to restorative sleep. A sleep expert can help with this part of treatment, but it is important to have a sleep study done before considering any sleep inducers.
In a study by my group, we found that about half of C.F.S. patients develop some level of sleep apnea over time, a treatable condition that could be worsened with some sleep medications.
'As someone with chronic fatigue syndrome, I had to change my life to get relief'
Zachary Sklar, former executive editor of the Nation magazine and co-author of the screenplay for the film "JFK" – Comments : email@example.com - Washington Post, October 27, 2009
So, maybe we're not all slackers. Maybe it's not all in our heads, as many employers, psychiatrists, friends and even family members have implied or thought to themselves over the years. Maybe the debilitating set of symptoms known as chronic fatigue immune dysfunction syndrome is a legitimate illness, like pneumonia or tuberculosis. And maybe, according to a study published recently in the prestigious journal Science, it's actually caused by a virus.
Many of the millions of people around the world who suffer from chronic fatigue syndrome welcomed the news of this study. Not only might it vindicate us, it also offers hope that a cure is possible, if not imminent.
But as someone who has lived with the syndrome for 23 years, I remain skeptical that this terrible illness is caused by a single virus, identified as the retrovirus XMRV. I have no doubt that XMRV was found in many of the 101 chronic fatigue patients in the study. But we've been down this road before. In the 1990s another retrovirus was announced with fanfare as the culprit. Many were disappointed when subsequent studies could not confirm any link between it and the illness.
And of course nearly everyone with chronic fatigue has been tested for other viruses that were once thought to be the cause : Epstein-Barr, cytomegalovirus, even HIV. Often those viruses are found in the blood of those tested. But so far, they have not been proved to be the cause of our illness.
I am not a scientist, I don't have the skills to evaluate the study and I am aware that researchers were only suggesting that XMRV "may be a contributing factor". But based on my own experience, I believe that chronic fatigue syndrome is an environmental illness in the broadest sense : an erosion of the immune system that can be caused by any number of factors, including chemicals in our food, pollution in our air and water, exposure to radiation, the stresses of modern life, unhealthful diet, lack of sleep, excessive use of drugs (prescription and recreational), psychological stresses, overwork and, yes, viruses, too.
I came down with the illness in 1986, when I was 38 years old. It hit me suddenly and felt like a severe flu : trembling, nausea, fever, headache, night sweats, digestive problems. It just never went away. From the blood tests, it's clear that my immune system was so weakened that it was unable to fight off completely whatever attacked it.
Why was my immune system compromised ? I have my own theories. I led an extremely stressful life in New York. I ate a lot of fast food, high in sugar and low in organics. For six years I missed two nights of sleep every week working at Time and Life magazines. I once spent my vacation time picking coffee on a peace brigade in Nicaragua and ended up with intestinal parasites.
But there's something else. I grew up in Los Angeles during the 1950s, when nuclear testing in the atmosphere was still permitted. As subsequent studies have made clear, a spree of nuclear tests in Nevada in October 1958, called Operation Hardtack II, spread radiation fallout over the L.A. basin. When records of those tests were released to the public years later, Linus Pauling, a two-time Nobel laureate for chemistry and for activism against nuclear testing, predicted that over a period of 30 years, 25,000 cancer deaths would result from one of those blasts alone. I was 10 years old in 1958 and I got sick 28 years later. I don't know if that radiation contributed to my illness. But after reading numerous reports of high cancer rates in areas exposed to nuclear fallout, I'm convinced it didn't help.
My concern about the latest announcement of a possible viral cause is that many people with chronic fatigue syndrome -- and those who become afflicted in the future -- might be misled into waiting for a pill that will instantly cure them. Even if such a drug is eventually marketed, I wonder whether chronic fatigue patients will be able to overcome the illness without changing the way they live.
In my own case, after a miserable year of being treated by a dozen top New York specialists who prescribed medications that made me feel worse, a friend recommended that I see Shyam Singha, an osteopath and naturopath.
He was the first to zero in on my poorly functioning digestive system. He put me on a cleansing fruit fast, then raw food for a month, then a strict vegetarian diet, no sugar, no alcohol, no caffeine. I thought he was insane and protested that I was too weak to try such a radical diet. "Do it !" he replied. I did and after two days on the fruit fast I started to feel better.
The most important lesson that Singha taught me was that my cure was largely in my own hands. Though he offered guidance and knowledge, I had to take responsibility for changing the habits, the diet, the life patterns that contributed to my getting sick in the first place.
Over nearly 23 years since then, I have tried many approaches to speed my healing : acupuncture, homeopathy, low doses of doxycycline, thyroid supplements, anti-yeast diets and more. I've eliminated much of the clutter and stress in my life. I feel far better today at the age of 61 than I did at 38. Not all those suffering from chronic fatigue syndrome have been so lucky.
Obviously, my view about the cause of this syndrome is at odds with the notion that people get the illness simply because they are exposed to a particular virus. And my belief that we must actively participate in our own healing is not widely accepted, even among chronic fatigue patients. The CFIDS Association of America, the biggest chronic fatigue organization, has been lobbying and raising research funds for many years to find a viral cause and then develop a drug to destroy it -- the polio model.
I hope the group is right, that one day a virus will be identified and there will be a cure or a vaccine, as there was for polio. But despite the study published in Science, I am not convinced that such a cure will be here very soon. For now, I will continue to do what's worked for me and many others. And I will urge anyone who has this illness not to wait passively for doctors and pills to cure them but instead to change their lives and get on with the hard work of healing themselves.
De aanhoudend gunstige conclusies van vele onafhankelijke onderzoeken over pure chocola zijn inmiddels zo indrukwekkend, dat veel voedingswetenschappers erkennen dat pure chocola met een hoog cacaopercentage goed is voor hart en bloedvaten.
Er zijn aanwijzingen dat chocola de bloedstroom in de hersenen verbetert en de kans op dementie kan verkleinen. Chocola werkt volgens sommige onderzoeken goed tegen hoestklachten en helpt diarree voorkomen. Vermoed wordt dat chocola ook een anticarcinogene werking heeft (het beschermt tegen kanker), maar bewijs is daarvoor nog niet geleverd.
Voordat je gezin zich nu enthousiast op een rijtje chocolaletters stort : hou wel rekening met de totale dagelijkse calorie-inname. Pure chocola levert per 100 gram ruim 500 calorieën, een kwart van wat vrouwen dagelijks mogen innemen.
De gezondheidsclaims gelden niet of nauwelijks voor melkchocola en witte chocola, waarvan het cacaogehalte veel lager is. Ook in cacaopoeder zitten niet zo veel van de goede stoffen uit de cacaoboon.
Puisten heb je niet alleen als je in de pubertijd zit : veel mensen hebben er ook last van als ze volwassen zijn. Kijk snel waar ze door veroorzaakt worden en hoe je ze kunt bestrijden.
Puisten zijn ontstekingen van de talgklieren. Deze talgklieren heb je over je hele lichaam, maar ze komen het meest voor op het hoofd en de T-zone van het gezicht (voorhoofd, neus en kin). Deze talgklieren produceren talg, waarmee je huid goed gesmeerd wordt en wat je huid tegen uitdroging beschermt. Maar als er vuil van buiten in de talgkliertjes terecht komt, kunnen deze gaan ontsteken. Wanneer je huid hiervoor gevoelig is, kunnen er puisten ontstaan.
Veel mensen hebben tijdens de pubertijd last van acné: een huidaandoening waarbij je langere tijd last hebt van jeugdpuistjes. Tijdens de pubertijd is je hormoonhuishouding enorm door de war, en staan je poriën open, waardoor er gemakkelijker vuil in de huid kan komen waardoor een jeugdpuistje ontstaat. Daarnaast produceren je talgklieren in die periode meer talg, waardoor het kliertje verstopt kan raken, gaat ontsteken en er een puistje tevoorschijn komt.
Maar ook mensen die allang uit de pubertijd zijn, kunnen last van puisten hebben. Dit is deels genetisch bepaald : als je ouders een kwetsbare en onrustige huid hebben, is de kans groter dat jij hier ook last van kunt krijgen. Maar volgens schoonheidsspecialiste Mieke Laarkamp van Schoonheidsinstituut De Schermer speelt voeding ook een belangrijke rol, al beweren andere gezondheidsdeskundigen wel eens van niet : ‘In mijn praktijk kom ik wel degelijk mensen tegen die bijvoorbeeld door varkensvlees te laten staan, minder last van puisten hebben. Ook hebben veel mensen extra last van puisten als ze chocolade eten. Ik adviseer ze sowieso altijd om voldoende water te drinken, zodat afvalstoffen goed worden afgevoerd.’ Andere oorzaken van puisten kunnen volgens Laarkamp zijn : stress, alcohol drinken, slaaptekort, roken en een slechte doorbloeding.
Hoe een huid op voeding of invloeden van buitenaf reageert, is volgens Laarkamp voor iedereen verschillend : ‘Ik heb bijvoorbeeld mensen in mijn praktijk die heel gevoelig zijn voor een bepaald merk wasverzachter. Dan zie ik aan de puisten op hun wang op welke kant ze ’s nachts op het kussen liggen. Anderen kunnen slecht tegen bepaalde shampoo en als meiden gel of mousse in hun haar doen en die vette pony op hun voorhoofd hangt, kan dit pukkels ook in de hand werken’.
De puisten van mannen verschillen overigens vaak met die van vrouwen. Laarkamp : ‘Mannen hebben een grovere huidstructuur en meer talgklieren dan vrouwen. Zij zijn daardoor veel bevattelijker voor puisten. Ook scheren kan hieraan bijdragen. Wanneer je de haren beweegt, activeer je de binnenkant van je talgklier en als je daar gevoelig voor bent kan het gaan ontsteken. Bij mannen is ook vaak een kwestie van aanleg, de een krijgt er wel last van en de ander niet. Wel hebben mannen met een gevoelige huid of een hele sterke baardgroei vaak last van puisten. Als je met een scheermes een stukje van de huid afschaaft, wordt hij automatisch kwetsbaarder. Ik adviseer dan ook om met een scheerapparaat te scheren in plaats van met een mesje en schuim, zodat je de huid zo min mogelijk irriteert’.
Vrouwen kunnen bij hevige acne de anticonceptiepil gaan slikken. Hiermee worden hormonen onder controle gehouden, waardoor de talgproductie stabiel blijft. Voor mannen is dit niet mogelijk, terwijl zij nog meer last kunnen hebben van de puisten. Laarkamp : ‘Mannen kunnen ook last van puisten over heel hun lichaam hebben, bijvoorbeeld de rug of de kont. Bij heet douchen gaan de talgklieren ook meer talg produceren, waardoor de puisten op de rug toenemen’.
Voor hen zijn andere ‘sterkere middelen’. Bijvoorbeeld het medicijn Roaccutane. Laarkamp : ‘Dit zet de gehele talgproductie in het lichaam stil, waardoor de huid uitdroogt. Hierdoor krijgen puisten minder snel een kans. Maar dit soort sterke medicijnen hebben behoorlijk heftige bijwerkingen. Het legt namelijk de talgproductie helemaal stil, waardoor niet alleen de huid uitdroogt, maar mensen die ze gebruiken hebben last van droge lippen, een droge neus, zijn overgevoelig voor de zon en hebben soms zelfs last van depressieve gevoelens of leverfalen’.
Er zijn op internet veel ‘remedies’ te vinden tegen puisten. Tandpasta erop smeren is een veelgehoorde oplossing. Laarkamp : ‘Hiermee droog je de puist uit, maar het is niet gezond voor de huid. Dit geldt ook voor pure alcohol op de puisten smeren. Ik heb ook een klant gehad die ergens had gelezen dat spruitjes erop leggen nut had. Dat lijkt me niet’.
Je huid goed schoonhouden is volgens Laarkamp succesvoller : ‘Je hebt speciale producten op de markt die de overmatige talgproductie van de huid tegengaan. Als je om de zes weken naar de schoonheidspecialist gaat, wordt dit op een professionele manier gedaan. Met een peeling worden dode huidcellen verwijderd. Vervolgens wordt het gezicht gestoomd, waardoor de poriën open gaan staan en de puisten het makkelijkst uitgeknepen kunnen worden. Vervolgens worden de puisten uitgeknepen’. Overigens hoef je je geen zorgen te maken over een hoge kostenpost als je naar de schoonheidsspecialist gaat : de meeste behandelingen worden vergoed.
Wie een muisarm wil voorkomen kan beter gaan sporten in de lunchpauze dan telkens kort te stoppen met computerwerk. Deze conclusie trekt bewegingswetenschapper Janneke Richter in haar proefschrift, waarop zij is gepromoveerd aan het Erasmus MC. Dat maakt het Rotterdamse medisch centrum vrijdag bekend.
Kantoorwerkers die dagelijks uren achter de computer zitten, worden vaak met speciale software gedwongen te pauzeren : de computer gaat op slot, de werknemer moet even iets anders gaan doen. Onderzoek van Richter wijst uit dat de spieractiviteit bij mensen die computerwerk doen nauwelijks verschilt met die van mensen die aan het bureau werkzaam zijn zonder de pc te gebruiken.
Intensief computerwerk kan leiden tot spierklachten aan de arm, nek of schouders. Voorheen stonden deze klachten bekend als 'Repetitive Strain Injury (RSI)'. Tegenwoordig zijn ze samengevoegd onder de noemer 'KANS' ('Klachten aan arm, nek of schouder').
Volgens Richter is het bestuderen van computergebruik niet voldoende om het ontstaan van KANS te verklaren. „Het lijkt erop dat ander bureauwerk ook risicofactoren bevat voor het ontstaan van KANS”, stelt ze. Uit haar onderzoek blijkt dat mensen die computerwerk (toetsen en muis) verrichten vaak al spontane pauzes nemen, zoals het halen van koffie, een gesprek met een collega of papierwerk. Pauzesoftware verandert het werk-pauzepatroon niet noemenswaardig.
Richter pleit daarom voor meer variatie tijdens de werkdag dan alleen normale- of softwarepauzes om spierkklachten te voorkomen. Sporten op het werk is volgens haar beter.
Studenten, werkenden, werklozen, gepensioneerden, iedereen die dat wil kan nog gewoon gelukkig zijn. Juist in deze tijd, waarin de economie en de politiek zo allesoverheersend zijn, is het van belang om nog beslister te kiezen voor gelukkig zijn. Geluk is dus zeker niet afhankelijk van wat er in de wereld en rondom jou gebeurt. Geluk is iets wat je zélf moet (her)ontdekken en dan nog liefst op een gewone manier. Welke zaken kunnen het delicate geluk in de weg staan ?
Elke dag leer ik op school weer honderdduizend dingen Maar nooit krijg ik eens onderwijs in lachen en in zingen Geschiedenis en tekenen, handvaardigheid en sport Maar hoe je vrolijk op moet staan schrijft niemand op het bord Ik weet hoe ik moet rekenen en foutloos zinnen schrijven Maar dat geeft geen garantie dat ik altijd blij zal blijven En als ik op de blinde kaart haast alle steden ken Dan wil dat nog niet zeggen dat ik straks gelukkig ben Dus hou nou alsjeblieft een keer je snater Met die stomme vraag; wat word je later ?
Wat ga je later doen ? Ik wil gewoon gelukkig zijn Verdien je een miljoen? Ik wil gewoon gelukkig zijn Heb je een buitenhuis ? Ik wil gewoon gelukkig zijn Je chauffeur die brengt je thuis Ik wil gewoon gelukkig zijn
Wat ga je later doen ? Ik wil gewoon gelukkig zijn Verdien je een miljoen ? Ik wil gewoon gelukkig zijn Heb je een buitenhuis ? Ik wil gewoon gelukkig zijn Je chauffeur die brengt je thuis Ik wil gewoon gelukkig zijn
Als ik naar grote mensen kijk raak ik geïrriteerd Ze hebben op hun eigen school geen malle moer geleerd Het kunnen dan wel knappe en geleerde koppen zijn Maar heb je daar wat aan wanneer je bol staat van chagrijn ? Van mij mogen ze vrolijk zijn als vak verplicht gaan stellen Dan ben je beter af dan als je goed tot tien kunt tellen Ik wil een tien voor aardig zijn en lol op mijn rapport Dan weet ik zeker dat ik later heel gelukkig word Dus hou nou alsjeblieft een keer je snater Met die stomme vraag; wat word je later ?
Wat ga je later doen ? Ik ga lekker hele dagen paardrijden Wat ga je later doen ? Ik begin gewoon een eigen snoepfabriek Wat ga je later doen ? Misschien word ik wel minister van gelukszaken Wat ga je later doen ? Of beter nog; ik ga de mensen gratis aan het lachen maken
Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn
Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon gelukkig zijn Wat ga je later doen ? Ik wil gewoon…
Gelukkige mensen zijn met geluksgenen geboren
Gezondheid.be, 16-10-2003 - Bron : Nieuwsblad
Om een leven lang gelukkig te blijven moet je met de juiste genen geboren zijn. Wie het met minder goede genen moet stellen, doet er best aan te trouwen.
Die wijsheid komt uit een onderzoek door het wetenschappelijk tijdschrift New Scientist.
Sommige mensen hebben nu eenmaal een opgewekt karakter, terwijl anderen van nature eerder zwartkijkers zijn. Wetenschappers schrijven dat verschil toe aan de genen. Hoe mensen hun leven aanvoelen hangt maar voor de helft af van de omstandigheden. We zijn van nature uit geneigd tot optimisme of sombere gedachten.
Het huwelijk kan aardig helpen om gelukkig te zijn. Dat leren tenminste de statistieken. Vooral het jaar voor en na de eigenlijke huwelijksceremonie zouden tijden van eindeloos geluk zijn. Gehuwde mensen zijn ook op langere termijn meestal gelukkiger dan vrijgezellen.
Vriendschap levert ook extra geluk op. Goede sociale relaties zijn bijzonder waardevol.
België ontcijferd, 07-09-2007 - In samenwerking met Algemene Directie Statistiek (FOD Economie)
Tussen maart en juni 2006 ondervroeg de onderzoeksgroep TOR-VUB van de Vrije Universiteit Brussel 4.500 Belgen van 19 tot 81 jaar over hun geluk. De respondenten moesten op een schaal van 1 tot 10 aanduiden hoe gelukkig ze zijn. Tevens stelden de onderzoekers een twintigtal aanvullende vragen. Op basis van al de gezamenlijke antwoorden berekenden Mark Elchardus en Wendy Smits een "geluksscore" op een schaal van 100.
Het algemeen gemiddelde bedraagt 60,99. Dat betekent dat de doorsnee Belg zichzelf een 6 op 10 geeft inzake geluk. Mannen zijn met een geluksscore van 61,71 gemiddeld iets gelukkiger dan vrouwen, die een score van 60,26 halen. Voor alle leeftijdsgroepen geldt overigens dat mannen gemiddeld gelukkiger zijn dan hun vrouwelijke evenknieën. Alleen vrouwen van 36 tot 45 jaar zijn (iets) gelukkiger dan hun mannelijke leeftijdsgenoten.
Het onderzoek toont duidelijk aan dat er een relatie is tussen leeftijd en geluk. Jonge volwassenen tussen 19 en 25 zijn gelukkiger dan de doorsnee Belg. Daarna daalt het geluk vrij rechtlijnig tot 55 jaar, om daarna opnieuw toe te nemen. Het gelukkigst zijn mensen in de leeftijdscategorie van 66 tot 75 jaar. Eens boven die leeftijd gekomen, neemt het geluk weer af.
Het diploma blijkt een sterk bepalende factor te zijn. Hoe hoger het onderwijsniveau, hoe groter de geluksscore. Volgens de onderzoekers heeft dat te maken met het feit dat een hoger diploma vaak leidt tot een hoger inkomen, een hogere plaats op de maatschappelijke ladder en meer controle over het eigen leven. Heel belangrijk inderdaad is de financiële situatie.
Mensen die in een slechte financiële situatie verkeren rapporteren veel minder vaak dat ze gelukkig zijn, mensen die in een goede financiële situatie verklaren dan weer vaker dat ze (heel) gelukkig zijn. “Geld maakt dus wel degelijk gelukkig”, zo stellen Elchardus en Smits. Lees ook 'Niet geld, maar slaap maakt gelukkig' van Olav Velthuis op : http://www.hartenziel.nl/artikel/niet_geld_maar_slaap_maakt_gel –.
Uit de cijfers van de TOR-VUB blijkt dat het al dan niet hebben van een relatie ook een belangrijke factor is. Mensen met een relatie zijn door de band gelukkiger dan mensen zonder een relatie. Samenwonenden zijn net iets gelukkiger dan gehuwden en een stuk gelukkiger dan mensen met een LAT-relatie. Bij mensen zonder relatie valt het op dat gescheiden mensen het ongelukkigst zijn.
Meeste Nederlanders zijn gelukkig Nationale Geluksonderzoek
de Volkskrant, 12-03-2008
ANP - Ruim 85 procent van de Nederlanders is het eens met de uitspraak 'het glas is half vol'. Zij voelen zich vooral tevreden met hun werk en hun uiterlijk.
Dat bleek woensdag uit het Nationale Geluksonderzoek van onderzoeksbureau Multiscope onder 2800 ondervraagden.
Nederlanders blijken tevreden over hun geluk en zijn over het algemeen optimistisch ingesteld. Het eigen geluk krijgt een 7,4 als rapportcijfer in het online onderzoek. Men voelt zich gemiddeld vijf dagen per week gelukkig.
Ruim 77 procent van de ondervraagden meent dat je zelf invloed hebt op de mate van geluk. Volgens de helft van de Nederlanders maakt geld gelukkig. Drie op de vier zijn het eens met de stelling : ‘ik word gelukkig van mijn werk’. Met het eigen uiterlijk is 62 procent gelukkig.
Als meest gelukkige BN'ers worden Marco Borsato, Frans Bauer, prinses Máxima, Paul de Leeuw en Jan Smit genoemd. Het meest ongelukkig zijn volgens Nederland : Geert Wilders, Gordon, Jan Peter Balkenende, Patty Brard en Linda de Mol.
Give yourself permission to be human When we accept emotions -- such as fear, sadness or anxiety -- as natural, we are more likely to overcome them. Rejecting our emotions, positive or negative, leads to frustration and unhappiness.
Geef jezelf de mogelijkheid om mens te zijn Aanvaard je emoties in plaats van ze te bestrijden.
Happiness lies at the intersection between pleasure and meaning Whether at work or at home, the goal is to engage in activities that are both personally significant and enjoyable. When this is not feasible, make sure you have happiness boosters, moments throughout the week that provide you with both pleasure and meaning.
Geluk ligt tussen plezier en betekenis Engageer je in activiteiten die je belangrijk en plezierig vindt, zowel op je werk als thuis.
Keep in mind that happiness is mostly dependent on our state of mind, not on our status or the state of our bank account Barring extreme circumstances, our level of well being is determined by what we choose to focus on (the full or the empty part of the glass) and by our interpretation of external events. For example : do we view failure as catastrophic or do we see it as a learning opportunity ?
Geluk is afhankelijk van onze gemoedstoestand, niet van onze bankrekening Leer je te focussen op de juiste zaken, het halfvolle glas in plaats van het halflege.
Simplify ! We are, generally, too busy, trying to squeeze in more and more activities into less and less time. Quantity influences quality and we compromise on our happiness by trying to do too much.
Vereenvoudig ! Probeer niet te veel in te weinig tijd te doen.
Remember the mind-body connection What we do -- or don't do -- with our bodies influences our mind. Regular exercise, adequate sleep and healthy eating habits lead to both physical and mental health.
Denk aan de verbinding tussen lichaam en geest Een gezonde geest heeft een gezond lichaam nodig.
Express gratitude, whenever possible We too often take our lives for granted. Learn to appreciate and savor the wonderful things in life, from people to food, from nature to a smile.
Laat je dankbaarheid zien Neem niet te veel voor vanzelfsprekend aan, maar apprecieer de zaken die je gelukkig maken, een lach, de natuur, lekker eten.
Je kan ook gewoon gelukkig zijn - 10 Stappen naar geluk -
Roland Verschaeve (illustraties : D. Demets) - Standaard Uitgeverij, februari 2007 – ISBN 10 : 9002222505 - ISBN 13 : 9789002222504 - Recensie van Tine Van Puyenbroeck, 05-09-2007 -
“Gelukkig zijn...” Raymond Van Het Groenewoud zong er ook al over...
Elke verjaardag, elke Nieuwjaar, elk huwelijk, elke geboorte... elke keer wensen we opnieuw en opnieuw geluk voor elkaar. Spreekwoorden te over vertellen hoe we gelukkig(er) kunnen zijn : denk maar aan “Geluk zit in de kleine dingen”... En toch blijft het bereiken van "het geluk" een zoektocht voor velen.
Dit dunne boekje van Roland Verschaeve met als ondertitel “10 stappen naar geluk” is een compacte reisgids naar geluk. Bewust kort gehouden en vlot leesbaar en met gewoon begrijpbare woorden geschreven, is dit al wat een mens nodig heeft om -mits wat wil en bewustwording- te beseffen dat geluk inderdaad in kleine dingen zit ! Gewoon bewust zijn van je leven, gewoon blij zijn met kleine gebaren, gewoon genieten van wat je hebt (en niet van wat je zou willen hebben), gewoon gelukkig zijn dat je er bent... meer is volgens de auteur niet nodig om op een hoger niveau van geluk te komen.
Mijn eigen conclusie ? Geluk begint vooral met bewustwording. Van zodra je bewust bent van een aantal zaken, ga je er op een andere manier mee om. En dat ene woordje “anders” – dus niet “beter” - maakt al een hele wereld van verschil. In ieder geval, als iedereen een tiende onthoudt van al wat hier neergeschreven staat, dan is mijn vermoeden groot dat het Bruto Nationaal Geluk er enorm op vooruit zou gaan (waar ik me de vraag stel wat de correlatie zou zijn met het gekende bruto nationaal product ?... een antwoord laat zich raden) !
Een kleine bedenking bij dit voor de rest absoluut fantastisch boekje : zoveel goede raad in zo weinig bladzijden kan, volgens mij, voor sommige mensen overweldigend zijn, waardoor ze niet ten volle in zich opnemen wat er allemaal staat. Vanuit die optie bekeken, scoort dit boekje als aanrader om op je nachtkastje te leggen en af en toe of zelfs regelmatig en al is het slechts voor her en der een stukje, terug vast te nemen. Immers, goede raad en vooral herhaling, over hoe we gewoon een ietsje gelukkiger kunnen zijn, wie wil dat niet ?
Chronic Fatigue Syndrome - La bÃªte noire of the Belgian Health Care System
.../... Het is nu duidelijk .../... dat de CVS Centra hebben gefaald in hun primaire missies. Het bleek zelfs onmogelijk om vanuit de ervaring van de CVSreferentiecentra gefundeerde wetenschappelijke richtlijnen op te stellen voor de diagnose en behandeling van CVS .../...
Niettegenstaande de royale financiering van deze Centra, zijn de klinische behandelresultaten van de CVS centra zo goed als onbestaande en is er ook geen wetenschappelijke output .../...
Duizenden patienten worden nog steeds .../... geoormerkt als zijnde luiaards, hypochonders, hysterica en psychosomatische klagers ofschoon deze patienten lijden aan ernstige, maar toch vaak te behandelen ziektebeelden.
Nog steeds worden duizenden patienten .../... langdurig behandeld met nonsens therapieen zoals CBT, magnesiumbaxters, rilatine, glucocorticoiden, botox behandelingen, herhaalde operaties, injecties, NSAIDs, psychoanalytische therapieen, morfine pompen etc. .../...
Dus worden patienten, die eigenlijk ernstig ziek zijn.../... onderworpen aan een ellenlange lijdensweg omdat ze verkeerd behandeld worden met : - GET - een training die ze meestal niet aankunnen en soms zelfs schadelijk is. - CBT - een psychologische therapie die de biochemische oorzaak van de CVS niet behandeld en die de patient stigmatiseert, namelijk “het zit tussen de oren”.
Deze onethische aanpak leidt bovendien tot een overconsumptie in de gezondheidszorg. .../...
The World Health Organization acknowledges Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) to be a medical illness. ME/CFS is characterized by disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways. In 2002, the Belgian government started with the development of CFS “Reference Centers”, which implement a “psychosocial” model. The medical practices of these CFS Centers are defined by the Superior Health Council, e.g. treatment should be based upon Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) and biological assessments and treatments of ME/CFS should not be employed. Recently, the Belgian government has evaluated the outcome of the treatments at the CFS Centers. They concluded that a “rehabilitation therapy” with CBT/GET yielded no significant efficacy in the treatment of ME/CFS and that CBT/GET cannot be considered to be curative therapies. In case reports, we have shown that patients who were “treated” at those CFS centers with CBT/GET in fact suffered from IO&NS disorders, including intracellular inflammation, an increased translocation of gram-negative enterobacteria (leaky gut), autoimmune reactions and damage by O&NS. Considering the fact that these findings are exemplary for ME/CFS patients and that GET may even be harmful, it means that many patients are maltreated by the Belgian CFS Centers. Notwithstanding the above, the government and the CFS Centers not only continue this unethical and immoral policy, but also reinforce their use of CBT/GET in patients with ME/CFS treated at those Centers.
Het eerste wat we van een ander willen weten is of hij te vertrouwen is en daarom is deugdzaamheid de eerste factor.
De 'Big Eight'' is gebaseerd op de manier waarop mensen over elkaar praten :
Die acht factoren die worden gemeten in de persoonlijkheidstest die door de Groningse psychologen Boele de Raad en Dick Barelds is ontwikkeld, hebben deels zeer herkenbare namen, maar hun betekenis is niet helemaal gelijk aan die van het woordenboek.
De persoonlijkheidstest op www.hartenziel.nl vraagt deelnemers zichzelf te beoordelen op grond van een aantal kenmerken, waarvan is aangetoond dat die een sterke samenhang vertonen met de genoemde factoren. Het gaat daarbij om zeer concrete gedragingen, waarvan iedereen zich snel een voorstelling kan maken. De test vraagt daardoor niet meer dan 10 minuten voor het invullen. Daarna heb je een scherp beeld van hoe je je eigen persoonlijkheid waarneemt.
En als dat nog niet genoeg zelfkennis oplevert, bestaat de mogelijkheid ook anderen te vragen de eigen persoonlijkheid te beoordelen. Wie zichzelf wil leren kennen heeft daarvoor immers ook altijd anderen nodig.
Doe de 'Personlijkheidstest'
Wilt u in niet meer dan tien minuten inzicht krijgen in uw persoonlijkheid ? In deze test krijgt u 120 stellingen voorgelegd waarvan u moet beoordelen in hoeverre die op u van toepassing zijn. De stellingen zijn eenvoudig, daarom kost het invullen zo weinig tijd.
Goede of foute antwoorden bestaan niet
Het is de bedoeling dat u de uitspraken over zichzelf doet op basis van een vergelijking met anderen. Als u aangeeft dat u het helemaal eens bent met de stelling dat u betrouwbaar bent, dan wil dat zeggen dat u vindt dat u in vergelijking met gemiddelde anderen betrouwbaarder bent.
De test heet 'Big Eight' omdat hij een beoordeling geeft op basis van acht persoonlijkheidskenmerken : deugdzaamheid, competentie, extraversie, mildheid, zorgvuldigheid, neuroticisme, hedonisme en volgzaamheid.
GROOTEGAST - Zwangeren die binnenkort gaan bevallen en hun huisgenoten willen laten inenten tegen de Mexicaanse griep, worden door de GGD terug naar de huisarts gestuurd. De huisarts mag echter geen mensen inenten die buiten de risicogroepen vallen.
Vaccinatie risicogroepen H1N1 volgende week van start LHV – Medischcontact.artsennet.nl, Nr. 45, rubriek 'Federatienieuws', p. 1890 – 04-11-2009 Deze week ontvangen alle huisartspraktijken in Nederland de vaccins voor de eerste vaccinatieronde tegen het H1N1-virus, de Mexicaanse griep. In totaal worden ruim 5 miljoen vaccins afgeleverd bij de huisartsen voor de eerste ronde. Een week later kan deze eerste vaccinatieronde beginnen. De doelgroep voor deze vaccinatie komt grotendeels overeen met de risicogroepen die de huisarts jaarlijks voor vaccinatie tegen de seizoensgriep oproept. Mensen met een medisch risico en gezonde 60-plussers hebben van hun huisarts een uitnodiging gekregen voor de pandemische vaccinatie. De vaccinatie wordt ook aangeboden aan mantelzorgers van mensen met een zeer hoog risico op ernstige ziekte en sterfte door griep. Onder mantelzorgers wordt verstaan: huisgenoten die contact hebben met genoemde patiëntencategorieën en daarmee vergelijkbare contacten. LHV en NHG adviseren hun leden om aan de hand van de lijst met opgeroepen patiënten te bepalen voor welke patiënten het nuttig is om de mantelzorgers te vaccineren. De betreffende patiënten kunnen vervolgens hun mantelzorgers vragen naar hun eigen huisarts te gaan. Het vaccin wordt ook beschikbaar gesteld aan gezonde zwangeren vanaf de vierde maand, maar de huisarts roept hen niet actief op. De Gezondheidsraad heeft bewust gekozen voor de omschrijving van ‘vaccin moet beschikbaar zijn’ in plaats van ‘adviseren om te vaccineren’ voor gezonde zwangeren. De reden is dat het vaccin tegen Nieuwe Influenza A (H1N1) nog niet getest is bij zwangeren. Onderzoeksresultaten van het vaccin tegen de jaarlijkse seizoensgriep bij zwangeren laat zien dat zich hierbij geen bijzonderheden voordoen. Voor de zekerheid is gekozen voor een contra-indicatie in het eerste trimester, omdat dat de meest kwetsbare periode is voor de vrucht. Om zwangeren goed te informeren, verstrekt VWS voorlichtingsfolders aan verloskundigen, gynaecologen en verloskundig actieve huisartsen. Tot slot heeft ook een deel van het zorgpersoneel recht op vaccinatie. Dit gaat bijvoorbeeld om medewerkers van ziekenhuizen, ambulancediensten en verloskundigen. Criterium is het risico voor kwetsbare patiënten. Vaccinatie van zorgpersoneel loopt via de werkgever. De LHV heeft met de KNOV afgesproken dat verloskundigen bij hun huisarts terecht kunnen voor vaccinatie. Mensen die niet tot een risicogroep behoren, komen niet in aanmerking voor H1N1-vaccinatie. Minister Klink van VWS vroeg de Gezondheidsraad op 19 oktober om de eerdere adviezen over vaccinatie tegen het licht te houden. Hij wil weten of deze nog overeenkomen met de nieuwste inzichten over Nieuwe Influenza A. Zo vroeg hij onder andere of jongeren in aanmerking moeten komen voor vaccinatie. Cfr. : http://medischcontact.artsennet.nl/blad/Tijdschriftartikel/Vaccinatie-risicogroepen-H1N1-volgende-week-van-start.htm
De GGD verwijst ook mensen die op vakantie zijn tijdens de inentingsdagen naar de huisarts. Maar deze kan en mag deze mensen niet inenten. Minister Klink heeft zelfs gedreigd met de tuchtrechter als dokters mensen gaan vaccineren die niet in een risicogroep vallen. Op dit moment is nog niet bekend hoe deze grensgevallen behandeld gaan worden.
Huisgenoten van zwangeren die gaan bevallen, vallen niet binnen de risicogroepen en krijgen dus geen oproep van de GGD. Het nog niet geboren kind is namelijk nog niet bekend bij de Gemeentelijke Basis Administratie (GBA) van waaruit pasgeboren kinderen en hun huisgenoten opgeroepen worden.
De GGD verwijst ook mensen die op vakantie zijn tijdens de inentingsdagen naar de huisarts. Maar deze kan en mag deze mensen niet inenten.
Minister Klink heeft zelfs gedreigd met de tuchtrechter als dokters mensen gaan vaccineren die niet in een risicogroep vallen. Op dit moment is nog niet bekend hoe deze grensgevallen behandeld gaan worden.
Geopereerd Prof. Johann Bauer - Een update (Greta)
Zoals beloofd hou ik jullie op de hoogte...
Cfr. 'Geopereerd Prof. Johann Bauer' – dit blog dd. 08-11-2009
Op 16-11-2009 schreef Greta in mijn dagboek :
Dag Jules en allen die op dit blog een kijkje nemen,
Zoals beloofd hou ik jullie op de hoogte na mijn operatie van 21-10-2009 door prof. Bauer in Baar (Zwitserland), 4 weken geleden al ondertussen.
Wat Dr. Bauer me voorspelde qua pijn klopt heel precies : omdat ik in zo'n erge mate fibro heb, had hij gezegd dat ik na de operatie nog veel meer pijn zou kunnen hebben dan ervoor en dat ik die 1ste operatie niet zoveel zou voelen.
Dat is ook zo, al heb ik in mijn eerste berichtje hier (cfr. 'Geopereerd Prof. Johann Bauer' – dd. 08-11-2009) geschreven dat ik me werkelijk beter voelde...
Dat wás ook zo - ik zag het weer volkomen zitten - maar vorige week was de hevige pijn er weer. Ik ben ondertussen mijn morfine met 12,5 mg ook aan het afbouwen en dat voel ik enorm, dat is weer afkicken... Ik ben vorige week echt heel erg ziek geweest. Ik kon zelfs mijn bed niet uit en ik kon weer niks meer eten. Ik voel maar al te goed dat dit mede komt door de stress hier thuis is : ik kan werkelijk tegen niks meer !
Ja, als je weer thuis komt... We hebben een eigen zaak en ik mag niet meer werken. Dat is voor mij niet om aan te zien ! Al was ik genoeg verwittigd dat ik de eerste weken na de operatie nog niks mocht doen heb ik vorige week weer ietske teveel hooi op de vork genomen. Maar wat moet ik doen ? Er is niks geregeld, door niemand : ik zorg altijd zélf voor alles... Nu voel ik werkelijk dat ik niet meer kán. Ik ben gewoon heel erg moe en wil slapen ! Ik moét afstand nemen, maar dat is heel erg moeilijk voor mij...
Gisteren zondag 15/11 lag ik hier alweer doodziek in bed.
Slapen ging heel erg slecht de afgelopen dagen, zelfs na inname van mijn slaapmedicatie. De krampen in mijn benen en voeten zijn heel veel verergerd.
Zoals gezegd had Prof. Bauer dat voorspeld. Hij had gelijk, dat geef ik hier eerlijk toe !
Gisteren hat ik dan ook in een serieuze dip.
Ik had alweer de pijn aan mijn rechtervoet. Daar begint het altijd. Maar met de morfinepleisters aan mijn rechtervoet te vernieuwen (om de 2 dagen) ben ik vandaag een stuk beter.
Als gevolg van een week niet kunnen slapen heb ik een hele grote afte in mijn mond gekregen. Vroeger had ik er soms 4 ineens ! Deze keer had ze de grootte van een 2-eurocentje. Ik kan amper iets eten. Niet te verwonderen dat ik al bij al zeker nog niet ben verzwaard...
Vandaag is er toch weer wat hoop, al heb ik nu op het ogenblik alweer ferme krampen in mijn voeten en benen. Ik heb boodschappen gedaan met mijn dochter. Bovendien was ik gisteren zeer zenuwachtig, want afhankelijk zijn van iemand ligt niet in mijn aard : ik heb altijd ánderen geholpen, ik ben geen vrager, maar een gever, altijd geweest...
Nu is het uitkijken naar mijn 2de operatie (aan mijn R-been).
Ik weet het, de prof had me eerlijk gezegd dat het er na die eerste operatie nog niet in zat, maar ik hoop dat ik na deze tweede operatie toch al een beetje verschil zal merken. Morgen stuur ik hem een mailtje.
Ondertussen is de operatiepleister verwijderd. Het wondje is nu een heel mooi fijn naadje, echt heel fijn gedaan ! Ik moet het nu elke dag inwrijven met Johannesolie van A. Vogel (want zalf mag niet op de wonde komen).
Zo beste allemaal, tot zover mijn verhaal.
Ik hoop dat ik toch nog iets mag ondervinden van de eerste operatie.
Het enige wat ik nu precies niet meer voel is de pijn in mijn kaakgewrichten en kaakbeenderen (het gevoel alsof ik slaag gekregen heb in mijn gezicht is verdwenen). Dat is toch iets positief.
Ook mijn darmen zijn wel beter. Alleen ben ik ook nog heel misselijk, maar dat is veeleer van de morfine.
Ik hoop de volgende keer iets positever te kunnen schrijven. Maar, nogmaals, de prof had me verwittigd dat ik veel slechter kon worden. Hij is eerlijk geweest.
Ik ben hier nu ook eerlijk geweest, maar ik laat de moed niet zakken ! Ik moet doorgaan !
Ik heb al een lange weg afgelegd... door de hel die zo stilaan haar poorten mag sluiten.
Met geduld kom ik er wel... er zijn nog zóveel mensen die ook heel veel pijn hebben en er óók mee moeten leven.
Ik wil alle mensen met fibro en cvs hierbij een hart onder de riem steken !
Weersfactoren die hoofdpijn uitlokken zijn onder andere dalende luchtdruk, toenemende bewolking, stijgende vochtigheid, temperatuurswisselingen en toenemende wind. Van al deze factoren is dalende luchtdruk het meest van invloed.
In het najaar kan de luchtdruk van dag tot dag snel veranderen en worden in de regel de laagste waarden van het jaar gemeten. Wanneer de luchtdruk snel daalt, zet de lucht in onder andere bij- en voorhoofdsholten uit, waardoor er meer druk op bloedvaten komt te staan. Dit kan hoofdpijn tot gevolg hebben.
Uiteraard lost het drukprobleem zich uiteindelijk vanzelf op. Je lichaam stelt zich erop in of de luchtdruk gaat weer omhoog.
Dr. Mark J Pellegrino Dr. Pellegrino has seen more than 20,000 FM patients in his practice at the Ohio Rehab Center – cfr. : http://www.ohiorehabcenter.com/index.html - and has been a fibromyalgia patient himself since childhood.
Though Dr. Pellegrino published these observations before discovery of the XMRV virus, the questions they raise are if anything more relevant today.
All of us involved with Fibromyalgia, either by treating it or having it, have come to appreciate how complicated this condition is
Fibromyalgia has different types and subsets (cfr. also Dr. Pellegrino’s articles on “The fibromyalgia spectrum – Part of the Big Picture in Understanding Fibromyalgia” at : http://www.prohealth.com//library/showArticle.cfm?libid=13042 -& “Fibromyalgia – Ultimately a disease of amplified pain” at : http://www.prohealth.com//library/showArticle.cfm?libid=13702 -). More than one factor may be involved in causing it. Causes may be recognized, but the exact mechanism of how fibromyalgia develops from this cause is not fully known. Most importantly, there is more than one way to get fibromyalgia; it is an “end point” condition with multiple ways leading to it.
I have compiled a list of probable causes of fibromyalgia. This list is based on my experiences and understanding of the current literature. My opinions on these probable causes may not be shared by everyone. My list of probable causes is as follows :
Like trauma, infection is one of those causes of fibromyalgia that just screams for common sense
I’ve seen hundreds and hundreds of people whose basic story goes like this : “I was fine, I got a virus, I developed fatigue and pain and I’ve never been the same since”.
The logical thinking in this scenario is that fibromyalgia was not present before the viral infection. There may have been a hereditary predisposition or a vulnerability, but fibromyalgia was not present. The virus caused the condition to develop and it has been present since the virus and continues to be present. This is a straightforward infectious cause.
Not all infections are as straightforward
Many people who have fibromyalgia get a viral infection and find it worsens the fibromyalgia. People with active viral infections are at risk for additional infections, particularly bacterial infections which can create additional problems.
Some people with fibromyalgia are more vulnerable to any type of infection because the fibromyalgia renders them more immunocompromised or more at risk for infection. The physician needs to sort out the various possibilities to determine whether an infection is the cause, a consequence or an aggravator of the fibromyalgia.
The mechanism by which an infection leads to fibromyalgia is probably related to inflammatory or autoimmune changes caused by the infection that starts the fibromyalgia cascade.
The actual clinical infection resolves and is long gone, yet fibromyalgia symptoms continue :
sometimes, the infecting virus or bacteria may hang around and create a persistent low grade infection which activates the autoimmune responses, thereby “triggering” the fibromyalgia
many times, though, the infection has long disappeared, but permanent changes occurred in the body and these changes caused fibromyalgia to develop.
Various viral infections can cause fibromyalgia
The Epstein-Barr virus which causes infectious mononucleosis is one;
Cytomegalovirus causes a syndrome similar to infectious mononucleosis;
Different strains of the influenza virus can also result in fibromyalglia;
The adenoviruses, especially Type II, cause common colds, bronchitis and various upper respiratory infections and may lead to fibromyalgia;
Human Herpes Virus 6 has also been implicated;
Reactive fibromyalgia has been described in patients with AIDS and hepatitis.
Sometimes viral titers can be directly measured to demonstrate that an acute infection has occurred. This concentration can be correlated with the clinical development of fibromyalgia. Many times, though, the exact offending virus is not known, but we can still categorize the fibromyalgia as one that was caused by an infection, probably a viral infection, if it fits clinically.
Bacterial infections can also cause fibromyalgia
I have seen patients who have developed fibromyalgia after sepsis (blood infection) and salmonella infections and one who, I felt, has gotten it from a Listeria infection. Some research studies found Mycoplasma incognitos and Chlamydia pneumoniae (for more on this subject cfr. “Chlamydia pneumoniae in chronic fatigue syndrome and fibromyalgia – An opinion” by Patient Advocate James Kepner (from the Chlamydia pneumoniae Help website) at : http://www.prohealth.com//library/showArticle.cfm?libid=127633 -) in patients with fibromyalgia and chronic fatigue syndrome (cfr. “Evidence for bacterial (mycoplasma, Chlamydia) and viral (HHV-6) co-infections in chronic fatigue syndrome patients” by Dr. Garth Nicolson and Dr. Darryl See at : http://www.informaworld.com/smpp/content~db=all?content=10.1300/J092v11n02_02 -). These infectious organisms may be causing some of the symptoms.
Indeed, some of the patients improve with antibiotic therapy. Gulf War Syndrome, in part, may have been related to infections from one of these bacteria. Symptoms of Gulf War Syndrome include fatigue, headaches, depression, joint and muscle pain, sleep disorders and poor memory (sound familiar ?).
As of November 2008, a research panel reported their finding that Gulf War illness is real and “is the result of neurotoxic exposures” (cfr. 'Gulf War Syndrome finally declared real - Illness caused by exposure to pesticides and other neurotoxic chemicals' at : http://www.prohealth.com/me-cfs/library/showArticle.cfm?libid=14093 -) as discussed in Chapter 10 under 'Chemical exposure as a probable cause of FM']
Fibromyalgia can be caused by yeast and parasite infections
I have seen some patients who developed it following a severe Candida yeast infection and others following parasite infections such as Giardia (cfr. : http://en.wikipedia.org/wiki/Giardia -). Most of the time, yeast or parasite infections occur in patients after the fibromyalgia has already developed. These infections may aggravate the preexisting fibromyalgia or cause it to flare up.
Fibromyalgia may predispose us to these infections by interfering with our immune function. On the other hand, these infections can sometimes cause the fibromyalgia by “triggering” the fibromyalgia cascade. Many of the symptoms of a chronic Candida yeast infection (cfr. also Dr. Pellegrino's article "Candidiasis - Yeast infection and nutritional tepair" at : http://www.prohealth.com/library/showArticle.cfm?libid=12385 -) such as fatigue, irritable bowel syndrome, bloating, allergies, altered immune response, and skin conditions - overlap with fibromyalgia symptoms. This can make it difficult to “separate” the two conditions and determine cause and effect relationships.
As I’ve mentioned, some infections come in, do their damage and disappear. The infectious agent is no longer present in the body and thus can’t be detected at a later point in time. Other infectious agents may hang around in the body and establish a chronic infection; one that perhaps can be detected with blood tests.
What remains to be seen is whether these chronic infections can be eradicated with antibiotic treatment and, if so, will the fibromyalgia symptoms disappear ? Or has the fibromyalgia already established itself as a separate entity which does not disappear with the antibiotic treatment ?
Hopefully we will have these answers in the near future. [But]… one thing is certain : we will continue to learn more about fibromyalgia and understand it better.
A 37 kDa 2-5A binding protein as a potential biochemical marker for Chronic Fatigue Syndrome De Meirleir K, Bisbal C, Campine I, De Becker P, Salehzada T, Demettre E, Lebleu B, Department of Human Physiology and Medicine, Vrije Universiteit Brussels, Belgium - Am J Med. 2000 Feb;108(2):99-105 - PMID: 11126321 Purpose - Recent studies have revealed abnormalities in the ribonuclease L pathway in peripheral blood mononuclear cells of patients with the chronic fatigue syndrome. We conducted a blinded study to detect possible differences in the distribution of 2-5A binding proteins in the cells of patients with chronic fatigue syndrome and controls. Patients and methods - We studied 57 patients with chronic fatigue syndrome and 53 control subjects (28 healthy subjects and 25 patients with depression or fibromyalgia). A radioactive probe was used to label 2-5A binding proteins in unfractionated peripheral blood mononuclear cell extracts and to compare their distribution in the three groups. Results - A 37 kDa 2-5A binding polypeptide was found in 50 (88%) of the 57 patients with chronic fatigue syndrome compared with 15 (28%) of the 53 controls (P < 0.01). When present, the amount of 37 kDa protein was very low in the control groups. When expressed as the ratio of the 37 kDa protein to the 80 kDa protein, 41 (72%) of the 57 patients with chronic fatigue syndrome had a ratio > 0.05, compared with 3 (11%) of the 28 healthy subjects and none of the patients with fibromyalgia or depression. Conclusion - The presence of a 37 kDa 2-5A binding protein in extracts of peripheral blood mononuclear cells may distinguish patients with chronic fatigue syndrome from healthy subjects and those suffering from other diseases. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11126321 Also read the comments on this article : - Chronic fatigue syndrome Van Houdenhove B, Vanthuyne S, Neerinckx E - Am J Med. 2000 Aug 15;109(3):257-9 - PMID: 11023437 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11023437?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract - Is there a Gulf War syndrome ? Podell RN - Am J Med. 2000 Dec 15;109(9):744 - PMID: 11188785 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11188785?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract - The biology of chronic fatigue syndrome Komaroff AL - Am J Med. 2000 Feb;108(2):169-71 - PMID: 11126311 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11126311?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract - Chronic fatigue syndrome - The fundamentals still apply Manu P - Am J Med. 2000 Feb;108(2):172-3 - PMID: 11126312 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11126312?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
A family history study of chronic fatigue syndrome Walsh CM, Zainal NZ, Middleton SJ, Paykel ES, University Department of Psychiatry, Addenbrooke's Hospital, Cambridge, UK - Psychiatr Genet. 2001 Sep;11(3):123-8 - PMID: 11702053 Chronic fatigue syndrome (CFS) is characterized by unexplained, disabling fatigue and is associated with high rates of comorbid depression. While the aetiology is unknown, findings from recent twin surveys suggest that genetic factors may be relevant to prolonged fatigue states (> 1 month). To date, however, there has been no exploration of the role of familial/genetic factors in operationally defined CFS. The aims of the present study were: (i) to examine whether CFS is familial by comparing the rates of CFS in the first-degree relatives of CFS cases and medical control subjects; and (ii) to determine whether the high rate of comorbid depression in CFS is reflected in a greater familial loading for affective disorder. Twenty-five CFS cases and 36 medical control subjects were assessed for fatigue symptoms based on the Centre for Disease Control (CDC) criteria for CFS and for lifetime psychiatric symptoms using the Schedule for Schizophrenia and Affective Disorders-Lifetime Version. Informant family history was obtained regarding first-degree relatives using the CDC criteria and the Family History Research Diagnostic Criteria. In addition, informant history was supplemented by sending a questionnaire to first-degree relatives. There were significantly higher rates of CFS in the relatives of CFS cases compared with the relatives of control subjects. The rate of depression in the CFS cases was similar to previous studies but did not appear to reflect a greater familial loading for depression when compared with control subjects. However, these analyses were complicated by higher than expected rates of depression in the control group. These findings suggest that familial factors are important in the aetiology of chronic fatigue syndrome. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11702053
Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome Peckerman A, LaManca JJ, Dahl KA, Chemitiganti R, Qureishi B, Natelson BH, Department of Neurosciences, CFS Cooperative Research Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA : firstname.lastname@example.org - Am J Med Sci. 2003 Aug;326(2):55-60 - PMID: 12920435 Background - Findings indicative of a problem with circulation have been reported in patients with chronic fatigue syndrome (CFS). We examined this possibility by measuring the patient's cardiac output and assessing its relation to presenting symptoms. Methods - Impedance cardiography and symptom data were collected from 38 patients with CFS grouped into cases with severe (n = 18) and less severe (n = 20) illness and compared with those from 27 matched, sedentary control subjects. Results - The patients with severe CFS had significantly lower stroke volume and cardiac output than the controls and less ill patients. Postexertional fatigue and flu-like symptoms of infection differentiated the patients with severe CFS from those with less severe CFS (88.5% concordance) and were predictive (R2 = 0.46, P < 0.0002) of lower cardiac output. In contrast, neuropsychiatric symptoms showed no specific association with cardiac output. Conclusions - These results provide a preliminary indication of reduced circulation in patients with severe CFS. Further research is needed to confirm this finding and to define its clinical implications and pathogenetic mechanisms. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12920435
Activation of human monocytes by the pineal hormone melatonin Morrey KM, McLachlan JA, Serkin CD, Bakouche O, Department of Molecular Pharmacology and Biologic Chemistry, Northwestern University Medical School, Chicago, IL 60611 - J Immunol. 1994 Sep 15;153(6):2671-80 - PMID: 8077674 To determine the effects of the pineal hormone melatonin on human monocytes, human monocytes were activated by different concentrations of melatonin. Above the activation threshold of 5 x 10(-11) M, melatonin was able to induce the cytotoxicity of human monocytes, the secretion of IL-1 and the production of reactive oxygen intermediates. Melatonin and LPS seemed to have a synergistic effect on human monocyte activation. Indeed, below their respective monocyte activation threshold (5 x 10(-11) M and 0.625 ng/ml), melatonin (10(-12) M) in association with LPS (0.2 ng/ml) was able to induce cytotoxicity, IL-1 secretion and reactive oxygen intermediates production. Melatonin alone at 10(-12) M or LPS alone at 0.2 ng/ml did not activate monocytes. Furthermore, melatonin was able to prime the monocytes for a subsequent activation by LPS. When monocytes were activated by LPS (0.25 ng/ml) at the time that they were plated and then activated by melatonin (10(-12) M) 8 h later, no IL-1 secretion and no cytotoxicity were detected. However, when the cells were first activated by melatonin (10(-12) M) and then 8 h later by LPS (0.25 ng/ml), IL-1 secretion and monocyte cytotoxicity were observed. Above its monocyte activation threshold, melatonin induces both cell-associated IL-1 alpha and IL-1 beta activities. Below this activation threshold, i.e., at 10(-12) M, melatonin does not induce the cell-associated IL-1 alpha and IL-1 beta activities, but does induce the mRNA for both IL-1 (alpha and beta). It seems that melatonin activates monocytes through protein kinase C. These data suggest that melatonin activates monocytes and induces their cytotoxic properties, along with the IL-1 secretion. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8077674
Anthrax vaccination and self-reported symptoms, functional status and medical conditions in the National Health Survey of Gulf War Era veterans and their families Mahan CM, Kang HK, Dalager NA, Heller JM, Veterans Health Administration, Department of Veterans Affairs, Washington, DC, USA - Ann Epidemiol. 2004 Feb;14(2):81-8 - PMID: 15018879 Purpose - To evaluate the health status of Gulf War veterans who reported receipt of anthrax vaccination and a small group of Gulf War veterans for whom documentation of anthrax vaccination exists. Methods - Among the 11,441 Gulf War veterans who completed a health survey, 4601 reported receiving the anthrax vaccine during the war; 2979 veterans reported not receiving it; 3861 were uncertain. Also, 352 of these respondents were documented by the Department of Defense as having received anthrax vaccination. We compared the medical history of these groups of veterans using multivariate analyses. Finally, we analyzed perception of exposure and its relation to reporting bias. Results - There were statistically significant differences in prevalence for almost all outcomes studied between those who reported having received anthrax vaccination and those who did not so report. However, when we compared the veterans for whom vaccination records exist to the group who self-reported that they had not received the vaccine, the significant differences in prevalence for almost all of the outcomes disappeared. Conclusions - The extent of a reporting bias should be carefully considered when one evaluates the health consequences of anthrax vaccination based on self-reported data. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/15018879
Arthritis in patients with chronic hepatitis C virus infection Rivera J, García-Monforte A, Pineda A, Millán Núñez-Cortés J, Instituto Provincial de Rehabilitación, Internal Medicine Department, Hospital General Universitario Gregorio Marañón, Madrid, Spain : email@example.com - J Rheumatol. 1999 Feb;26(2):420-4 - PMID: 9972979 Objective - To describe the clinical picture of arthritis in patients with chronic infection by hepatitis C virus (HCV). Methods - Two patient populations were studied. Patients with arthritis and evidence of serum elevation of alanine aminotransferase (ALT) at the consultation were checked for HCV infection. A second group of 303 consecutive patients with rheumatoid arthritis (RA) were also checked for the presence of HCV antibodies. All patients attended the outpatient rheumatology unit of a tertiary care teaching hospital. Chronic HCV infection was determined by the presence of viral RNA in serum. A group of 315 first-time blood donors served as controls. Results - Twenty-eight patients with arthritis and chronic HCV infection were identified. Seven fulfilled criteria for RA, psoriatic arthritis was found in one patient, systemic lupus erythematosus in one, gout in 2, chondrocalcinosis in 2, osteoarthritis in 7 and tenosynovitis in one. In 7 patients with a clinical picture of intermittent arthritis, a definitive diagnosis could not be made. In these patients, mixed cryoglobulinemia was present in 6/7 (86%), whereas mixed cryoglobulinemia was found in 6/21 (28%) of the other patients. Among patients with RA, 23 (7.6%) had HCV antibodies and active infection by HCV was found in 7 (2.3%) patients. The prevalence of HCV antibodies in a blood donor population was 0.95%, significantly different (p<0.001; 95% CI 0.03, 0.10) compared to patients with RA. The distribution of antibodies determined by recombinant immunoblot analysis was similar (p = NS) between RA patients and blood donors with HCV antibodies. Conclusion - There is not a single clinical picture of arthritis in patients with chronic HCV infection. There is a well defined picture of arthritis associated with the presence of mixed cryoglobulinemia that consists of an intermittent, mono or oligoarticular, nondestructive arthritis affecting large and medium size joints. Although a high prevalence of HCV antibodies is suspected in patients with RA, its occurrence may be coincidental and its interpretation is difficult to determine from the data in this study. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/9972979?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Single ItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmed Also read the comment on this article : Human immunodeficiency virus infection and arthritis Rivera J, Garcia-Monforte A - J Rheumatol. 2000 May;27(5):1322-3 - PMID: 10813314 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/10813314?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
Association of mycoplasma and human immunodeficiency virus infection - Detection of amplified Mycoplasma fermentans DNA in blood Hawkins RE, Rickman LS, Vermund SH, Carl M, Department of Internal Medicine, National Naval Medical Center, National Institutes of Health, Bethesda, Maryland - J Infect Dis. 1992 Mar;165(3):581-5 - PMID: 1538164 A cross-sectional study was undertaken to determine the prevalence of Mycoplasma fermentans infection in patients with human immunodeficiency virus (HIV) infection using polymerase chain reaction methodology. Targeted M. fermentans DNA sequences could be amplified from the DNA extracted from the blood of 6 (11%) of 55 HIV-seropositive patients but from none of 26 HIV-seronegative subjects at low risk for HIV infection (P = .17). There was no correlation between M. fermentans infection and HIV clinical stage. There was a nonsignificant trend toward an association between M. fermentans infection and a history of syphilis. Infection with M. fermentans may occur more commonly in HIV-infected patients; however, a role as a copathogen or opportunistic infection was not established in this study. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/1538164
Bacterial and Viral Co-Infections in Chronic Fatigue Syndrome (CFS/ME) Patients Bacterial and viral co-infections in chronic fatigue syndrome patients Garth L. Nicolson,(1) PhD, Marwan Y. Nasralla,(2) PhD, Kenny De Meirleir,(3) MD, PhD and Jeorg Haier,(4)MD, PhD – (1) The Institute for Molecular Medicine, Huntington Beach, California, USA – (2) International Molecular Diagnostics, Inc., Huntington Beach, California, USA – (3) Department of Internal Medicine, Free University of Brussels, Brussels, Belgium and (4) Department of Surgery, Wilhelm-University, Munster, Germany – Correspondence : Prof. Garth L. Nicolson, Office of the President, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, California 92649. Tel. : 714-903-2900; Fax : 714-379-2082; Email : firstname.lastname@example.org - Website : www.immed.org - ProHealth, June 14, 2002 A majority of Chronic Fatigue Syndrome (CFS) patients have systemic bacterial and viral infections. In our study of 200 CFS patients we found a high prevalence (52%) of Mycoplasmal infections. Using forensic polymerase chain reaction we also examined whether these same CFS patients showed evidence of co-infections with various Mycoplasmas, Chlamydia pneumoniae and/or Human Herpes Virus-6 (HHV-6). We found that 7.5% of the patients had C. pneumoniae and 30.5% had HHV-6 infections. Since the presence of one or more infections may predispose patients to other infections, we examined the prevalence of C. pneumoniae and HHV-6 infections in Mycoplasma-positive and -negative patients. Unexpectedly, we found that the incidence of C. pneumoniae or HHV-6 was similar in Mycoplasma-positive and -negative patients. Also, the incidence of C. pneumoniae in HHV-6-positive and -negative patients was similar. Control subjects had low rates of Mycoplasmal (6%), HHV-6 (9%) or chlamydial (1%) infections and there were no co-infections in control subjects. Differences in bacterial and/or viral infections in CFS patients compared to control subjects were significant (P<0.001). The results indicate that a very large subset of CFS patients show evidence of bacterial and viral co-infections. Full text at : - http://www.prohealth.com/library/showarticle.cfm?id=3635&t=CFIDS_FM - http://www.immed.org/Fatigue%20Illness/Netal_co_MycoAust02%5B1%5D.1.rtf
Bacterial products, cytokines and sleep JM Krueger L Johannsen, Department of Physiology and Biophysics, University of Tennessee, Memphis 38163 - J Rheumatol Suppl. 1989 Nov;19:52-7 - PMID: 2691682 Sleep deprivation, infection and administration of muramyl peptides or certain other immune response modifiers all alter sleep. Sleep, temperature and hematologic effects observed after bacterial infection are also elicited after administration of isolated bacterial cell walls. Macrophages have the capability to digest bacterial peptidoglycan and in the process produce pyrogenic and somnogenic substances of low molecular weight. Activated macrophages also produce cytokines and some of these e.g., interleukin-1 (IL-1), are somnogenic. Our results emphasize the close connection of the infection process, fever and sleep. Muramyl peptides and/or IL-1 may also be involved in daily regulation of sleep. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2691682
Baseline mood and psychosocial characteristics of patients developing depressive symptoms during interleukin-2 and/or interferon-alpha cancer therapy Capuron L, Ravaud A, Miller AH, Dantzer R, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA : email@example.com - Brain Behav Immun. 2004 May;18(3):205-13 - PMID: 15050647 It has been suggested that patients with subclinical mood symptoms prior to initiating cytokine treatment (as revealed by elevated baseline scores on depression rating scales) are more likely to become clinically depressed during the course of cytokine therapy. The present study was designed to identify which specific preexisting symptoms predict development of depressive symptomatology during treatment with the cytokines, interleukin-2 (IL-2) and/or interferon-alpha (IFN-alpha), in patients with cancer. Thirty-two patients with renal cell carcinoma or malignant melanoma eligible to receive treatment with IL-2 and/or IFN-alpha were enrolled in the study. At baseline and after one month of cytokine therapy (endpoint), depressive symptoms were assessed using the clinician-administered Montgomery-Asberg depression rating scale (MADRS). Illness-related coping strategies, social support, somatic complaints, quality of sleep and demographic factors were also assessed as relevant baseline predictive factors. MADRS scores significantly increased during cytokine therapy. Patients with moderate to marked depressive symptomatology at study endpoint exhibited higher baseline scores in dimensions of the MADRS scale assessing emotional (especially reported sadness), cognitive (especially pessimistic thoughts) and neurovegetative (sleep disturbances) symptoms compared to patients who remained free of depressive symptoms during cytokine therapy. Interestingly, only emotional symptoms and sleep disturbance at baseline, along with low social support, predicted severity of depressive symptoms at the end of the first month of therapy. By documenting specific behavioral vulnerability factors for cytokine-induced depressive symptoms, these findings may help identify patients at risk for mood disturbances during cytokine treatment and help target specific patient populations and specific symptoms for preventative strategies. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/15050647
Biochemical dysregulation of the 2-5A synthetase/RNase L antiviral defense pathway in chronic fatigue syndrome Suhadolnik RJ, Peterson DL, Cheney PR, Horvath SE, Reichenbach NL, O’Brien K et al. - Journal of Chronic Fatigue Syndrome 1999; 5:223-42
Biochemical evidence for a novel low molecular weight 2-5A-dependent RNase L in chronic fatigue syndrome Suhadolnik RJ, Peterson DL, O'Brien K, Cheney PR, Herst CV, Reichenbach NL, Kon N, Horvath SE, Iacono KT, Adelson ME, De Meirleir K, De Becker P, Charubala R, Pfleiderer W, Department of Biochemistry, Temple University School of Medicine, Philadelphia, PA, USA - J Interferon Cytokine Res. 1997 Jul;17(7):377-85 - PMID: 9243369 Previous studies from this laboratory have demonstrated a statistically significant dysregulation in several key components of the 2',5'-oligoadenylate (2-5A) synthetase/RNase L and PKR antiviral pathways in chronic fatigue syndrome (CFS) (Suhadolnik et al. Clin Infect Dis 18, S96-104, 1994; Suhadolnik et al. In Vivo 8, 599-604, 1994). Two methodologies have been developed to further examine the upregulated RNase L activity in CFS. First, photoaffinity labeling of extracts of peripheral blood mononuclear cells (PBMC) with the azido 2-5A photoaffinity probe, [32P]pApAp(8-azidoA), followed by immunoprecipitation with a polyclonal antibody against recombinant, human 80-kDa RNase L and analysis under denaturing conditions. A subset of individuals with CFS was identified with only one 2-5A binding protein at 37 kDa, whereas in extracts of PBMC from a second subset of CFS PBMC and from healthy controls, photolabeled/immunoreactive 2-5A binding proteins were detected at 80, 42, and 37 kDa. Second, analytic gel permeation HPLC was completed under native conditions. Extracts of healthy control PBMC revealed 2-5A binding and 2-5A-dependent RNase L enzyme activity at 80 and 42 kDa as determined by hydrolysis of poly(U)-3'-[32P]pCp. A subset of CFS PBMC contained 2-5A binding proteins with 2-5A-dependent RNase L enzyme activity at 80, 42, and 30 kDa. However, a second subset of CFS PBMC contained 2-5A binding and 2-5A-dependent RNase L enzyme activity only at 30 kDa. Evidence is provided indicating that the RNase L enzyme dysfunction in CFS is more complex than previously reported. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/9243369
Candidiasis - Yeast infection and nutritional repair - Causes, symptoms, testing, natural treatments and probiotic strategies, anti-yeast/weight loss diet and trigger avoidance Mark J. Pellegrino, MD – ProHealth, December 6, 2006 What would you say if I told you we had millions of Dr. Jekyll's living in our bodies, each waiting for the opportune time to turn into Mr. Hyde ? We all have little round whitish organisms in our body known as Candida albicans that can lose their innocence and become rather vicious creatures that attack our bodies. Candida albicans is fungus or yeast that normally thrives in the mouth, gastrointestinal tract, vagina and skin. In healthy individuals this yeast is helpful in digestion and vitamin production and it is harmless because it is kept in check by beneficial bacteria and other yeast such as Lactobacillus acidophilus that occupies the same space. When the balance of intestinal bacteria and yeast is altered or your immune system becomes compromised, the Candida can overgrow, transforming from a benign yeast into an aggressive fungus that releases numerous toxins and can cause many symptoms. When fungal growth exceeds the body’s ability to control it, the friendly Candida becomes unfriendly and cause a yeast infection. 1. - Causes of Candida Various causes of Candidiasis (Candida infection) include : - Chronic illnesses or stress For example, diabetic patients, hospitalized patients and cancer patients all have low resistance to infection. - Antibiotic use This destroys normal bacteria and Lactobacillus acidophilus, but spares the Candida. - Birth control pills The estrogen favors Candida multiplication. - Cortisone medicine - Immunosuppressive drugs - Pregnancy Hormonal changes favor increased Candida growth. - Diets high in sugar and carbohydrates Candida loves glucose ! - Thyroid medicine Increases Candida risk. - Warm moist areas Tight nylons, wet diapers, people who work as dish washers; all this can lead to Candida dermatitis. - Alcohol Another food for the Candida. Those with Fibromyalgia often have multiple risk factors, particularly the altered immune system, the chronic stress and the carbohydrate sensitivity. Throw in the woman... who is on birth control pills, thyroid medicine and recently took a course of antibiotics for bronchitis and you have a recipe for “Candisaster”! When Candida albicans transforms into an invasive fungal state, it produces rhizoids which are long root-like structures. Rhizoids can penetrate the intestinal walls and leave microscopic holes that allow toxins, undigested food particles, bacteria and yeast to enter the blood stream. This “invasion” leads to many symptoms. 2. - Candidiasis symptoms - Bloating - Irritable bowel syndrome (IBS) - Chronic heartburn - Oral thrush (white spots on the mouth and tongue) - Vaginal yeast infection - Skin rashes - Skin itching - Vulvar pain and itching - Rectal itching - Fatigue - Irritability - Fibrofog - Food cravings (especially carbohydrates) - Malnutition (poor nutrient absorption) - Food allergies - Depression - Bad breath. As you can see there is much overlap of Candidiasis symptoms with fibromyalgia symptoms. These two conditions “feed” into each other where the fibromyalgia makes one have more problems with the Candidiasis and the Candidiasis causes symptoms that can aggravate the fibromyalgia. If I suspect Candidiasis, I will treat it separately from the fibromyalgia because this often leads to much improvement of fibromyalgia symptoms as well as correcting the Candida problem. 3. - Testing for Candida A simple home test for Candidiasis can be performed. Dr. Kelly Hannigan described a test you can take (Health Points 8 (2) 2003). Before you go to sleep at night set a clear glass of water next to your bed. When you wake up in the morning (before you clear your throat, swallow or speak), deposit your saliva into the glass of water. If within 30 minutes your saliva sinks to the bottom or there are strands of saliva running down into the water or the water turns cloudy, you probably have an abundance of yeast in your body. Lab testing can be done for a definitive diagnosis of Candidiasis. Saliva, stool and blood samples can all be tested to look for specific immunoglobulin antibodies against Candida. These tests are not routinely covered by insurance companies so the patient has to pay for these tests, which are usually several hundred dollars. Since intestinal Candidiasis is so common and easily identified with careful history of symptoms and since treatments are low-risk and well-tolerated, I will usually treat Candidiasis based on the clinical exam (history and physical) and not always order a specific yeast test. 4. - Candidiasis treatment The strategies for treating Candidiasis are focused on rebalancing the intestinal bacteria and yeast. Candida that has overgrown needs to be killed and suppressed. The “good” yeast and bacterial needs to be replenished and the gastrointestinal tract needs to be rebalanced. Here are some strategies used to rebalance the intestinal tract. Antiyeast products - Prescribed medicines Prescribed medicines to treat Candida include Nystatin (mycostatin) and Fluconazole (Diflucan). Nystatin is available in tablet and liquid form. The liquid form is used to treat oral thrush (“swish and swallow”). The tablet forms are used for intestinal Candidiasis and they are usually well tolerated, although some people have some nausea or diarrhea with them. Patients may need to be on this medicine for several months and some of them need to be on maintenance dose for long-term Candida management. Nystatin kills off Candida, but does not harm the Lactobacillus or bacteria. Fluconazole is another antifungal medicine that is given to treat Candidiasis. Sometimes one tablet or two tablets only are used to treat a vaginal yeast infection. However, a vaginal yeast infection or recurring vaginal yeast infections in women are a sign of more widespread Candidiasis; the vaginal yeast infection is actually the “tip of the iceberg”. In treating intestinal or more widespread Candidiasis, Diflucan may need to be used for weeks instead of days. Antiyeast products - Natural treatments Natural antiyeast treatments include herbal products such as enteric coated oregano extract and olive leaf extract (Oleuropein). Olive leaf extract has the ability to attack Candida and other potential harmful microorganisms while sparing the helpful ones. To treat Candida, two capsules every eight hours on an empty stomach are recommended. Olive leaf extract can be used in conjunction with the prescribed antibiotic or can be used as a first line anti-Candida treatment. 5. - Herxheimer's reaction Herxheimer’s reaction can occur when the Candida die off (this reaction typically involves flu-like symptoms and results when infective agents are killed/toxins are released faster than the kidneys and liver can remove them via the natural detoxification process). A sudden die-off of Candida can release a lot of toxins and the result may be aggravation of symptoms. Whereas this is not necessarily a bad thing, this type of reaction can cause significant discomfort, so we usually back off on the medicine to a lower dose to avoid a rapid die-off and to allow a slower and steadier die-off of Candida. To minimize Herxheimer’s reaction when taking Nystatin I have patients start with one Nystatin tablet on the first day and then increase by one tablet a day until the desired dose of six tablets a day is being taken. A slow die-off of the Candida is preferred as it allows the gastrointestinal tract to better rebalance and not create sudden changes that a rapid die-off can cause. Plus a slower die-off allows the friendly yeast and bacteria to gradually fill the spaces and help rebuild the intestines. 6. - Friendly replenishers (probiotics & prebiotics) Lactobacillus acidophilus and the good bacteria are called probiotics. These “friendly” yeast and bacteria help with digestion and vitamin production and when Candida has died off, these friendly probiotics are necessary to help rebuild the gastrointestinal flora by filling the spaces where Candida used to be and restoring proper balance. An acidophilus supplement is recommended to help replenish the flora. Fructooligosaccharides (FOS) are the food source for healthy bacteria. Any good nutrient (FOS) for the probiotics (acidophilus and other friendly bacteria) is called prebiotic. I like to use a…prebiotic and probiotic blend that helps counteract Candida buildup and maintain healthy intestinal flora. Acidophilus supplements have done an excellent job of treating irritable bowel syndrome, which reinforces the theory that a lot of irritable bowel flare-up can be related to Candidiasis. I usually have patient continue the acidophilus on an ongoing basis, especially when fibromyalgia increases their risk of Candidiasis.
Infection as one possible cause of fibromyalgia - Part II
Infection as one possible cause of fibromyalgia
7. - Dietary strategies The Candida thrive on high sugar concentrations, so a basic diet strategy is cutting back the number of carbs. Fermented foods such as soy sauce, vinegar, pickles, cheese and yogurt have high sugar concentrations that feed yeast so these should be avoided. The fibromyalgia diet that I described in Chapter 17 is also a good antiyeast diet (cfr. “Why weight gain is a problem with fibro and what to do about it” at : http://www.prohealth.com/library/showarticle.cfm?id=7468&t=CFIDS_FM -). In addition to watching the carbohydrates, you should make sure to get enough fiber in your diet because that will help eliminate toxins and unwanted yeast in the bowel. Many people can learn to control Candida yeast overgrowth simply by modifying the diet. Often a combination of yeast antibiotic and friendly replenishers is also necessary along with dietary changes. 8. - Avoid aggravating factors If possible, avoid drugs, chemicals and foods that can trigger the Candida and its symptoms. Since alcohol can aggravate Candida, it should be avoided or used in moderation. Obviously it is not practical to stop thyroid medicine, hormone medicines or other necessary prescribed medicines. Likewise, if you develop a bacterial infection, you may require an antibiotic. If you must take an antibiotic for a bacterial infection, you might want to also take Nystatin or a natural yeast antibiotic to counteract the potential for Candida overgrowth while on the antibiotic. Any prescription medication that you have identified as a cause of Candidiasis should be reviewed with your doctor to see if it can be reduced or changed. If you have Candidiasis, you can successfully transform the Candida back to Dr. Jekyll where he can live peacefully in the normal flora neighborhood... Cfr. : - http://www.prohealth.com/library/showArticle.cfm?libid=12385 - http://www.prohealth.com/library/showarticle.cfm?id=7553&t=CFIDS_FM
Cardiac insufficiency hypothesis M.E. Society of America, (last updated) February 22, 2009 There is new research from a New Jersey team, authored by Doctors Arnold Peckerman, Benjamin Natelson et al., which found left-ventricular dysfunction following exertion and orthostatic stress in patients with myalgic encephalomyelitis/chronic fatigue syndrome. The WedMD article and the press release are available at the link below. In an NIH-funded study on impedance cardiography also linked below, Peckerman and Natelson found that low cardiac output correlated with symptom severity in ME/CFS. Dr. A. Martin Lerner holds U.S. patents for the diagnosis of ME/CFS in the chronic mononucleosis subset of this disease using 24-hour Holter monitoring. He argues that a prominent subset of the disease is a prolonged, chronic mononucleosis following infection with Epstein Barr virus (EBV), Human Cytomegalovirus (HCMV) or both and/or possibly Human Herpes Virus 6 (HHV-6). Viral infection persists in the heart, causing left-ventricular dysfunction, producing exercise intolerance. Exercise, in turn, worsens the cardiac dysfunction. He has also postulated that the disease is an early dilated cardiomyopathy that in later stages might result in progressive, end-stage dilated cardiomyopathy, a type of heart failure. Dilated cardiomyopathy is sometimes viewed as "idiopathic" or "Idiopathic Dilated Cardiomyopathy" (IDC). In an editorial response titled "Microbial Persistence and Idiopathic Dilated Cardiomyopathy" Dr. Lerner has postulated that these viruses may be the etiological link. More recently, physicist, physician, long-time ME/CFS researcher and clinician and heart-transplant recipient Paul Cheney, M.D., Ph.D., has offered an alternative theory that a subset of ME/CFS patients suffer from a diastolic cardiomyopathy, a problem with ventricular filling resulting from mitochondrial dysfunction and low ATP energy in the heart. To view a streaming video of a three-hour talk by Dr. Cheney on diastolic cardiomyopathy and ME/CFS, click : http://www.cfids-cab.org/MESA/CFS_Dist.htm -. This video can be accessed with a broadband connection only. The video cannot be properly viewed using a dial-up modem. Because there may be many people trying to access the video at once, our server may become temporarily overloaded. Please try back again if you encounter this problem or if the video does not play for the full three hours. Note that some of the most informative parts of this three-hour talk occur in the second half when Dr. Cheney discusses and shows charts on cardiac output in litres per minute, comparing ME/CFS patients with controls. To purchase a videocassette of this seminar by Dr. Cheney from the Dallas-Fort Worth CFS group, click : http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0509B&L=CO-CURE&P=R911 -. A detailed discussion of Dr. Cheney's views is available below in an interview by Carol Sieverling, and is recommended reading along with the Peckerman/Natelson article on impedance cardiography for those who want to study the insightful issues addressed in the video. To purchase a DVD set of another talk by Dr. Cheney illustrating more recent echocardiographic and other objective data on ME/CFS and heart failure, click : http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0610E&L=CO-CURE&P=R346 -. Some of Dr. Lerner's significant articles, as well as his patent issued in 2002, are linked below in Portable Document File (PDF) format. .../... Cfr. : http://www.cfids-cab.org/MESA/Lerner.html
Central nervous system manifestations of Mycoplasma pneumoniae infections Tsiodras S, Kelesidis I, Kelesidis T, Stamboulis E, Giamarellou H, 4th Academic Department of Internal Medicine and Infectious Diseases, Attikon University Hospital, University of Athens Medical School, 1 Rimini Street, Xaidari, 12462 Athens, Greece : firstname.lastname@example.org - J Infect. 2005 Dec;51(5):343-54. Epub 2005 Sep 19 - PMID: 16181677 Mycoplasma pneumoniae infection is associated with several manifestations from the central nervous system (CNS) such as encephalitis, aseptic meningitis, acute transverse myelitis, stroke and polyradiculopathy. In the current paper epidemiologic, clinical, laboratory and treatment data on these manifestations are reviewed. The M. pneumoniae induced immune dysregulation and its contributing role in the pathogenesis of neurological insult is discussed. The recent introduction in clinical practice of newer molecular diagnostic techniques has helped in establishing a firmer association between M. pneumoniae infection and CNS disease especially encephalitis. Clinicians should be aware of the potential association between M. pneumoniae infection and several CNS manifestations. The role of various anti-microbial or immunomodulating therapies in treating such manifestations should be further explored. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/16181677?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleIt emSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedreviews&logdbfrom=pubmed
Central sensitivity syndromes - A unified concept for Fibromyalgia and other similar maladies Muhammad Yunus, Section of Rheumatology, University of Illinois College of Medicine Peoria, Illinois, USA - Journal of Indian Rheumatism Association. 2000 Mar; 8(1): 27-33 Fibromyalgia syndrome(FMS) and similar other conditions, e.g., myofascial pain syndrome, irritable bowel syndrome, chronic fatigue syndrome, headaches and restless legs syndrome share several characteristics, including pain, poor sleep, fatigue, hyperalgesia and an absence of structural tissue pathology. These syndromes are bound by a common pathophysiological mechanism, i.e., neurohormonal dysfunctions, which are generally different from those in psychiatric diseases. Central nervous system (CNS) sensitivity, either intrinsic or due to CNS neuroplasticity secondary to peripheral stimuli, results in amplified, widespread and persistent pain. This central sensitivity seems to be the most important aberration among the neuroendocrine dysfunctions. Thus, FMS and other overlapping syndromes have been called "central sensitivity syndromes" (CSS) as a group. Current research suggests that central sensitivity is present among the CSS members and is likely to be the common biopathophysiological glue that binds them. Cfr. : http://medind.nic.in/imvw/imvw4222.html
Chronic fatigue illnesses - Chronic fatigue syndrome, fibromyalgia syndrome and other fatigue conditions Prof. Garth L. Nicolson Chronic fatigue is reported by 20% of all patients seeking medical care and is considered as a nonspecific sign that is associated with many well known medical conditions. Chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME) and fibromyalgia syndrome (FMS) patients suffer from complex overlapping signs and symptoms (cfr. : 'Signs/Symptoms' Questions, above) CFS is primarily characterized by persisting or relapsing fatigue without previous history of comparable symptoms that does not resolve with rest. In these patients other clinical conditions are absent that can explain the signs and symptoms such as malignancies or autoimmune diseases. In contrast, FMS patients have overall muscle pain, tenderness and weakness as primary complaints, but they have most if not all of the commonly found signs and symptoms for CFS. We previously proposed that CFS/ME patients might be suffering from chronic infections that can cause, in part, their complex signs and symptoms. For example, systemic mycoplasmal infections can cause chronic fatigue, muscle pain and a variety of additional signs and symptoms, some of which are related to dysfunctional immune responses and in extreme cases autoimmune-like disorders. Some mycoplasmas can invade virtually every human tissue and can compromise the immune system, permitting opportunistic infections by other bacteria, viruses, fungi and yeast. When mycoplasmas exit certain cells, such as synovial cells, nerve cells, among others that can be infected, they can stimulate autoimmune response. Our recently published studies demonstrated a possible link between mycoplasmal infections and CFS and FMS, since we found high frequencies of mycoplasmal infections in these patients. Previously we examined patients with chronic illnesses for the presence of mycoplasmal infections. We found that about one half of patients with Gulf War Illness and two third of patients with CFS/ME and FMS were positive for mycoplasmal infections in their blood. The Gulf War Veterans suffer from signs and symptoms similar to patients diagnosed with CFS and FMS. They can be treated using antibiotics effective against mycoplasmal infections and once they recover, their blood is no longer positive for the presence of mycoplasmal infections. Our recent results indicate that Rheumatoid Arthritis is also associated with mycoplasmal infections (cfr. 'Autoimmune Diseases'). Recent reports and publications indicate that in addition to mycoplasmal infections, CFS/ME and FMS patients have other chronic infections caused by other intracellular bacteria and viruses. For example, patients with Lyme Disease, caused by intracellular Borrelia infections, have been diagnosed with CFS/ME. Also, CFS/ME and FMS patients can have intracellular Chlamydia species infections. These patients can also have infections by other bacteria that enter their bodies through 'leaky gut' problems. Chronically ill patients often have inflammatory bowel syndrome and other gut problems and this can allow pathogenic bacteria to enter their systems. Patients with CFS/ME and FMS can also have viral infections that complicate their conditions and cause morbidity. Such infections can occur with or without the bacterial infections described above. Viruses that have been associated with CFS/ME and FMS are Human Herpes Virus-6 (HHV-6) and Cytomeglovirus (CMV). These viruses have been found at high incidence in chronically ill patients and especially those with CFS/ME. Patients with CFS/ME or FMS can have predominantly intracellular bacterial infections, predominantly viral infections or a combination of intracellular bacterial and viral infections. This may be one reason why the underlying causes of these chronic illnesses are so difficult to determine and effectively treat. The other reason could be the persistent nature of the infections and their ability to hide inside cells where they are essentially refractory to immune system responses, their slow growing natures and their relative insensitivity to therapeutic drugs (see references below). A new direction at the Institute is studying the role of decreased cellular energy in causing fatigue. Cellular energy is mainly produced by the mitochondria, subcellular organelles that contain the machinery that converts fats and sugars to energy in the form of the high-energy molecules, such as ATP. Mitochondrial function requires an intact inner membrane where the electron transport chain or energy machinery is located. When the inner mitochondrial membrane is damaged, the efficiency of the electron transport chain is reduced along with the ability of cells to produce the energy that they need for vital functions—thus fatigue becomes a problem. Various environmental insults and even aging produce excess oxidation molecules that can damage the mitochondrial membrane, including chronic infections of the type mentioned above. At the Institute for Molecular Medicine clinical studies have shown the benefits of dietary membrane lipids (Lipid Replacement Therapy) in replacing damaged mitochondrial membrane lipids, increasing the efficiency of the electron transport chain, increasing energy and reducing fatigue. A number of non-pharmaceutical approaches to decreasing fatigue are being investigated at the Institute. Cfr. : http://www.immed.org/illness/fatigue_illness_research.html
Chronic fatigue illnesses associated with service in Operation Desert Storm - Were biological wWeapons used against our forces in the Gulf War ? Nicolson GL, Nicolson NL - Townsend Lett Doctors 1996; 156:42-48 Cfr. : http://www.all-natural.com/part-1.html
Chronic fatigue syndrome - A working case definition Holmes GP, Kaplan JE, Gantz NM, Komaroff AL, Schonberger LB, Straus SE, Jones JF, Dubois RE, Cunningham-Rundles C, Pahwa S et al., Division of Viral Diseases, Centers for Disease Control, Atlanta, Georgia - Ann Intern Med. 1988 Mar;108(3):387-9 - PMID: 2829679 The chronic Epstein-Barr virus syndrome is a poorly defined symptom complex characterized primarily by chronic or recurrent debilitating fatigue and various combinations of other symptoms, including sore throat, lymph node pain and tenderness, headache, myalgia and arthralgias. Although the syndrome has received recent attention and has been diagnosed in many patients, the chronic Epstein-Barr virus syndrome has not been defined consistently. Despite the name of the syndrome, both the diagnostic value of Epstein-Barr virus serologic tests and the proposed causal relationship between Epstein-Barr virus infection and patients who have been diagnosed with the chronic Epstein-Barr virus syndrome remain doubtful. We propose a new name for the chronic Epstein-Barr virus syndrome--the chronic fatigue syndrome--that more accurately describes this symptom complex as a syndrome of unknown cause characterized primarily by chronic fatigue. We also present a working definition for the chronic fatigue syndrome designed to improve the comparability and reproducibility of clinical research and epidemiologic studies and to provide a rational basis for evaluating patients who have chronic fatigue of undetermined cause. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2829679
Chronic fatigue syndrome patients subsequently diagnosed with lyme disease borrelia burgdorferi - Evidence for mycoplasma species co-infections Garth L. Nicolson a; Nancy L. Nicolson a; Joerg Haier b - a Institute for Molecular Medicine, Huntington Beach, CA - b Department of Surgery, University Hospital, Munster, Germany - Journal Of Chronic Fatigue Syndrome, Volume 14, Issue 4 June 2008 , pages 5 – 17 Objective - We examined the blood of 48 North American chronic fatigue syndrome (CFS) patients subsequently diagnosed with Lyme disease (Borrelia burgdorferi infection) and compared these with 50 North American CFS patients without evidence of Borrelia burgdorferi infections for presence of Mycoplasma species coinfections using forensic polymerase chain reaction. Results - We found that 68.75% of CFS/Lyme patients show evidence of mycoplasma coinfections (odds ratio [OR] = 41.8; confidence limits [CL] = 11.3-155; and p < .001) compared with controls, whereas 50% of CFS patients without a diagnosis of Lyme disease show Mycoplasma coinfections (OR = 19.0; CL = 5.3-69; and p < .001) compared with controls. Because CFS patients without a diagnosis of Lyme disease have a high prevalence of one of four Mycoplasma species and a majority show evidence of multiple infections, we examined CFS/Lyme patients' blood for various Mycoplasma species. We found that CFS patients with Lyme disease mostly had single species Mycoplasma infections (OR = 31.7; CL = 8.6-116; and p < .001) with a preponderance of Mycoplasma fermentans infections (50% of patients; OR = 59.0; CL = 7.6-460; and p < .001), whereas the most commonly found Mycoplasma species in CFS patients without Lyme disease was Mycoplasma pneumoniae(34% of patients; OR = 14.94; CL = 3.3-69; and p < .001). Conclusions - The results indicate that a subset of CFS patients show evidence of infection with Borrelia burgdorferi, and a large fraction of these patients were also infected with Mycoplasma fermentans and to a lesser degree with other Mycoplasma species. Cfr. : http://www.informaworld.com/smpp/content~content=a903736316~db=all~jumptype=rss
Chronic Infections in Fibromyalgia Syndrome - Sources of morbidity and illness progression Prof. Garth Nicolson, The Institute for Molecular Medicine 16371 Gothard St. H, Huntington Beach, CA 92647 - Fibromyalgia Survivor 2000 Fibromyalgia Syndrome (FMS) is characterized by muscle pain and tenderness at specific sites, but there are also a number of other less specific chronic signs and symptoms. Among these are disabling fatigue, impairments in short-term memory, headaches, gastrointestinal and vision problems and sometimes intermittent low-grade fevers, joint pain and other signs and symptoms. In many patients the diagnosis of FMS is accompanied by other secondary diagnoses, such as Chronic Fatigue Syndrome (CFS), Rheumatoid Arthritis (RA), Inflammatory Bowel Diseases and other syndromes, which can also present with overlapping signs and symptoms. This suggests that although the exact causes of these illnesses are not known and may be different in each patient, there are similarities in these conditions that may be important in patient morbidity (sickness) or in illness progression (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176). Instead of concentrating on possible causes of FMS, we have been interested in the progression of chronic illnesses like FMS and in the potential role that chronic infections may play in FMS. The complex signs and symptoms that evolve in many FMS, CFS and RA patients may be due, in part, to systemic chronic infections (bacteria, viruses, fungi). Such infections can follow acute or chronic chemical, environmental or other insults (trauma, chemical exposures, acute viral illness etc.) that have the potential to suppress the immune system and cause metabolic imbalances (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176). Illness progression in FMS patients Illnesses like FMS evolve over time, probably in a multistep process that may require multiple toxic exposures, including infections that could be causative for the illness in a few patients, cofactors for the illness (not causative but important in patient morbidity) in others or more likely in most patients, opportunistic infections that cause morbidity. Such infections need not be present at the onset of illness to be important. Because of their dysfunctional metabolic and immune systems, many FMS patients may be particularly susceptible to chronic infections that worsen their illness. Of course, illness progression in FMS patients could also be caused by other factors, psychological stress, physical trauma, other illnesses and many other factors (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21). Chronic infections are usually held in check by our immune systems, but they can take hold if they can avoid immune surveillance and penetrate and hide in various tissues and organs, including muscle cells and nerve cells. When such “stealth” viral and bacterial infections occur, they can cause many of the complex signs and symptoms seen in FMS, CFS, RA and GWI, including enhanced immune dysfunction and metabolic imbalances (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21 -&- “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21). Changes in environmental responses as well as increased titers to various endogenous viruses that are commonly found to be expressed in these patients have been seen in FMS, CFS and GWI patients. If infectious agents are involved, few can produce the complex chronic signs and symptoms found in these patients. One that can is represented by a small, primitive class of bacteria called mycoplasmas (cfr. “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32).
Infection as one possible cause of fibromyalgia - Part IV
Infection as one possible cause of fibromyalgia
Mycoplasmas and other bacteria (Chlamydia, Coxiella, Brucella, Borelia etc.), although not as well known as other agents in causing various diseases, are now considered important emerging pathogens in various chronic illnesses. As chronic illnesses such as FMS, CFS and RA progress, there are a number of accompanying clinical problems, and in some patients show increases in autoimmune signs and symptoms. This suggests that they do not have classical autoimmune diseases but they may have incomplete diagnoses for these diseases. Although it is certainly not proven, this pattern is consistent with certain chronic infections, such as mycoplasmal infections, that penetrate into nerve cells, synovial cells in joints, muscle cells and other cell types. Microorganisms like mycoplasmas can incorporate into their own surface structures pieces of host cell membranes that contain important host membrane antigens that can trigger autoimmune responses (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176) and they can also mimic host cell antigen structures (cfr. “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32). Thus patients with such infections may respond immunologically to microorganism antigens as well as their own membrane antigens, producing unusual autoimmune signs and symptoms. This could explain why such patients do not have all of the clinical characteristics expected in these usually rare autoimmune diseases. Microorganisms can cause morbidity in FMS patients Microorganisms like Mycoplasmas are not considered important human pathogens when they are found at superficial sites, such as the oral cavity or gut, but some species, such as M. fermentans, M. penetrans, M. pneumoniae, M. genitalium, M. Pirum and M. hominis, among others, have the capacity to penetrate into the blood circulation and colonize various tissues and these cell-penetrating microorganisms have been closely associated with various human diseases (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176 -&- “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32). Do such infectious agents actually cause FMS, CFS or RA ? Probably not on their own, but some bacteria and viruses appear to be an important element in causing chronic illness progression, patient morbidity or exacerbating the major signs and symptoms seen in patients with chronic illnesses. We have found that ~70% of FMS, ~60% of CFS and ~50% of RA and Gulf War Illness patients have mycoplasmal blood infections that can explain many of the chronic signs and symptoms found in these patients. In the majority of FMS and CFS patients we have found multiple pathogenic mycoplasmas in their white blood cells but these infections are only found in 0-9% of controls (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176 -&- “Multiple mycoplasmal infections detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients” - Nasralla, M., Haier, J. and Nicolson, G.L. - Eur. J. Clin. Microbiol. Infect. Dis. 1999; 18:859-865). Interestingly, the majority of CFS and FMS patients had multiple mycoplasmal infections but none were found in controls (cfr. “Multiple mycoplasmal infections detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients” - Nasralla, M., Haier, J. and Nicolson, G.L. - Eur. J. Clin. Microbiol. Infect. Dis. 1999; 18:859-865); however, single infections are found in some nonsymptomatic subjects (0-9%). The tests that we use to identify mycoplasmal infections, Forensic Polymerase Chain Reaction, are very sensitive and highly specific. These tests are a dramatic improvement over the relatively insensitive serum antibody and other tests that have been used to assay for systemic infections. New treatments for FMS and other chronic illnesses When microorganism infections are identified in the blood of patients, they should be treated as medical not psychiatric patients, just like any other patients with blood infections. This does not mean that psychological or psychiatric problems are not important in chronic illness patients. But if such infections are important in these disorders, then appropriate treatments with antibiotics or other medications that suppress chronic infections should result in improvement and even recovery. This is exactly what has been found (cfr. “Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis” - Nicolson, G.L., Nasralla, M, Hier, J., Erwin, R., Nicolson, N.L. and Ngwenya, R. - Med. Sentinel 1999; 4:172-176 -&- “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21). The majority of patients with confirmed pathogenic mycoplasmal infections eventually recover from 50-100% of their premorbid health on therapies that are directed specifically against their chronic infections not against possible psychological problems (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21). The recommended treatment for confirmed mycoplasmal blood infections is long-term antibiotic therapy, usually multiple 6-week cycles of doxycycline (200-300 mg/day), ciprofloxacin or Cipro (1,500 mg/day), azithromycin or Zithromax (500 mg/day) or clarithromycin or Biaxin (750-1,000 mg/day). Multiple cycles are required, because few patients recover after only a few cycles, possibly because of the intracellular locations of the infections, the slow-growing nature of these microorganisms and their inherent insensitivity to antibiotics. We now recommend that patients who have been diagnosed with blood infections receive continuous oral antibiotics for at least 6 months before using the 6-week cycles of treatment. Although patients starting such therapy usually have Herxheimer reactions and feel initially worse due to die-off or release of toxic materials from damaged microorganisms, they eventually stabilize within days to a few weeks and then slowly begin to recover. Unfortunately, the treatment requires long-term therapy, and recovery is usually very slow. Patients that have been sick for many years are unlikely to recover within a year of therapy (cfr. “Considerations when undergoing treatment for chronic infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses - Part 1 - Antibiotics Recommended when indicated for treatment of Gulf War Illness/CFIDS/FMS (Part 2)” - Nicolson, G.L. - Intern. J. Med. 1998; 1:115-117, 123-128). The clinical responses that are seen are not due to placebo effects, because administration of some antibiotics, such as penicillins, resulted in patients becoming more not less symptomatic. In addition, they are not due to immunosuppressive effects of some of the antibiotics, because other antibiotics that do not cause immune suppression are also effective but only if they suppress the chronic infections. If they don’t have these infections, then antibiotics should not work (cfr. “The role of microorganism infections in chronic illnesses - Support for antibiotic regimens” - Nicolson, G.L. - CFIDS Chronicle 1999; 12(3):19-21). Some patients recover to a certain point and then fail to continue to respond to the recommended antibiotics, suggesting that other problems, such as viral infections, environmental exposures and other toxic events and even stress, also play an important role in these illnesses, and may even play a predominant role in some patients. What results have been obtained with antibiotics for chronic illnesses like FMS ? Although a majority of patients diagnosed with chronic blood infections appear to benefit from antibiotic therapy, many patients respond and have some alleviation of most signs and symptoms but do not fully recover. A 3-year follow-up of antibiotic therapy in Northern California indicates that a majority (~80%) of FMS/CFS) patients from Shasta County that were confirmed with mycoplasmal infections recovered from 50-100% of their pre-illness health within this time period and even some patients who did not test positive showed benefit from antibiotics, suggesting other bacterial infections. Similar to other therapies for chronic illnesses, not every patient benefited from antibiotic therapy and the time required for recovery was quite variable in different patients (cfr. “Mycoplasmas - Sophisticated, reemerging and burdened by their notoriety” - Baseman, J.B. and Tully, J.G. - Emerg. Infect. Dis. 1997; 3:21-32). In some patients oxygen therapy has proved useful. Oxygen suppresses the anaerobic chronic infections like mycoplasmas. In addition to antibiotics, patients must take vitamins, minerals, immune enhancement and other supplements to help boost immunity. For example, these patients are often depleted in vitamins B complex, C and E, among others and certain minerals (cfr. “Considerations when undergoing treatment for chronic infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses - Part 1 - Antibiotics Recommended when indicated for treatment of Gulf War Illness/CFIDS/FMS (Part 2)” - Nicolson, G.L. - Intern. J. Med. 1998; 1:115-117, 123-128). Amino acids, fish oils, probiotic bacteria (Lactobacillus acidophillus) and a number of natural remedies have proven useful during therapy (cfr. “Considerations when undergoing treatment for chronic infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses - Part 1 - Antibiotics Recommended when indicated for treatment of Gulf War Illness/CFIDS/FMS (Part 2)” - Nicolson, G.L. - Intern. J. Med. 1998; 1:115-117, 123-128). Complex causes of chronic illnesses Do chronic infections explain illnesses like FMS ? It is unlikely that there is only one or even a few explanations for complex chronic illnesses like FMS or CFS. Rather, these illnesses are probably due to a combination of multiple toxic exposures, chemical and biological, in combination with genetic susceptibility (immune systems and/or detoxification systems, cellular metabolism) that determines whether a person becomes chronically ill. These considerations probably also play an important role in determining who will recover to various extents on different types of therapy. In addition, recovery can be complicated by patients’ over-dependence on drugs, such as certain antidepressants or other drugs that can suppress portions of the immune system. Interestingly, those patients that slowly recover after several cycles of antibiotics are generally less environmentally sensitive, suggesting that their immune systems may be returning to pre-illness states. If such patients had illnesses that were solely caused by psychological or psychiatric problems or by environmental or chemical exposures, they should not respond to the recommended antibiotics and recover their health. In addition, if such treatments were just reducing the autoimmune responses, then patients should not maintain recovery after the treatments are discontinued. For further information Contact : Prof. Garth L. Nicolson, The Institute for Molecular Medicine 16371 Gothard St. Bld H, Huntington Beach, CA 92647 – Tel. : 714-596-6636 – Fax : 714-596-3791 – E-mail : email@example.com – Website : www.immed.org -. Cfr. : www.immed.org/Fatigue%20Illness/.../FMSurvivorNewslett00.rtf
Chronic Lyme Disease" as the incorrect diagnosis in patients with Fibromyalgia VM Hsu, SJ Patella, LH Sigal, Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019 - Arthritis Rheum. 1993 Nov;36(11):1493-500 - PMID: 8240427 Objective - To evaluate a large number of patients referred with persistent symptoms thought to represent chronic Lyme disease. Methods - We retrospectively reviewed the charts of nearly 800 patients referred with persisting nonspecific musculoskeletal and/or neurologic symptoms thought to represent chronic Lyme disease. Results - Seventy-seven patients were found to have fibromyalgia, not ongoing Lyme disease, as the explanation of their chronic symptoms. Many had received multiple courses of antibiotic therapy for symptoms of fibromyalgia mistakenly attributed to chronic Lyme disease. No patient reported permanent and/or total resolution of fibromyalgia symptoms following antibiotic therapy. Appropriate therapy for fibromyalgia in those who remained compliant, however, was often effective in improving some if not all of the chronic symptoms. Conclusion - Fibromyalgia is a treatable and potentially curable disorder and should be considered in the evaluation of patients with "refractory Lyme disease". Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8240427 Also read the comment on this article : Do infections trigger fibromyalgia ? Goldenberg DL - Arthritis Rheum. 1993 Nov;36(11):1489-92 - PMID: 8240426 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8240426?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
Clinical experiences with post-traumatic fibromyalgia syndrome Romano TJ, Department of Medicine, West Virginia University School of Medicine - W V Med J 1990;86(5):198-202 Fibromyalgia syndrome (FS) is a musculoskeletal problem that has become more and more widely recognized. There are three types : primary (PFS idiopathic), secondary (associated with another disorder) and post-traumatic (PTFS). The latter condition, PTFS, is especially intriguing since quite often litigation is involved and doubt is cast as to whether the patient is actually suffering. Accusations of malingering have been made. A retrospective chart review of 14 PTFS patients was made in an effort to ascertain the likelihood of malingering. Over the past two years, 14 patients (three male, 11 female) were treated for PTFS. The mean age was 37 years for both men and women. All had classic PTFS with a chronic musculoskeletal problem that started immediately after a traumatic event, classic myofascial tender points, poor sleep and normal standard laboratory tests. Twenty-three per cent went to trial; 77 per cent settled out of court. All were given a monetary award. The vast majority (77 per cent) returned to a rheumatologist for continued treatment, suggesting that patients who meet strict FS criteria are not malingering and are indeed in need of medical help. Cfr. : http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19921926
Cloning and characterization of a RNAse L inhibitor - A new component of the interferon-regulated 2-5A pathway Bisbal C, Martinand C, Silhol M, Lebleu B, Salehzada T, Institut de Génétique Moléculaire-UMR 9942, CNRS-Université de Montpellier I et II, France - J Biol Chem. 1995 Jun 2;270(22):13308-17 - PMID: 7539425 The 2-5A/RNase L system is considered as a central pathway of interferon (IFN) action and could possibly play a more general physiological role as for instance in the regulation of RNA stability in mammalian cells. We describe here the expression cloning and initial characterization of RLI (for RNase L inhibitor), a new type of endoribonuclease inhibitor. RLI cDNA codes for a 68-kDa polypeptide whose expression is not regulated by IFN. Its expression in reticulocyte extracts antagonizes the 2-5A binding ability and the nuclease activity of endogenous RNase L or the cloned 2DR polypeptide. The inhibition requires the association of RLI with the nuclease and is dependent on the ratio between the two proteins. Likewise RLI is coimmunoprecipitated with the RNase L complex by a nuclease-specific antibody. RLI does not lead to 2-5A degradation or to irreversible modification of RNase L. The overexpression of RLI in stably transfected HeLa cells inhibits the antiviral activity of IFN on encephalomyocarditis virus but not on vesicular stomatitis virus. RLI therefore appears as the first described and potentially important mediator of the 2-5A/RNase L pathway. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/7539425
Co-Infections in Fibromyalgia Syndrome, Chronic Fatigue Syndrome and Other Chronic Illnesses Prof. Garth Nicolson - Fibromyalgia Frontiers 2002; 10(3):5-9, 27-28
Considerations when Undergoing Treatment for chronic and autoimmune diseases Prof. Garth L. Nicolson, The Institute for Molecular Medicine, 16371 Gothard St. H, Huntington Beach, California 92647 USA – Tel. : (714) 596-6636 – Fax : (714) 596-3791 – E-mail : firstname.lastname@example.org - Website: www.immed.org - Reprinted from Intern. J. Medicine 1998; 1:123-128 - Plus Supplemental Suggestions : Prof. Nicolson 11/15/05 Several people have asked me for instructions on a cost-effective way to remove heavy metals like uranium without weekly clinic visits. Also, I have received questions on our Lipid Replacement Therapy protocol to restore mitochondrial function and restore cellular energy. I have attached our updated treatment information on these topics as a MS Word 9 rich text format doc. The Institute for Molecular Medicine is a nonprofit research organization and does not make any money on any of the products listed in the information. This is provided only as a public service. Antibiotic therapy for chronic infections Please consult “Antibiotics/antivirals recommended when indicated for treatment of Gulf War illness/CFS/FMS/arthritis” - Prof. Garth L. Nicolson, The Institute for Molecular Medicine at :http://gulfwarcouncil.com/Nicolson-Consideration%20When%20Undergoing%20Treatment%20for%20Chronic%20and%20Autoimmune%20Diseases.htm - for general information. We are finding that subsets of GWI (~45%) and FMS/CFS (~60%) patients have chronic mycoplasmal infections and probably other infections as well. We usually recommend several 6-week cycles of doxycycline, ciprofloxacin, azithromycin, clarithromycin or minocycline etc. with 2-week cycles of Augmentin in between or concurrently, if needed. To overcome Herxheimer reactions or die-off that cause chills, low grade fever, night sweats, muscle aches, joint pain, short term memory loss and fatigue or adverse responses i.v antibiotics have been used and a whole lemon/olive drink is useful (1 blended whole lemon, 1 cup fruit juice, 1 tbs olive oil--strain and drink liquid). This period usually passes within 1-2+ weeks. Some physicians add the antiviralFamvir (500 mgX3/day) for first 2 weeks in each 6-week cycle of antibiotics. The rational is that mycoplasmas have some characteristics of viruses, and antivirals can have a useful effect. Alternatively, viral infections may also be important in these illnesses. Other therapies for chronic infections One therapy that appears to be useful is oxidative therapy. This can be done at home with peroxide baths(2-4X 16 oz. bottles of 3% hydrogen peroxide in 20 inch bath (or Jacuzzi) with 2 cups of Epsom salt. Soak in hot water + salt until pores open (about 5 min), then add peroxide solution. Repeat daily or 3X per week at bedtime; no vitamins 8 hr before bath. Peroxide (3%, one 16 oz. bottle) can also be directly applied to skin after a work-out or hot shower/tub (for better effect apply Swedish Beauty type A tanning accelerator for 5 min before peroxide). Leave peroxide on for 5 min and then wash off. For oral irrigation, mix 1 part 3% peroxide with 2 parts water 3X per day and use like a mouth wash. General nutritional considerations GWI/CFS/FMS patients are often immunosuppressed and could be susceptible to a variety of opportunistic infections, so proper nutrition is important. You should not smoke or drink alcohol or caffeinated products. Drink as much fresh fluids as you can, lots of fruit juices or pure water are best. Try to avoid high sugar and fat foods, such as military (MRE) or other fast foods and acid-forming, allergen-prone and stressing foods or junk foods. Increase your intake of fresh vegetables, fruits and grains and decrease your intake of fats and eliminate simple or refined sugars that can suppress your immune system. To build up your immune system cruciferous vegetables, soluble fiber foods, such as prunes and bran, wheat germ, yogurt, fish and whole grains are useful. In some patients exclusive use of 'organic' foods have been beneficial. Vitamins and minerals GWI/CFS/FMS patients are often depleted in vitamins (especially B, C and E) and certain minerals. Unfortunately, illnesses like GWI result in poor absorption. Therefore, high doses of some vitamins must be used and others, such as vitamin B complex, cannot be easily absorbed by the gut (oral capsules). Sublingual (under the tongue) natural B-complex vitamins in small capsules or liquids (such as Total B, Real Life Research, Norwalk, CA, 310-926-5522) should be used instead of oral capsules that are swallowed. General vitamins plus extra C, E, CoQ-10, beta-carotene, folic acid, bioflavoids and biotin are best. L- cysteine, L-tyrosine, L-carnitine and malic acid are reported by some to be useful. Certain minerals are also often depleted in GWI/CFS/FMS patients, such as zinc, magnesium, chromium and selenium. Some recommend doses as high as 300 mg/day sodium selenite for a few days, followed by lower maintenance doses. Minerals should not be taken at the same time of day that antibiotics are taken because the minerals can affect the absorption of certain antibiotics. Replacement of natural gut flora GWI/CFS/FMS patients are often undergoing treatment with antibiotics and other substances that can destroy the normal gut flora. Antibiotic use that depletes normal gut bacteria and can result in over-growth of less desirable bacteria. To supplement bacteria in the gastrointestinal system yogurt and especially Lactobacillus acidophillus tablets are recommended. One product is a mixture of Lactobacillus acidophillus, Lactobacillus bifidus and FOS (fructoologosaccharides) to promote growth of these “friendly” bacteria in the gut (example, DDS-Plusor Multi-Flora ABF, UAS Labs (800-422-3371); Intestinal Care-DF, Ethical Nutritionals (Vitamin Park, 714-251-1800). L. acidophillus or mixtures above should be taken 3X daily to restore gut flora. Natural immunoenhancers or immunomodulators A number of natural remedies, such as ginseng root, herbal teas, whole lemon/olive extract drink or an extract of olive leaves with antioxidants are available and are potentially useful, especially during or after antibiotic therapy has been completed. Some examples are Eden, Echinacea-C (NF Formulas, 800-547-4891), Super-Immunotone (Phyto Pharmica, 800-553-2370), Immunocal (800-337-2411) olive leaf extract (Immuno-screen, 818-966-1610), NSC-100 (Nutritional Supply, 888-246-7224), Nu-Life Formula (Sophista-Care, 760-837-1908), Tahitian Noni (Morinda, 800-445-8596) or Super Defense Plus (BioDefense Nutritionals, 800-669-9205). These have been used to boost immune systems. Although these products appear to help many CFS/FMS patients, their clinical effectiveness in GWI/CFS/FMS patients has not been evaluated. They appear to be useful during therapy to boost the immune system or after antibiotic therapy in a maintenance program to prevent relapse of illness. Yeast/fungal or bacterial overgrowth Yeast overgrowth can occur, especially in female patients (vaginal infections). Gynecologists recommend Nizoral, Diflucan, Mycelex or anti-yeast creams for women on antibiotics. In some cases, use of metronidazole (Flagyl, Prostat) have been used to prevent fungal or parasite overgrowth or other antifungals (Nystatin, Amphotericin B, Fluconazole, Diflucan) have been administered for fungal infections that can occur while on antibiotics. As described above, L. acidophillus should be taken daily to restore gut flora. Bacterial overgrowth can also occur, for example, in between cycles of antibiotics or after antibiotics have been stopped. This can be controlled with 2 week courses of Augmentin (3 X 500 mg/day) in between cycles or concurrent with other antibiotics. Flying and exercise Flying, especially in unpressurized aircraft, excessive exercise and lack of sleep can make signs/ symptoms worse. Some exercise is essential (don’t over do it ! A common problem !). Adjust your exercise level to help the recovery process without causing a relapse. Dry saunas help rid the system of contaminating chemicals and saunas should be taken at least 3-5X per week--moderate exercise, followed by 15-20 min of dry sauna and tepid shower. The sauna can be repeated, by not more than 2X per day. The idea is to work up a good sweat, eliminating chemicals without placing too much stress on your system. During exercise GWI/CFS/FMS patients should always try to avoid pollutant and allergen exposures. For recovery after exercise and to decrease muscle soreness, some use a Jacuzzi or hot tub, but only after a sufficient cool-down period. Don’t get overheated in the process. Cfr. : - http://gulfwarcouncil.com/Nicolson-Consideration%20When%20Undergoing%20Treatment%20for%20Chronic%20and%20Autoimmune%20Diseases.htm - http://compkarori.com/arthritis/pi16007.htm
Controversies in neurological infectious diseases Greenlee JE, Rose JW, Neurology Service, Veterans Affairs Medical Center and Department of Neurology, University of Utah Health Science Center, Salt Lake City 84148-001, USA - Semin Neurol. 2000;20(3):375-86 - PMID: 11051301 The past several years have seen major advances in our understanding of neurological infectious diseases, their diagnosis, and their treatment. Along with these advances, however, new information about infectious agents and new therapeutic options have also introduced both uncertainty and controversy in the approach and management of patients with diseases of the central nervous system. Here, we discuss six such areas: the long-term efficacy of HAART therapy in treatment of HIV infection; the role of viral infection in chronic fatigue syndrome; Rasmussen's encephalitis as an infectious or autoimmune disease; the spectrum of neurological diseases caused by rickettsial infection; the role of Mycoplasma pneumoniae in human central nervous system disease; and the possible association of Chlamydia pneumoniae and human herpesvirus 6 with multiple sclerosis. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11051301
Cytokines and chronic fatigue syndrome Patarca R, Department of Medicine, University of Miami School of Medicine, Florida 33101, USA : email@example.com - Ann N Y Acad Sci. 2001 Mar;933:185-200 - PMID: 12000020 Chronic fatigue syndrome (CFS) patients show evidence of immune activation, as demonstrated by increased numbers of activated T lymphocytes, including cytotoxic T cells, as well as elevated levels of circulating cytokines. Nevertheless, immune cell function of CFS patients is poor, with low natural killer cell cytotoxicity (NKCC), poor lymphocyte response to mitogens in culture and frequent immunoglobulin deficiencies, most often IgG1 and IgG3. Immune dysfunction in CFS, with predominance of so-called T-helper type 2 and proinflammatory cytokines, can be episodic and associated with either cause or effect of the physiological and psychological function derangement and/or activation of latent viruses or other pathogens. The interplay of these factors can account for the perpetuation of disease with remission/exacerbation cycles. A T-helper type 2 predominance has been seen among Gulf War syndrome patients and this feature may also be present in other related disorders, such as multiple chemical sensitivity. Therapeutic intervention aimed at induction of a more favorable cytokine expression pattern and immune status appears promising. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12000020
Cytomegalovirus-related sequence in an atypical cytopathic virus repeatedly isolated from a patient with Chronic Fatigue Syndrome W. J. Martin, L. C. Zeng, K. Ahmed and M. Roy, Department of Pathology, USC School of Medicine, Los Angeles 90033 - American Journal of Pathology 1994; 145: 440-51 An atypical virus, cytopathic for human and animal fibroblasts, was repeatedly cultured from a patient with chronic fatigue syndrome. Viral particles, suggestive of cytomegalovirus (CMV) were seen by electron microscopy. Infected cells did not, however, stain with antisera specific for CMV, herpes, simplex virus or human herpes-virus-6. Polymerase chain reaction (PCR) assays for these viruses were also negative. Two distinct products of approximately 1.5 kilobase pairs were amplified from virally infected cells using the human T lymphotropic virus-II tax gene reactive primer, SK44, in low stringency PCR. Sequencing of one of the amplified products showed a region of highly significant partial homology with the UL34 gene of CMV. The sequence of the other PCR product did not correspond with CMV or any other virus. DNA was extracted from the material pelleted by ultracentrifugation of filtered culture supernatants. It migrated in agarose gels as a single band of approximately 20 kpb. The banded DNA was digested with EcoRI and cloned. A 2.2 kbp plasmid containing the CMV-related sequence identified within the PCR product was recovered. Sequencing of this plasmid extended the region of partial sequence homology with CMV to include a portion of the UL35 gene of CMV. Initial sequencing of additional plasmids has confirmed the partial relatedness to CMV. The data indicate a novel type of CMV-related "stealth" virus that is able to establish a clinically persistent human infection. Cfr. : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1887390/
Deregulation of the 2.5A synthetase RNase L antiviral pathway by mycoplasmas in subsets of Chronic Fatigue Syndrome Nijs J, De Meirleir K, Coomans D, De Becker P, Nicolson GL - J Chronic Fatigue Syndr 2003; 11(2):37-50 The deregulation of the 2.5A synthetase RNase L antiviral pathway and the prevalence of Mycoplasma spp. in subsets of Chronic Fatigue Syndrome [CFS] have been separately reported in the scientific literature. We hypothesised that a co-morbid pathophysiological mechanism involving infection by Mycoplasma spp. and the deregulation of the 2,5A synthetase / RNase L antiviral pathway may exist in CFS. Therefore, 186 consecutive CFS patients were enrolled. Mycoplasma detection was performed using forensic polymerase chain reaction. For RNase L determination, a radioactive probe was used to label 2,5A binding proteins in unfractionated peripheral blood mononuclear cell extracts. Mycoplasmainfected CFS patients presented with significantly elevated RNase L-ratio, compared to noninfected age- and sex-matched patients [p = 0.016]. These results suggest that Mycoplasma infections may cause deregulation of the 2,5A synthetase RNase L antiviral pathway in patients with CFS. Cfr. : http://www.name-us.org/ResearchPages/ResearchArticlesAbstracts/ImmuneArticles/Nijsi2003RNaseLMyco Full.pdf
Detection of Chlamydia in the peripheral blood cells of normal donors using in vitro culture, immunofluorescence microscopy and flow cytometry techniques Cirino F, Webley WC, West C, Croteau NL, Andrzejewski C Jr, Stuart ES, Department of Microbiology, University of Massachusetts, Amherst, Massachusetts 01003, USA : firstname.lastname@example.org - PMID: 16472397 (erratum in : BMC Infect Dis. 2006;6:165) Background - Chlamydia trachomatis (Ct) and Chlamydia pneumoniae (Cp) are medically significant infectious agents associated with various chronic human pathologies. Nevertheless, specific roles in disease progression or initiation are incompletely defined. Both pathogens infect established cell lines in vitro and polymerase chain reaction (PCR) has detected Chlamydia DNA in various clinical specimens as well as in normal donor peripheral blood monocytes (PBMC). However, Chlamydia infection of other blood cell types, quantification of Chlamydia infected cells in peripheral blood and transmission of this infection in vitro have not been examined. Methods - Cp specific titers were assessed for sera from 459 normal human donor blood (NBD) samples. Isolated white blood cells (WBC) were assayed by in vitro culture to evaluate infection transmission of blood cell borne chlamydiae. Smears of fresh blood samples (FB) were dual immunostained for microscopic identification of Chlamydia-infected cell types and aliquots also assessed using Flow Cytometry (FC). Results - ELISA demonstrated that 219 (47.7%) of the NBD samples exhibit elevated anti-Cp antibody titers. Imunofluorescence microscopy of smears demonstrated 113 (24.6%) of samples contained intracellular Chlamydia and monoclonals to specific CD markers showed that in vivo infection of neutrophil and eosinophil/basophil cells as well as monocytes occurs. In vitro culture established WBCs of 114 (24.8%) of the NBD samples harbored infectious chlamydiae, clinically a potentially source of transmission, FC demonstrated both Chlamydia infected and uninfected cells can be readily identified and quantified. Conclusion - NBD can harbor infected neutrophils, eosinophil/basophils and monocytes. The chlamydiae are infectious in vitro and both total and cell type specific Chlamydia carriage is quantifiable by FC. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/16472397
Detection of Chlamydophila pneumoniae in the bone marrow of two patients with unexplained chronic anaemia Nebe CT, Rother M, Brechtel I, Costina V, Neumaier M, Zentgraf H, Böcker U, Meyer TF, Szczepek AJ, Central Laboratory, University Hospital Mannheim, Mannheim, Germany : email@example.com - Eur J Haematol. 2005 Jan;74(1):77-83 - PMID: 15613113 Anaemia of chronic disease (ACD) is a common finding involving iron deficiency and signs of inflammation. Here, we report on two patients with ACD where a persistent infection with Chlamydophila (Chlamydia) pneumoniae (CP) was detected in bone marrow (BM) biopsies. Infection was suspected by routine cytology and confirmed by immunofluorescence, electron microscopy, polymerase chain reaction (PCR) including different primer sets and laboratories and sequencing of the PCR product. This is a first report of chlamydial presence in the BM of anaemic patients. The cases are presented because persistent chlamydial infection may contribute more frequently to chronic refractory anaemia than previously suspected. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/15613113
Detection of Mycoplasma genus and Mycoplasma fermentans by PCR in patients with Chronic Fatigue Syndrome Vojdani A, Choppa PC, Tagle C, Andrin R, Samimi B, Lapp CW, Immunosciences Laboratory, Beverly Hills, CA 90211, USA : firstname.lastname@example.org - FEMS Immunol Med Microbiol. 1998 Dec;22(4):355-65 - PMID: 9879928 Mycoplasma fermentans and other Mycoplasma species are colonizers of human mucosal surfaces and may be associated with human immunodeficiency virus infection. While many infectious agents have been described in different percentages of patients with Chronic Fatigue Syndrome (CFS), little is known about the prevalence of mycoplasmas and especially M. fermentans in CFS patients. A polymerase chain reaction (PCR)-based assay was used to detect Mycoplasma genus and M. fermentans genomes in peripheral blood mononuclear cells (PBMC) of CFS patients. Blood was collected from 100 patients with CFS and 50 control subjects. The amplified products of 717 bp of Mycoplasma genus, and 206 bp of M. fermentans were detected in DNA purified from blood samples in 52% and 34% of CFS samples, respectively. In contrast, these genomes were found in only 14% and 8% of healthy control subjects respectively (P < 0.0001). All samples were confirmed by Southern blot with a specific probe based on internal sequences of the expected amplification product. Several samples, which were positive for Mycoplasma genus, were negative for M. fermentans indicating that other Mycoplasma species are involved. A quantitative PCR was developed to determine the number of M. fermentans genome copies present in 1 microg of DNA for controls and CFS patients. Mycoplasma copy numbers ranging from 130 to 880 and from 264 to 2400 were detected in controls and CFS positive subjects, respectively. An enzyme immunoassay was applied for the detection of antibodies against p29 surface lipoprotein of M. fermentans to determine the relationship between M. fermentans genome copy numbers and antibody levels. Individuals with high genome copy numbers exhibited higher IgG and IgM antibodies against M. fermentans specific peptides. Isolation of this organism by culture from clinical specimens is needed in order to demonstrate specificity of signal detected by PCR in this study. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/9879928
Detection of Mycoplasma pneumoniae by using the polymerase chain reaction C Bernet, M Garret, B de Barbeyrac, C Bebear, and J Bonnet, Institut de Biochimie Cellulaire et Neurochimie du Centre National de la Recherche Scientifique, Bordeaux, France - J Clin Microbiol. 1989 November; 27(11): 2492–2496 The polymerase chain reaction (PCR) technique was used to detect Mycoplasma pneumoniae. A specific DNA sequence for M. pneumoniae was selected from a genomic library and two oligonucleotides were chosen in this sequence to give an amplified fragment of 144 base pairs. We show that DNA from different M. pneumoniae strains can be detected by PCR, with DNA from other Mycoplasma species giving negative results. Analysis of biological samples (throat swabs) obtained from hamsters that were experimentally infected with M. pneumoniae showed that PCR was more sensitive and reliable than conventional culture techniques for the detection of M. pneumoniae. Initial experiments on artificially seeded human bronchoalveolar lavages showed that PCR can be used to detect 10(2) to 10(3) organisms. Cfr. : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC267064/
Infection as one possible cause of fibromyalgia - Part V
Infection as one possible cause of fibromyalgia
Detection of Mycoplasma pneumoniae in the airways of adults with chronic asthma Monica Kraft, Gail H. Cassell, Jan E. Henson, Harold Watson, Jan Williamson, B.P. Marmion, Charlotte A. Gaydos and Richard J. Martin, Department of Medicine, National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, Colorado; Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama; Royal Hobart Hospital, University of Tasmania, Hobart, Tasmania; Institute of Medical and Veterinary Science, University of Adelaide, Australia; and Department of Medicine, The Johns Hopkins University, Baltimore, Maryland - Am. J. Respir. Crit. Care Med., Volume 158, Number 3, September 1998, 998-1001 Infection with Mycoplasma pneumoniae has been shown to exacerbate asthma in humans. However, the role of M. pneumoniae in the pathogenesis of chronic asthma has not been defined. Eighteen asthmatics with chronic, stable asthma and 11 nonasthmatic control subjects underwent evaluation of the upper and lower airways and serologic analysis to determine the presence of M. pneumoniae, Chlamydia pneumoniae and seven respiratory viruses through culture, enzyme-linked immunoassay (EIA) and polymerase chain reaction (PCR). M. pneumoniae was detected by PCR in 10 of 18 asthmatics and one of 11 control subjects (p = 0.02). In nine of the 10 patients, the organism was detected in bronchoalveolar lavage or bronchial biopsies. Seven of 18 asthmatics and one of 11 control subjects were also positive for M. fermentans and M. genitalium by PCR. All patients' cultures, EIAs and serology were negative for M. pneumoniae. All PCR and cultures were negative for C. pneumoniae and all EIAs for respiratory viruses were negative in all subjects. Nine asthmatics and one control subject exhibited positive serology for C. pneumoniae (p = 0.05). M. pneumoniae was present in the lower airways of chronic, stable asthmatics with greater frequency than control subjects and may play a role in the pathogenesis of chronic asthma. Cfr. : http://ajrccm.atsjournals.org/cgi/content/abstract/158/3/998
Detection of Mycoplasmal infections in blood of patients with rheumatoid arthritis Haier J. (1), Nasralla M. (1), Franco A. R. (2), Nicolson G. L. (1) - (1) Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041, Etats-Unis - Arthritis Center of Riverside, Riverside, CA 92501,Etats-Unis - Rheumatol 1999; 38:504-509 Objective - Mycoplasmal infections are associated with several acute and chronic illnesses. Some mycoplasmas can enter a variety of tissues and cells and cause system-wide or systemic signs and symptoms. Methods - Patients (14 female, 14 male) diagnosed with rheumatoid arthritis (RA) were investigated for mycoplasmal infections in their blood leucocytes using a forensic polymerase chain reaction (PCR) procedure. Amplification was performed with genus- and species-specific primers and a specific radiolabelled internal probe was used for Southern hybridization with the PCR product. Patients were investigated for the presence of Mycoplasma spp. and positive cases were further tested for infections with the following species : M. fermentans, M. hominis, M. pneumoniae and M. penetrans. Results - The Mycoplasma spp. sequence, which is not entirely specific for mycoplasmas, was amplified from the peripheral blood of 15/28 patients (53.6%) and specific PCR products could not be detected in 13 patients (46.4%). Significant differences (P < 0.001) were found between patients and positive healthy controls in the genus test (3/32) and in the specific tests (0/32). Moreover, the incidence of mycoplasmal infections was similar in female and male patients. Using species-specific primers, we were able to detect infections with M. fermentans (8/28), M. pneumoniae (5/28), M. hominis (6/28) and M. penetrans (1/28) in RA patients. In 36% of the patients, we observed more than one Mycoplasma species in the blood leucocytes. All multiple infections occurred as combinations of M. fermentans with other species. Conclusions - The results suggest that a high percentage of RA patients have systemic mycoplasmal infections. Systemic mycoplasmal infections may be an important cofactor in the pathogenesis of RA and their role needs to be explored further.Cfr. : http://rheumatology.oxfordjournals.org/cgi/reprint/38/6/504.pdf
Development of an amplification and hybridization assay for the specific and sensitive detection of Mycoplasma fermentans DNA Berg S, Lüneberg E, Frosch M, Institut für Medizinische Mikrobiologie, Medizinische Hochschule, Hannover, Germany - Mol Cell Probes. 1996 Feb;10(1):7-14 - PMID: 8684379 A polymerase-chain-reaction-based detection system for Mycoplasma fermentans was established. The highly conserved tuf gene, which encodes elongation factor Tu of prokaryotes, served as target sequence for the PCR. With two PCR oligodeoxynucleotides, which were selected from M. fermentans specific sequences of the tuf gene, we amplified a 850 base pair DNA fragment. Via the biotin-moiety of one primer the PCR fragments were immobilized on streptavidin-coated microtitre plates. After alkaline denaturation a digoxigenin-labelled M. fermentans specific DNA probe was hybridized to the single stranded immobilized PCR fragment. Detection was performed by addition of an alkaline phosphatase conjugated anti-digoxigenin antibody. 4-methyl-umbelliferyl-phosphate was used as a fluorogenic substrate. Amplification of 10 fg chromosomal target DNA was detected by this 'DNA enzyme immuno assay (DEIA)' technique, corresponding to seven genome copies. Our study supports the presumption that the tuf gene proves to be a suitable target sequence for the PCR based detection of any bacterial species. Furthermore, hybridization of PCR fragments with radio-labelled DNA probes should no longer be necessary, because a very sensitive non-radioactive test system can easily be established with the 'DEIA' technique. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8684379
Diagnosis and integrative treatment of intracellular bacterial infections in Chronic Fatigue and Fibromyalgia Syndromes, Gulf War Illness, Rheumatoid Arthritis and other chronic illnesses Nicolson GL, Nasralla M, Franco AR, Nicolson NL, Erwin R, Ngwenya R, Berns PA - Clin. I'racl. Ail.Med, 2000; 1:92-102 Cfr. : http://www.immed.org/
Diagnosis and treatment of chronic infections in chronic fatigue syndrome, fibromyalgia syndrome and Gulf War illness G.L. Nicolson and N.L. Nicolson - International Journal of Occupational Medicine, Immunology and Toxicology 1996 ; 5 : 69-78 Cfr. : http://www.immed.org/
Diagnosis and treatment of chronic mycoplasmal infections in Fibromyalgia and Chronic Fatigue Syndromes - Relationship to Gulf War Illness Nicolson GL. Nasralla M. Haier and Nicolson NL - Biomed. Ther, 1998;16:266-71 Cfr. : http://www.immed.org/
Diagnosis and treatment of mycoplamsmal infections in Persian Gulf War Illness – CFIDS patients Nicolson GL, Nicolson NL - International Journal of Occupational Medicine, Immunology and Toxicology 1996; 5: 67-78 Veterans of Operation Desert Storm returned from the Persian Gulf Theater of Operations and developed multiple signs and symptoms characterized by disabling fatigue, arthralgia, intermittent fever, myalgia, impairments in short-term memory, headaches, skin rashes, diarrhea and additional symptoms that have defied a disease case definition but has been called Gulf War Illness (GWI). In a sampling of GWI patients and symptomatic family members (n=30) we have used the technique of Gene Tracking and have found evidence of mycoplasmal infections in the blood leukocytes of approximately one-half of these cases. Mycoplasma-positive patients can be successfully treated with several 6 week courses of doxycycline (200 mg/d) or other antibiotics. Of the 14/30 patients that were mycoplasma-positive, 11/14 completely recovered after multiple cycles of antibiotics and 3/14 are still undergoing antibiotic therapy and relapsing. Cfr. : www.immed.org/Fatigue%20Illness/_GWI_IJO.rtf
Dietary supplement Healthy Curb for reducing weight, girth, body mass, appetite and fatigue while improving blood lipid values with NTFactor Lipid Replacement Therapy Garth L Nicolson, PhD, Rita Ellithorpe, MD, Robert Settineri, MS - J. IiME 2009; 3(1): 39-48 – Source : Journal of IiME, May 28, 2009 (note : the full text of this article with charts is available free online in the Spring 2009 issue of the Journal of IiME - http://bit.ly/3PvOQ -; dr. Nicolson presented the results at the recent International IiME Conference] Often Chronic Fatigue Syndrome (CFS) patients have weight issues and weight reduction regimens can increase fatigue. Therefore, we initiated a weight loss clinical trial using an all natural oral supplement mixture containing an FDA-approved amylase inhibitor plus NTFactor®, which is known to safely reduce fatigue in aged subjects, chronic fatigue and CFS. The objective was to see if subjects could safely lose weight without increasing appetite and fatigue and without changing eating or exercise patterns or using drugs, herbs or caffeine. A 2-month open label clinical trial was initiated with 30 patients who used an oral mixture (Healthy Curb™) of amylase inhibitor (500 mg white kidney bean extract) plus 500 mg of NTFactor 30 min before each meal. Weight and measurements were taken weekly, appetite was assessed and fatigue was determined using the Piper Fatigue Scale. - Sixty-three percent of the participants lost an average of 3 pounds, with average reductions of 1.5 and 1 inch waist and hip circumference, respectively. - Participants experienced gradual and consistent weight loss along with waist and hip, body mass index (BMI) and basal metabolic rate (BMR) reductions during the entire trial. - There was a 44% reduction in overall hunger with reduced cravings for sweets; therefore, notable appetite suppression occurred. - Using the Piper Fatigue Scale the entire test group showed an average of 23% decrease in overall fatigue. - Blood lipid profiles generally improved, suggesting improved cardiovascular health and - no adverse effects were noted clinically or found in blood chemistries. Conclusions - The vast majority of the subjects in this trial lost weight, showed decreased waist and hip measurements and overall body mass. Their overall fatigue was reduced and they experienced marked appetite suppression. The product was completely safe and void of any side effects and was extremely well tolerated. Healthy Curb appears to be a safe and effective means for CFS patients to manage weight without changes in eating or exercise patterns. Cfr. : http://www.prohealth.com/alzheimers/library/showarticle.cfm?libid=14581
Doxycycline treatment and Desert Storm Garth L. Nicolson, PhD, The University of Texas M. D. Anderson Cancer Center Houston - Nancy L. Rosenberg-Nicolson, PhD, Rhodon Foundation for Biomedical Research Kingwood, Tex – JAMA 1995;273(8):618-619 Cfr. : http://jama.ama-assn.org/cgi/content/summary/273/8/618-a
Effective treatment of chronic fatigue syndrome and fibromyalgia—A randomized, double-blind, placebo-controlled, intent-to-treat study Jacob E. Teitelbaum a; Barbara Bird a; Robert M. Greenfield b; Alan Weiss b; Larry Muenz c; Laurie Gould d - a Annapolis Research Center for Effective FMS/CFIDS Therapies and the Anne Arundel Medical Center, Annapolis, MD, USA - b Anne Arundel Medical Center, Annapolis, MD, USA - c Larry Muenz resides in Gaithersburg, MD, USA - d Annapolis Research Center for Effective FMS/ CFIDS Therapies, Annapolis MD, and also the USDA, Beltsville, MD, USA - Journal Of Chronic Fatigue Syndrome, Volume 8, Issue 2 May 2000 , pages 3 – 15 Cfr. : http://www.informaworld.com/smpp/content~db=jour~content=a903600733~tab=citations
Emerging concepts in the neurobiology of chronic pain - Evidence of abnormal sensory processing in fibromyalgia Bennett RM, Division of Arthritis and Rheumatic Diseases, Oregon Health Sciences University, Portland 97201, USA - Mayo Clin Proc. 1999 Apr;74(4):385-98 - PMID: 10221469 Chronic pain often differs from acute pain. The correlation between tissue pathology and the perceived severity of the chronic pain experience is poor or even absent. Furthermore, the sharp spatial localization of acute pain is not a feature of chronic pain; chronic pain is more diffuse and often spreads to areas beyond the original site. Of importance, chronic pain seldom responds to the therapeutic measures that are successful in treating acute pain. Physicians who are unaware of these differences may label the patient with chronic pain as being neurotic or even a malingerer. During the past decade, an exponential growth has occurred in the scientific underpinnings of chronic pain states. In particular, the concept of nonnociceptive pain has been refined at a physiologic, structural and molecular level. This review focuses on this new body of knowledge, with particular reference to the chronic pain state termed "fibromyalgia". Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/10221469 Aslo read the comment on this article : Fibromyalgia and pain management Sartin JS - Mayo Clin Proc. 2000 Mar;75(3):316-7 - PMID: 10725965 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/10725965?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
Empiric parenteral antibiotic treatment of patients with fibromyalgia and fatigue and a positive serologic result for Lyme disease - A cost-effectiveness analysis Lightfoot RW Jr, Luft BJ, Rahn DW, Steere AC, Sigal LH, Zoschke DC, Gardner P, Britton MC, Kaufman RL, Division of Rheumatology, Kentucky Clinic J515, University of Kentucky Medical Center, Lexington 40536-0284 - Ann Intern Med. 1993 Sep 15;119(6):503-9 - PMID: 8357117 Purpose - To examine the cost-effectiveness of empirical, parenteral antibiotic treatment of patients with chronic fatigue and myalgia and a positive serologic result for Lyme disease who lack classic manifestations. Data sources - Peer-reviewed journals, opinion of experts in the field and published epidemiologic reports. Study selection - Consensus by authors on articles that indicated methods for patient selection; on criteria used for diagnosis; on immunologic methods used for classifying patients; on the dose and duration of therapy; and on criteria by which responses to therapy were ascertained. Data extraction - In a cost-effectiveness model, the costs and benefits of empirical parenteral therapy for patients seropositive for Lyme disease were compared with a strategy in which only patients having classical symptoms of Lyme disease were treated. Data synthesis - In areas endemic for Lyme disease, the incidence of false-positive serologic results in patients with nonspecific myalgia or fatigue exceeds by four to one the incidence of true-positive results in patients with nonclassical infections. Treatment of the former group of patients costs $86,221 for each true-positive patient treated. The empirical strategy causes 29 cases of drug toxicity for every case in the more conservative strategy. If patients were willing to pay $3485 to eliminate anxiety about not treating possible true Lyme disease, the empirical strategy would break even. Conclusion - For most patients with a positive Lyme antibody titer whose only symptoms are nonspecific myalgia or fatigue the risks and costs of empirical parenteral antibiotic therapy exceed the benefits. Only when the value of patient anxiety about leaving a positive test untreated exceeds the cost of such therapy is the empirical treatment cost-effective. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8357117 Also read the comments on this article : - Appropriateness of parenteral antibiotic treatment for patients with presumed Lyme disease - A joint statement of the American College of Rheumatology and the Council of the Infectious Diseases Society of America Ann Intern Med. 1993 Sep 15;119(6):518 - PMID: 8357119 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8357119?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract - Simplifying the diagnosis of obstructive sleep apnea Pack AI - Ann Intern Med. 1993 Sep 15;119(6):528-9 - PMID: 8204127 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8204127?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
Established fibromyalgia syndrome and parvovirus B19 infection Berg AM, Naides SJ, Simms RW, Arthritis Section, Boston University, MA - J Rheumatol. 1993 Nov;20(11):1941-3 - PMID: 8308782 Objective - To determine the seroprevalence of prior and persistent parvovirus B19 (B19) infection in a group of patients with fibromyalgia (FS) compared with controls. Methods - Fifteen female patients with FS who recalled a viral prodrome (+VP) preceding the onset of FS symptoms and eleven patients with FS who did not recall any such illness (-VP) were selected from a referral practice. We excluded patients with FS who described a history of trauma prior to the onset of FS symptoms. Twenty-six female medical workers served as controls. Serum IgM and IgG anti-B19 antibodies were measured by ELISA. Polymerase chain reaction (PCR) products from serum were analyzed by dot blot hybridization for B19 DNA. Fisher's 2-tailed exact test was used to compare the proportion of positive serologies in each group. Results - No patient or control had positive IgM levels. For all patients with FS, the prevalence of prior B19 infection was comparable to that of healthy controls (11/26 vs 12/26, p = 1.00) and that of the general population. No significant difference was found in the prevalence of prior B19 infection in FS + VP and FS-VP patients (8/15 vs 3/11, p = 0.25). None of the patients or controls showed evidence for persistent B19 viremia, as determined by PCR analysis. Conclusion - Our data do not suggest that B19 plays a pathogenic role in this population of patients with FS. Testing for IgM against B19 within 2-3 months of symptom onset may prove more helpful in further defining the role of B19 in FS. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8308782
Examination of Mycoplasmas in blood of 565 chronic illness patients by polymerase chain reaction Marwan Y. Nasralla, Jörg Haier, Nancy L. Nicolson and Garth L. Nicolson.*, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041 USA, Tel. : 1-714-903-2900 – Fax : 714-379-2082 - *Correspondence to: Prof. Garth L. Nicolson, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041 USA, Tel: 1-714-903-2900, Fax: 1-714-379-2082 – Website : www.immed.org – E-mail : email@example.com - International Journal Medicine Biology Environment 2000; 28(1):15-23 Mycoplasmal infections are associated with several acute and chronic illnesses. Patients with Chronic Fatigue Syndrome (CFS), myalpic encepthalomyelitis (ME) and/or Fibromyalgia Syndrome (FMS) were examined for systemic mycoplasmal infections by analysis of blood specimens. Using an optimized protocol for forensic polymerase chain reaction (PCR) blood samples from 565 CFS or FMS patients (401 female, 164 male) and 71 healthy controls were investigated for presence of Mycoplasma spp. and M. fermentans infections. The Mycoplasma spp. sequence was amplified from the peripheral blood of 300/565 patients (53.1 %). Specific PCR products could not be detected in 265 patients (46.9 %). A significant difference (p<0.001) was found between mycoplasma-positive patients and healthy controls (7/71; 9.9%). The prevalence of M. fermentans infections (24.6%) was also significantly (p<0.001) higher in CFS/FMS patients than in controls (2/71; 2.8%). Moreover, the prevalence of mycoplasmal infections was similar in female and male CFS patients. The data indicate that mycoplasmas can be detected in blood specimens from a high proportion of CSF/FMS patients. M. fermentans can be an opportunistic infection, cofactor or causative agent resulting in morbidity in these patients.
Fibromyalgia - Is there an infectious connection ? The Road Back Foundation Fibromyalgia (FM) is a commonly misunderstood, sometimes misdiagnosed rheumatic disease. The main symptoms are achiness, pain (more in the muscles than in the joints), stiffness, fatigue, accompanied by headaches, depression, sleep disorders, Raynaud's and irritable bowel syndrome. The sites of pain are located in specific areas call-ed tender or trigger points. The painful tender points are located where the ligament attaches the muscle to the bone. There are 18 tender point locations. Sensitivity at 11 points defines a diagnosis of fibromyalgia. FM is not life threatening nor does it cause physical deformities. Many lab tests are within normal range. In fact, most patients look extremely well and fit, making it difficult to account for the degree of clinical suffering they are experiencing, yet 10-30% of fibromyalgia patients are disabled to some degree because of their disease symptoms. It is 9 times more common among women than men, usually between the ages of 40 and 60, is more common in Caucasians than other races and is the second or third most common disorder treated by rheumatologists. Potential Pathogens As is the case of most forms of "arthritis", no known cause has been established, but a number of possibilities are mentioned in the medical literature. Like many forms of arthritis, the cause of FM is probably not limited to one single factor. 55% of patients identify a "flu-like" or viral type illness, 33% physical trauma/injury and 14% emotional stress as a precursor to the onset of symptoms. The connection of FM to infections is well documented in the literature, especially in relation to Lyme disease, mycoplasma, Chlamydia pneumoniae., Hepatitis C, Parvovirus B19, HIV and Epstein-Barr. It is believed as many as 25-40% of long-term Lyme patients develop fibromyalgia-like symptoms, particularly pain and fatigue; as many as 25% of HIV patients, 57% of RA patients and 24% of Psoriatic Arthritis patients also have FM symptoms. A 1993 Annals of Internal Medicine article (Lightfoot et al) found 10% of patients with Lyme Disease would have arth-ritis develop as a result of the spirochete infection. Because this organism (like mycoplasma) is difficult to culture, the diagnoses is based on the occurrence of (1) one or more of the classical features and (2) serum antibodies to the etiologic spirochete after the first 4 to 6 weeks of illness. Some Lyme/FM patients do not respond to courses of antibiotics, causing researchers to dismiss the possibility of an organism as a trigger for the disease and antibiotics as a therapy. This might be a misleading assumption as explained by Garth Nicholson, PhD, in a recent article (Environmental Phys, 1997). "Are chronic, systemic mycoplasmal infections the answer to CFS, FMS, GWI* and other disorders ? Of course not ! This is likely to be an appropriate explanation for a rather large subset of CFS, FMS, GWI* and some arthritis patients, but certainly not every patient will have the same chronic infections. Some patients may have chemical exposures or other environmental problems as the underlying reason for their chronic signs and symptoms. In these patients, antibiotics should have no effect whatsoever". Nicholson has found mycoplasma infections in approximately one half of patients with FM as well as arthritis. "The identification of mycoplasma infections in the leukocyte blood fractions of a rather large subset of CFS, FMS and arthritis patients suggests that mycoplasmas and probably other chronic infections as well, may be an important source of morbidity in these patients. If such infections are important in these disorders, then appropriate treatment with antibiotics should result in improvement and even recovery. This is exactly what has been found" (Nicholson JAMA 1995). "Only antibiotics that are effective against the pathogenic mycoplasmas result in recovery, and some antibiotics, such as penicillins, can worsen the condition" (Nicholson, 1996, & 1997). Goldenberg suggests two possibilities for an infectious cause : 1) the infectious agent would either directly invade tissues such as the joints or central nervous system or 2) "trigger" factors that would cause the chronic myalgias, fatigue, headaches, sleep disturbances and mood disturbances... Infectious agents are capable of activating cytokines which may in turn cause severe myalgias, fatigue and neurocognitive disturbances... The potential role of a microbial agent as a trigger to fibromyalgia remains tenable. Antibodies to Chlamydia pneumoniae have been found in 78.3% of FM patients tested or 67.4% for unselected rheumatic patients. These high numbers point to a possible connection between Chlamydia pneumoniae and fibromyalgia. In a Spanish study, Rivera et al found 15% of 112 FM patients had Hepatitis C viral Infection (HCV) and among HCV patients, 10% had FM. The incidence of FM in the control group was less than 2%; the prevalence of FM in the general population was 2%. "The presence of active infection by HCV is more likely to trigger FM than the stress and anxiety produced by the disease" (Rivera et al, 1997). Other researchers have described HCV infection as a trigger for autoimmune disorders (Pawlotsky 1994 & Agnello 1992). "In the remaining 85%, other known and unknown viruses that can produce chronic infections, could be responsible for FM symptoms. We think the presence of such viruses should be sought in patients with FM symptoms" (Rivera et al, 1997). Parvovirus B19 infection as a trigger for autoimmune disorders (Pawlotsky 1994 & Agnello 1992). "In the remaining 85%, other known and unknown viruses that can produce chronic infections, could be responsible for FM symptoms. We think the presence of such viruses should be sought in patients with FM symptoms" (Rivera et al, 1997). Parvovirus B19 has been implicated as a cause in cases of chronic arthritis and may mimic rheumatoid arthritis. Berg et al identified patients with established FM who had symptoms consistent with recent or distant B19 infection. In fact, 30-60% of the general population test positive for Parvovirus B19 and the incidence increases with age. The timing of testing for PV B19 appears to be critical. Testing too early or too late will yield negative results. 25% of HIV patients experience fibromyalgia symptoms, adding additional discomfort and anxiety. Epstein Barr Virus (EBV) has been considered a possible cause of FM or CFS because of similarity of symptoms, but so far, a connection has not been proven. Most observers currently believe that no single infectious agent is likely to be the cause of CFS (or FM). Yet it has been shown that chronic persistent viruses may often be reactivated during this illness. Is this merely an epiphenomenon ? Or, once reactivated, do these viruses go on to produce many of the symptoms of the disease ? And what reactivates these viruses ? If it is some defect in immunologic containment, what causes the defect ? Could it be stress ? Genetics ? infection with other viruses ? In the view of Komaroff et al, it is reasonable to speculate that all these factors are capable triggers, with different factors playing different roles in different individuals. Common FM symptoms - Chronic, widespread pain - most fatigue : 70-90% - morning stiffness : 80% - migraine headaches : 50% - depression : 25-50% - sleep disturbances : 70% - anxiety : 25% - Raynaud's-like syndrome : 33% - numbness, tingling : 75% - irritable bowel syndrome : 50% - positive ANA : 10%. Organisms that might be connected to FM - Borellia borgdorferi (Lyme) - Hepatitis C - Epstein-Barr Virus - Mycoplasma - Chlamydia pneumoniae - Parvovirus B19 - HIV References .../... Cfr. : http://www.roadback.org/index.cfm/fuseaction/education.display/display_id/135.html
Fibromyalgia - Up close and personal Mark J. Pellegrino, MD - Anadem Publishing; 2 edition (January 2005) - ISBN-10: 1890018503 - ISBN-13: 978-1890018504 'Fibromyalgia - Up close & personal' is packed with 43 chapters of "inside" medical information and "hands-on" practical advice for everyday living. Dr. Mark J. Pellegrino brings readers up-to-date with the newest drug and physical treatments for fibromyalgia. He also presents the latest thinking on diet and exercise to help people with this condition lead a full life. Recognized by fibromyalgia sufferers for understanding what they are going through, Dr. Pellegrino is a welcoming and encouraging presence for everyone with this condition and this quality comes through very clearly in his writing. It’s as if each person reading his book is having a private consultation about their shared disease. In 'Up close & personal' Dr. Pellegrino has enlisted two leading attorneys to bring readers much needed insight into disability and personal injury issues. Also, he asked a knowledgeable physician to contribute a chapter on common pain problems. Cfr. : - https://www.prohealth.com/shop/product.cfm/product__code/BK90 - http://www.amazon.com/Fibromyalgia-Personal-Mark-J-Pellegrino/dp/1890018503
Infection as one possible cause of fibromyalgia - Part VI
Infection as one possible cause of fibromyalgia
From time to time there may be an acute exacerbation of a problem leading to a lot of pain signals being generated and if a lot of pain signals are dumped at once into the spinal cord sponge, only a little bit gets absorbed and a lot gets passed through and perceived as acute pain. In Fibromyalgia, however, the different pain generators continue to send signals and eventually the dry sponges becomes a wet sponge and it can’t soak up any more. The additional oncoming continuous signals will spill over the wet sponge and this leads to persistent pain. The two main changes that occur at the spinal cord include : - pain amplification (by specialized nerves called NMDA receptors) and - loss of pain filtering (by the diffuse noxious inhibitory control system). Spinal cord nerves are bombarded by continuous stimulation from the peripheral nerves, causing a progressive increase in electrical signals to be sent up to the brain. This phenomenon is called “wind-up” and is the neurological mechanism for the amplification of pain. Once this wind-up phenomenon occurs, a central sensitization results in which various types of sensory signals - not just pain - will arrive in the spinal cord, become amplified and be sent to the brain as pain. The spinal cord becomes more sensitized to sending pain, lots of it. Once this happens, the spinal cord is not able to properly sort out and filter various sensory signals. As a result, different sensory signals such as touch, pressure, temperature and joint movement all become amplified and sent up the pain pathways, resulting in pain signals instead of the appropriate touch, pressure, temperature or joint motion signals. This defect in pain transmission where there is increased sensitivity to all stimuli – even those which normally do not evoke pain – is called allodynia. Unfortunately for the person with Fibromyalgia, the spinal cord is now “wired” to interpret nearly all sensory signals as pain – severe pain ! We can still appreciate touch, pressure, temperature, joint movement and other non-pain signals, but pain contaminates these signals and we feel the pain. Another key change at the spinal cord level is an increased formation of Substance P and other neurotransmitters. Substance P’s primary role at the spinal cord level is to transmit pain signals and to sensitize the spinal cord so it is readily available to transmit pain. When Substance P reaches high concentrations (as it does in Fibromyalgia), it can migrate up and down the spinal cord, away from the initial location of the pain signal. As a result, multiple levels of the spinal cord undergo sensitization and send increased pain signals, leading to a “generalization” of the Fibromyalgia. This spreading of pain explains how one can develop generalized Fibromyalgia from an initial regional area of pain. A common example of this occurs following a motor vehicle accident where a particular body part, such as the neck, was injured. Over time, the pain begins to involve the mid-back, low back and ultimately the whole body, even though these areas were never injured. The Substance P-induced spinal cord changes can explain this migration of pain from the neck to the entire body. Brain Our poor brains have no chance, do they ? Any pain memory stored in the past will be re-awakened by this process. Fibromyalgia is notorious for causing previously injured areas to hurt more once it develops. This previously injured area may have settled down and become essentially pain-free, but the pain memories remained, although inactive. Thanks to the Fibromyalgia pain amplification process, the inactive memories are reactivated. The pain centers of our brain, the limbic system and the cerebral cortex, are continuously fed these amplified signals from the spinal cord. Changes occur : - serotonin levels decrease, - brain waves change, - sleep stages are affected, - blood flow and glucose [blood sugar] metabolism are affected. The brain gets overwhelmed with these pain signals and spends a lot of attention and energy monitoring the pain. Fibrofog occurs. Emotional components are “attached” to pain, including fear, depression, anxiety, anger, hopelessness and helplessness, which can further amplify the pain. In patients with Fibromyalgia, functional reorganization (brain plasticity) in both sensory and motor portions of the brain has been observed and appears directly related to the chronicity of the pain (Dr. H. Flor, 2003). These brain changes may be viewed as pain memories that influence how painful and non-painful signals affect the body’s sensory and motor responses. The brain makes these changes to enhance its ability to perceive pain – brain amplified pain. This type of abnormal brain plasticity can be measured. Doctors Richard H. Gracely, Richard A. Harris, Daniel J. Clauw et al. at the University of Michigan Chronic Pain and Fatigue Research Center have published studies which demonstrated abnormal “hyperactive” areas of the brains and abnormal “quiet” areas of the brains in Fibromyalgia test subjects who underwent functional MRIs. This provides objective evidence to support brain plasticity with both hypersensitive amplified pain, and turning off the ability to inhibit pain. Fibromyalgia pain summary To summarize, Fibromyalgia changes our pain pathways. It may start off as a peripheral irritant, but eventually it becomes a self-perpetuating process that affects the entire pathway from the nociceptors to the brain. The main problem, in a nutshell, is amplified pain. The amplified pain is the result of our nervous system gaining the ability to magnify pain and losing the ability to inhibit pain. What comes in at a signal of a “1” does not end up in the brain as a signal of a “1” as it would in people without Fibromyalgia. Our pain signal of a “1” gets amplified and magnified and by the time it reaches our brain, it is a “10” ! Other non-painful signals get thrown into this pain amplification pathway and arrive at our brain as pain signals. Even tiny subconscious pain signals can get amplified or the nerve pathways can automatically “fire away” without any obvious noxious stimulus to cause spontaneous pain. These are not your everyday aches and pains, these are severe pains that cannot be ignored. This severe, chronic pain can completely disrupt one’s life. And by the way, while all of this is happening, we continue to look completely normal on the outside. Cfr. : - http://www.prohealth.com//library/showArticle.cfm?libid=13702 - http://www.prohealth.com/library/showarticle.cfm?id=8892&t=CFIDS_FM - http://www.prohealth.com/library/print.cfm?libid=13702
Fibromyalgia and its relation to chronic fatigue syndrome, viral illness and immune abnormalities Goldenberg DL, Newton-Wellesley Hospital, Department of Medicine, Tufts University School of Medicine, MA 02162 - J Rheumatol Suppl. 1989 Nov;19:91-3 - PMID: 2607516 Fibromyalgia and chronic fatigue syndrome have similar clinical and demographic features. We found that most patients with chronic fatigue syndrome have a tender point examination similar to patients with fibromyalgia. Similar pathophysiologic mechanisms are also being explored in each syndrome, including a potential role for viral induced immune dysfunction. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2607516
Fibromyalgia and other chronic fatigue syndromes - Is there evidence for chronic viral disease ? Goldenberg DL, Department of Medicine, Boston University School of Medicine, MA 02118 - Semin Arthritis Rheum. 1988 Nov;18(2):111-20 - PMID: 3064302 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/3064302
Fibromyalgia and overlapping disorders - The unifying concept of central sensitivity syndromes Yunus MB, Section of Rheumatology, The University of Illinois College of Medicine at Peoria, One Illini Drive, Peoria, IL 61605, USA - Semin Arthritis Rheum. 2007 Jun;36(6):339-56. Epub 2007 Mar 13 - PMID: 17350675 Objectives - To discuss fibromyalgia syndrome (FMS) and overlapping conditions eg, irritable bowel syndrome, headaches and chronic fatigue syndrome, within the concept of central sensitivity syndromes (CSS). Methods - A critical overview of the literature and incorporation of the author's own views. Results - The concept of CSS seems viable. It is based on mutual associations among the CSS conditions as well as the evidence for central sensitization (CS) among several CSS members. However, such evidence is weak or not available in other members at this time, requiring further studies. The biology of CSS is based on neuroendocrine aberrations, including CS, that interact with psychosocial factors to cause a number of symptoms. Conclusions - CSS is an important new concept that embraces the biopsychosocial model of disease. Further critical studies are warranted to fully test this concept. However, it seems to have important significance for new directions for research and patient care involving physician and patient education. Each patient, irrespective of diagnosis, should be treated as an individual considering both the biological and psychosocial contributions to his or her symptoms and suffering. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/17350675
Fibromyalgia and parvovirus infections Lawrence J. Leventhal, MD *, Stanley J. Naides, MD, Bruce Freundlich, MD, From the Section of Rheumatology, Department of Medicine, University of Pennsylvania School of Medicine and the Presbyterian Medical Center, Philadelphia, Pennsylvania and the Division of Rheumatology, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City - * Correspondence to : Lawrence J. Leventhal, Address reprint requests to Lawrence J. Leventhal, MD, 570 Maloney Building, Hospital of the University of Pennsylvania, 3600 Spruce Street, Philadelphia, PA 19104 An infectious cause of fibromyalgia (FM) has been hypothesized based upon the observed similarity of this entity and chronic fatigue syndrome. Three patients developed symptoms of FM after documented episodes of acute parvovirus B19 infections. B19 antibody determinations were obtained approximately 1 month after the symptoms began; both IgM and IgG titers were positive at that time. All 3 patients met criteria for FM. Polysomnography performed on 2 of the patients revealed profound alpha-wave intrusion throughout non-rapid eye movement sleep. A more careful search for viral infections in FM patients whose symptoms appear following a flu-like illness appears warranted. Cfr. : http://www3.interscience.wiley.com/journal/112208394/abstract
Fibromyalgia and related central sensitivity syndromes - Twenty-five years of progress John B. Winfield, MD, University of North Carolina School of Medicine - Seminars in Arthritis and Rheumatism, Volume 36, Issue 6, Pages 335-338 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/17303220
Fibromyalgia in human immunodeficiency virus infection Buskila D, Gladman DD, Langevitz P, Urowitz S, Smythe HA, University of Toronto Rheumatic Disease Unit, Wellesley Hospital, ON, Canada - J Rheumatol. 1990 Sep;17(9):1202-6 - PMID: 2290162 Tenderness was assessed by point count and by scored palpation in 51 patients with human immunodeficiency virus (HIV) infection as well as 51 patients with rheumatoid arthritis (RA) and 50 patients with psoriatic arthritis (PsA). Fifteen of 51 (29%) patients with HIV infection met criteria for fibromyalgia, based on the presence of 10 tender (of 14) "fibrositic" points. Similar results were observed among patients with PsA (24%). The prevalence of fibromyalgia was higher among patients with RA (57%). Patients with HIV and PsA were less tender than patients with RA. Fibromyalgia in patients with HIV was significantly associated with myalgia and arthralgia, but not with age, duration of HIV infection, stage of HIV disease or zidovudine therapy. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2290162
Fibromyalgia-associated hepatitis C virus infection Rivera J, de Diego A, Trinchet M, García Monforte A, Rheumatology Unit, Hospital General Universitario Gregorio Marañón, Madrid, Spain - Br J Rheumatol. 1997 Sep;36(9):981-5 - PMID: 9376995 The objective was to determine whether there might be an association between hepatitis C virus (HCV) chronic infection and fibromyalgia (FM). We determined the prevalence of HCV infection in 112 FM patients, in comparison with matched rheumatoid arthritis (RA) patients from the out-patient clinic of a teaching tertiary care general hospital. Furthermore, we looked for evidence of FM in 58 patients diagnosed with chronic hepatitis due to HCV, compared with matched surgery clinic patients, HCV antibodies were determined by enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA). Serum RNA of HCV (HCV-RNA) was determined by polymerase chain reaction. In the group of FM patients, HCV antibodies were found by ELISA in 17 (15.2%) patients and in six (5.3%) of the RA controls (P < 0.05). RIBA was positive in 16 and indeterminate in one of the FM patients. Serum HCV-RNA was found in 13 of these FM patients. In eight (47%) FM patients, alanine aminotransferase (ALT) was normal, although HCV-RNA was detected in four (50%) of them. In the group of patients with chronic hepatitis due to HCV, all patients had HCV antibodies and the presence of HCV-RNA in serum. Within these patients, 31 (53%) had diffuse musculoskeletal pain, while six (10%) fulfilled FM diagnostic criteria. In the control group, 13/58 (22%) had diffuse musculoskeletal pain (P < 0.001), whereas only one female patient (1.7%) fulfilled FM criteria (P < 0.05). Serum ALT was 51.7 +/- 38.4 in FM patients, whereas it was 122 +/- 76.3 in patients with HCV chronic hepatitis but without FM (P < 0.001). There were no statistical differences in autoimmune markers between patients with and without FM. These data suggest that there exists an association between FM and active HCV infection in some of our patients. FM is not associated with liver damage or autoimmune markers in these patients. HCV infection should be considered in FM patients even though ALT elevations were absent. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/9376995
Fibromyalgia, chronic fatigue syndrome and myofascial pain syndrome Goldenberg DL, Newton-Wellesley and Tufts University School of Medicine, Massachusetts, USA - Curr Opin Rheumatol. 1995 Mar; 7(2):127-35 - PMID: 7766493 Two important studies in which nuclear magnetic resonance spectroscopy was used convincingly demonstrated that muscle is not the primary pathologic factor in fibromyalgia. There were further studies reporting that fibromyalgia-chronic fatigue syndrome may follow well treated Lyme disease or mimic Lyme disease. The longest therapeutic trial to date in fibromyalgia demonstrated an initial modest effect of tricyclic medications, but at 6 months that efficacy was no longer evident. Investigation in both fibromyalgia and chronic fatigue syndrome now focuses on the central nervous system. The use of new technology, eg, neurohormonal assays and imaging such as single-photon emission computed tomography scan, may be important in understanding these elusive conditions. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/7766493?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleI temSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmed
Fibromyalgia, infection and vaccination - Two more parts in the etiological puzzle Jacob N. Ablina, Yehuda Shoenfeldb and Dan Buskilac - aDepartment of Rheumatology, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel-Aviv University, 6 Weizman St., 64239 Tel-Aviv, Israel - bDepartment of Medicine ‘B’ and Center for Autoimmune Diseases, Sheba Medical Center Tel-Hashomer and Sackler Faculty of Medicine, Tel-Aviv University, Israel - cRheumatic Disease Unit, Department of Medicine, Soroka Medical Center, Beer Sheba, Israel As the pathogenesis of fibromyalgia continues to raise debate, multiple putative triggers have been implicated. The current review summarizes the available data linking fibromyalgia to either infection or vaccination. Multiple infectious agents have been associated with the development of either full-blown fibromyalgia (e.g. hepatits C) or with symptom complexes extensively overlapping with that syndrome (e.g. chronic Lyme disease). The cases of Lyme disease, mycoplasma, hepatits C and HIV are detailed. Despite the described associations, no evidence is available demonstrating the utility of antibiotic or anti-viral treatment in the management of fibromyalgia. Possible mechanistic links between fibromyalgia and HIV are reviewed. Associations have been described between various vaccinations and symptom complexes including fibromyalgia and chronic fatigue syndrome. The case of Gulf War syndrome, a functional multisystem entity sharing many clinical characteristics with fibromyalgia is discussed, with emphasis on the possibility of association with administration of multiple vaccinations during deployment in the Persian Gulf and the interaction with stress and trauma. Based on this example a model is proposed, wherein vaccinations function as co-triggers for the development of functional disorders including fibromyalgia, in conjunction with additional contributing factors. Cfr. : http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WHC-4M7CDJ5-1&_user=10&_coverDate=11%2F30%2F2006&_alid=1081388956&_rdoc=3&_fmt=high&_orig=search&_cdi=6847&_docancho r=&view=c&_ct=134&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md 5=7cd5ea72fb8f7bab0830aa8998b5326d
Gulf War Illnesses - Chemical, radiological and hiological exposures resulting in chronic l'aliQuing illnesses can be idemificd and treated Nicolson GL, Berns P, Nasralla M, Haicr J, Nicolson NL, Nass M - Chronic tigne Syndr. 2003; ll(l):21-36
Health and exposures oT United Kingdom Gull war veterans - Part II - The relation of health to exposure Cherry N. Creed 1'. Sii man A, Dunn G. Baxter G, S medley J. et al. - J. Occup. Environ. Med, 2001;58:299-306
Hepatitis C virus infection in Italian patients with fibromyalgia C. Palazzi1, E. D’Amico2, S. D’Angelo3, 5, A. Nucera4, A.Petricca1 and I.Olivieri3 – 1 Division of Rheumatology, Villa Pini Clinic, Chieti, Italy – 2 Liver Unit, Spirito Santo Hospital, Pescara, Italy – 3 Rheumatology Department of Lucania, S. Carlo Hospital of Potenza and Madonna delle Grazie Hospital of Matera, Potenza, Italy – 4 Section of Medical Statistics & Epidemiology, Department of Health Sciences, University of Pavia, Pavia, Italy – 5 Rheumatology Department of Lucania, San Carlo Hospital, Contrada Macchia Romana, Via Potito Petrone—Padiglione E, 85100 Potenza, Italy - Clin Rheumatol. 2008 Jan; 27(1):101-3. Epub 2007 Oct 18 We evaluated the prevalence of hepatitis C virus (HCV) infection in Italian patients suffering from fibromyalgia (FM), in comparison with patients affected by non-HCV related rheumatic degenerative disorders. Consecutive patients with FM and a statistically comparable group of patients suffering from peripheral osteoarthritis (OA) or sciatica due to L4-L5 or L5-S1 herniated disc were tested for HCV infection with a third-generation microparticle enzyme immunoassay (MEIA). In the positive cases, a third-generation recombinant immunoblot assay (RIBA) confirmatory test and serum HCV-RNA test were performed. Fisher’s exact test was performed to compare the prevalence of HCV infection (MEIA- and RIBA-positive results) obtained in the two enrolled groups. Enrolled were 152 subjects suffering from FM and 152 patients with peripheral OA or sciatica. Anti-HCV antibodies were found in 7/152 (4.6%) patients suffering from FM and in 5/152 (3.3%) of control subjects. No statistically significant differences in HCV prevalence were detected between cases and controls. Our present report does not confirm previous data indicating an increased prevalence of HCV in FM patients and does not seem to support a significant pathogenetic role of HCV under this condition. Cfr. : http://www.springerlink.com/content/126w3638641h7204/
High frequency of systemic mycoplasmal infections in Gulf War veterans and civilians with Amyotrophic Lateral Sclerosis (ALS) Nicolson GL, Berns P, Nasralla M, Haier J, Pomfret J - J Clin Neurosci 2002; 9:525-529 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12383408
High prevalence of mycoplasmal infections among European Chronic Fatigue Syndrome patients - Examination of four Mycoplasma species in Chronic Fatigue Syndrome patients Nijs J, Nicolson GL, De Becker P, Coomans D, De Meirleir K - FEMS Immunol Med Microbiol 2002; 34:209-214 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12423773
Higher prevalence of fibromyalgia in patients infected with human T cell lymphotropic virus type I Cruz BA; Catalan-Soares B; Proietti F, Rheumatology Department, Biocor Instituto, Nova Lima, Minas Gerais, Brazil : firstname.lastname@example.org - J Rheumatol. 2006 Nov;33(11):2300-3 - PMID : 17086610 Objective - Inflammatory rheumatic conditions including rheumatoid arthritis and Sjogren's syndrome have been reported in individuals infected with human T cell lymphotropic virus type I (HTLV-I). Other chronic lymphotropic virus infections such as hepatitis C and human immunodeficiency virus are associated with fibromyalgia (FM). There are no reports about the association between HTLV-I infection and FM. We evaluated the association between FM and HTLV-I infection. Methods - We conducted a case-control study with prevalent cases. Ex-blood donation candidates with HTLV-I infection from a blood bank cohort and healthy blood donors as a control group, were submitted to rheumatologic evaluation to compare the prevalence of FM. The following covariables were also evaluated: other rheumatic diseases, age, sex, personal income, level of education and depression. Results - One hundred individuals with HTLV-I infection and 62 non-infected blood donors were studied. Thirty-eight (38%) HTLV-I infected individuals and 3 (4.8%) individuals from the control group presented the diagnosis of FM (OR 12.05, 95% CI 3.53-41.17). Other rheumatic diseases were also more prevalent in the infected group (37% vs 12.9%; OR 3.80, 95% CI 1.63-8.86). In multivariate analysis adjusted by the covariables, the association between HTLV-I and FM was statistically significant (OR 9.14, 95% CI 2.42-34.52). Conclusion - Our study shows a greater prevalence of FM in HTLV-I infected individuals, suggesting that FM may be associated with this viral infection. Cfr. : http://www.uptodate.com/patients/content/abstract.do;jsessionid=21CED400A6252607545D B5AC431EF284.1102?topicKey=~IVIndOU9abHZK_&refNum=11
Identification of mycoplasma fermentans in synovial fluid samples from arthritis patients with inflammatory disease Johnson S, Sidebottom D, Bruckner F, Collins D - Journal of Clinical Microbiology 2000; 38: 90-3 Cfr. : http://jcm.asm.org/cgi/content/abstract/38/1/90
Illness, cytokines and depression Yirmiya R, Pollak Y, Morag M, Reichenberg A, Barak O, Avitsur R, Shavit Y, Ovadia H, Weidenfeld J, Morag A, Newman ME, Pollmächer T, Department of Psychology, Hebrew University, Hadassah Hospital, Jerusalem, Israel : email@example.com - Ann N Y Acad Sci. 2000;917:478-87 - PMID: 11268375 Various medical conditions that involve activation of the immune system are associated with psychological and neuroendocrine changes that resemble the characteristics of depression. In this review we present our recent studies, designed to investigate the relationship between the behavioral effects of immune activation and depressive symptomatology. In the first set of experiments, we used a double-blind prospective design to investigate the psychological consequences of illness in two models : (1) vaccination of teenage girls with live attenuated rubella virus and (2) lipopolysaccharide (LPS) administration in healthy male volunteers. In the rubella study, we demonstrated that, compared to control group subjects and to their own baseline, a subgroup of vulnerable individuals (girls from low socioeconomic status) showed a significant virus-induced increase in depressed mood up to 10 weeks after vaccination. In an ongoing study on the effects of LPS, we demonstrated significant LPS-induced elevation in the levels of depression and anxiety as well as memory deficits. These psychological effects were highly correlated with the levels of LPS-induced cytokine secretion. In parallel experiments, we demonstrated in rodents that immune activation with various acute and chronic immune challenges induces a depressive-like syndrome, characterized by anhedonia, anorexia, body weight loss and reduced locomotor, exploratory and social behavior. Chronic treatment with antidepressants (imipramine or fluoxetine) attenuated many of the behavioral effects of LPS, as well as LPS-induced changes in body temperature, adrenocortical activation, hypothalamic serotonin release and the expression of splenic TNF-alpha mRNA. Taken together, these findings suggest that cytokines are involved in the etiology and symptomatology of illness-associated depression. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11268375
Immune cell apoptosis and chronic fatigue syndrome Frémont M, D’Haese A, Roelens S, De Smet K, Herst CV, Englebienne P – In : 'Chronic Fatigue Syndrome - A biological approach' - Englebienne P, De Meirleir K, editors - Boca Raton: CRC Press 2002, p. 131-74 Cfr. : http://www.ncf-net.org/forum/TotalExposure.htm
Interferon-alpha-induced changes in tryptophan metabolism - Relationship to depression and paroxetine treatment Capuron L, Neurauter G, Musselman DL, Lawson DH, Nemeroff CB, Fuchs D, Miller AH, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia 30322, USA - Biol Psychiatry. 2003 Nov 1;54(9):906-14 - PMID: 14573318 Background - Tryptophan (TRP) degradation into kynurenine (KYN) by the enzyme, indoleamine-2,3-dioxygenase, during immune activation may contribute to development of depressive symptoms during interferon (IFN)-alpha therapy. Methods - Twenty-six patients with malignant melanoma were randomly assigned in double-blind fashion to receive either placebo or paroxetine, beginning 2 weeks before IFN-alpha treatment and continuing for the first 12 weeks of IFN-alpha therapy. At treatment initiation and at 2, 4, and 12 weeks of IFN-alpha treatment, measurements of TRP, KYN and neopterin (a marker of immune activation), were obtained, along with structured assessments of depression, anxiety and neurotoxicity. Results - Regardless of antidepressant treatment status, all patients exhibited significant increases in KYN, neopterin and the KYN/TRP ratio during IFN-alpha therapy. Among antidepressant-free patients, patients who developed major depression exhibited significantly greater increases in KYN and neopterin concentrations and more prolonged decreases in TRP concentrations than did nondepressed, antidepressant-free patients. Moreover, in antidepressant-free patients, decreases in TRP correlated with depressive, anxious and cognitive symptoms, but not neurovegetative or somatic symptoms. No correlations were found between clinical and biological variables in antidepressant-treated patients. Conclusions - The results suggest that reduced TRP availability plays a role in IFN-alpha-induced depressive symptoms, and paroxetine, although not altering the KYN or neopterin response to IFN-alpha, attenuates the behavioral consequences of IFN-alpha-mediated TRP depletion. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/14573318
Interrelations between fibromyalgia, thyroid autoantibodies and depression Ribeiro LS; Proietti FA, Department of Rheumatology, Governador Israel Pinheiro Hospital, Belo Horizonte, Brazil : firstname.lastname@example.org - J Rheumatol. 2004 Oct;31(10):2036-40 - PMID :15468372 Objective - To detect and quantify the association between fibromyalgia (FM) and thyroid autoimmunity. Methods - This cross-sectional study comprised 146 women with FM and 74 case-controls, all 18 years of age or older. FM was diagnosed according to the American College of Rheumatology 1990 classification criteria. The Mini-International Neuropsychiatric Interview (MINI) was applied for the diagnosis of depression, previously considered as an important confounding factor. Thyroid autoimmunity was defined as the occurrence of detectable antithyroid peroxidase antibodies and/or antithyroglobulin antibodies by the immunometric assay. Cases of diffuse connective tissue diseases and thyroid dysfunctions (hypo or hyperthyroidism) were excluded in both groups. Results - Univariate analysis detected an association between FM and thyroid autoimmunity (odds ratio, OR = 3.87, 95% confidence interval, CI = 1.54-10.13), depression (OR = 3.94, 95% CI = 1.97-7.93) and age (OR = 1.04, 95% CI = 1.01-1.07). In the final logistic regression model, after adjustment for depression and age, the association between FM and thyroid autoimmunity was strengthened (OR = 4.52, 95% CI = 1.86-11.0). Conclusion - Our results suggest an association between FM and thyroid autoimmunity. Cfr. : http://www.uptodate.com/patients/content/abstract.do;jsessionid=21CED400A6252607545D B5AC431EF284.1102?topicKey=~IVIndOU9abHZK_&refNum=12
Is RA27/3 rubella immunization a cause of chronic fatigue ? Allen AD, Biomedical Sciences Division, Algorithms, Incorporated, Northridge, California 91325 - Med Hypotheses. 1988 Nov;27(3):217-20 - PMID: 3211019 Patients with chronic fatigue syndromes (primary fibrositis syndrome, major affective disorder etc) have elevated IgG serum antibodies to multiple common viruses. Only IgG rubella antibodies are positively correlated with the intensity of symptoms and have a height that is clearly significant compared to healthy controls. The lymphotropic properties of the rubella virus could account for the multiple elevated antibodies. Adult women are over-represented in the population of patients with chronic fatigue and are especially susceptible to developing such symptoms following exposure to attenuated rubella virus. A new more potent strain of live rubella vaccine (strain RA27/3) was introduced in 1979. Within three years reports of patients with chronic fatigue began surfacing in the literature. Considering all this, the possible role of rubella immunization in the etiology of chronic fatigue syndromes deserves further study. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/3211019?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleIt emSupl.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed
Is there a biologic connection between inflammatory disease and depression ? Colby Stong - NeuroPsychiatry Reviews, September 2004, Vol. 5, No.7 Nearly a third of patients with an inflammatory disease may develop depression, which until recently has been attributed to their inability to cope with the disease. However, research on patients who are aided via immunotherapy has challenged this theory. Robert Dantzer, DVM, PhD, and Keith Kelley, PhD, believe that they have found strong evidence of a relationship between a molecular pathway in the brain and development of psychopathology. “Depression is a risk factor for a bad outcome,” said Dr. Dantzer in an interview with Neuropsychiatry Reviews : “What our research is showing is that you have to put everything in a different perspective. The idea is that the depression is linked biologically to the disease. It is not just the way that the molecules are involved in the disease process but [that] the physiology of the disease acts on the brain and is responsible for depression. Actually, the severity of the disease will result in a higher risk for depression. So it’s a mirror image of the usual interpretation that people give of the association between depression and disease”. Dr. Dantzer is an Adjunct Professor of Psychoneuroimmunology in the Department of Animal Sciences, University of Illinois at Urbana–Champaign and Director of the Laboratory of Integrative Neurobiology at the University of Bordeaux, France. The prevalence of depression in the general population is about 3% to 5%. In patients with chronic inflammation—such as occurs with coronary heart disease or type 2 diabetes mellitus—the prevalence of depression increases to between 12% and 30%. Immunotherapy, which involves the injection of cytokines, also causes depression in about a third of patients, noted Dr. Dantzer. Symptoms of depression begin within days to weeks of treatment and disappear when the treatment ends. Thus, Dr. Dantzer wanted to help patients avoid depression while they still benefited from the immune-boosting effects of cytokine treatments. Tryptophan, cytokines and depression Drs. Dantzer and Kelley conducted a series of experiments on mice to show how cytokine treatment causes serotonin depletion. They hypothesized that cytokines suppress serotonin by activating the enzyme indoleamine-2,3-dioxygenase (IDO) that catabolizes tryptophan. Dr. Dantzer explained that in the brain, IDO prevents tryptophan from being turned into serotonin, which causes decreased levels of serotonin and leads to the symptoms of depression. “From clinical studies, we have learned that depressed patients either suffering from chronic inflammatory disorders or who are treated with cytokines have decreased plasma levels of tryptophan,” he said : “Second, we have observed that the enzyme responsible for that is induced not only at the periphery but in the brain”. Dr. Dantzer pointed out that his current research is built on a concept that he had ignored a few years ago, which is the fact that the brain is representing what is going on in the body—“what we already knew for quite a long time, but in terms of inflammation and it is doing that with the same molecules as the ones that are promoting inflammation at the periphery. If you have an inflammatory response in your body, it will be represented in the brain with exactly the same molecules that in your body are responsible for inflammation. This normally is responsible for what we call sickness behavior—why you feel sick and behave in a sick way when you are ill”. On target for new treatments Dr. Dantzer said that if his hunches are correct, then logical targets for decreasing the risk of depression in patients with inflammatory disorders are the cytokine system or the IDO enzyme to avoid both the decrease in serotonin and the generation of neuroactive compounds derived from tryptophan. For example, he said, antioxidants may be used in an effort to decrease free radicals, which may enhance the IDO activation. By suppressing the IDO activity, more tryptophan should be available to be converted to serotonin, he theorized. If antioxidant treatment proves effective in the mice, then humans eventually may benefit from the approach. “The main potential of clinical application is the discovery of new targets for drugs aiming at decreasing the risk of developing mood disorders when you are sick,” he said. Treating all patients who will undergo interferon therapy with an antidepressant is not necessarily the right preventive solution, stressed Dr. Dantzer. It is not yet known whether antidepressant treatment will affect interferon treatment for the disease, he said—“in this case, the immune cells of the body and their ability to kill tumor cells. You are preventing the occurrence of depression with an antidepressant treatment, but at the same time this antidepressant treatment could also act on immune cells so that they are less able to do what they are supposed to do. My own advice would be to tell the clinician to try to identify those patients who are at risk for developing depression. We know that patients who are at risk for developing depression are already high in terms of depressed moods”. Suggested reading - Interferon-alpha-induced changes in tryptophan metabolism - Relationship to depression and paroxetine treatment - Capuron L, Neurauter G, Musselman DL et al. - Biol Psychiatry. 2003;54:906-914 at : http://www.ncbi.nlm.nih.gov/pubmed/14573318 - Baseline mood and psychosocial characteristics of patients developing depressive symptoms during interleukin-2 and/or interferon-alpha cancer therapy - Capuron L, Ravaud A, Miller AH, Dantzer R - Brain Behav Immun. 2004;18:205-213 at : http://www.ncbi.nlm.nih.gov/pubmed/15050647 -. Cfr. : http://www.neuropsychiatryreviews.com/sep04/sep04_npr_inflammatory.html
Lack of association of fibromyalgia with hepatitis C virus infection Narváez J, Nolla JM, Valverde-García J, Department of Rheumatology, Hospital Universitario de Bellvitge-IDIBELL, Barcelona, Spain : email@example.com - J Rheumatol. 2005 Jun;32(6):1118-21 - PMID: 15940777 Objective - An association between chronic hepatitis C virus (HCV) infection and fibromyalgia (FM) remains controversial, mainly because previous studies were based on prevalent case series or comparisons with less than optimal control groups. We investigated whether there might be an association between chronic HCV infection and FM. Methods - We prospectively investigated the prevalence of HCV infection in a series of 115 patients with FM and compared it with the prevalence in the general population of our community reported in the same period. Anti-HCV antibodies were determined by ELISA. In positive cases, infection was confirmed by recombinant immunoblot assay and HCV-RNA was detected by PCR using sera samples. Differences between prevalence rates were assessed by chi-square test. Results - : HCV infection was confirmed in 3 of 115 patients with FM (2.6%). Two of these patients (1.74%) had active HCV infection shown by the presence of viral RNA in serum, whereas HCV RNA was undetectable in the third patient. In these cases, liver disease had previously been undiagnosed and HCV infection manifested itself by extrahepatic symptoms. Although the prevalence of HCV infection was slightly higher in patients with FM than in the general population in the age groups 25-44 and 45-64 years, when we compared prevalence rates in the total group and the different age groups, no statistically significant differences were found. Conclusion - From our results, it seems unlikely that HCV infection plays a pathogenic role in FM. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/15940777
Melatonin inhibits expression of the inducible NO synthase II in liver and lung and prevents endotoxemia in lipopolysaccharide-induced multiple organ dysfunction syndrome in rats Elena Crespo,* Manuel Maci´as,* David Pozo,† Germaine Escames,* Miguel Marti'n,* Francisco Vives,* Juan M. Guerrero,† and Dari'o Acun˜ A-Castroviejo*,1 - *Departamento de Fisiologı´a, Instituto de Biotecnologı´a, Universidad de Granada, Spain - †Departamento de Bioquı´mica Me´dica y Biologı´a Molecular, Facultad de Medicina, Universidad de Sevilla, Spain - FASEB J. 13, 1537–1546 (1999) We evaluated the role of melatonin in endotoxemia caused by lipopolysaccharide (LPS) in unanesthetized rats. The expression of inducible isoform of nitric oxide synthase (iNOS) and the increase in the oxidative stress seem to be responsible for the failure of lungs, liver and kidneys in endotoxemia. Bacterial LPS (10 mg/kg b.w) was i.v. injected 6 h before rats were killed and melatonin (10–60 mg/kg b.w.) was i.p. injected before and/or after LPS. Endotoxemia was associated with a significant rise in the serum levels of aspartate and alanine aminotransferases, g-glutamyl-transferase, alkaline phosphatase, creatinine, urea, and uric acid and hence liver and renal dysfunction. LPS also increased serum levels of cholesterol and triglycerides and reduced glucose levels. Melatonin administration counteracted these organ and metabolic alterations at doses ranging between 20 and 60 mg/kg b.w. Melatonin significantly decreased lung lipid peroxidation and counteracted the LPSinduced NO levels in lungs and liver. Our results also show an inhibition of iNOS activity in rat lungs by melatonin in a dose-dependent manner. Expression of iNOS mRNA in lungs and liver was significantly decreased by melatonin (60 mg/kg b.w., 58–65%). We conclude that melatonin inhibits NO production mainly by inhibition of iNOS expression. The inhibition of NO levels may account for the protection of the indoleamine against LPS-induced endotoxemia in rats. Fullt text at : http://www.fasebj.org/cgi/reprint/13/12/1537.pdf
Multiple co-infections (mycoplasma, chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients - Association with signs and symptoms Nicolson GL, Gan R, Haier J, The Institute for Molecular Medicine, Huntington Beach, California 92649, USA : firstname.lastname@example.org - APMIS. 2003 May;111(5):557-66 - PMID: 12887507 Previously we and others found that a majority of chronic fatigue syndrome (CFS) patients showed evidence of systemic mycoplasmal infections and their blood tested positive using a polymerase chain reaction assay for at least one of the four following Mycoplasma species : M. fermentans, M. hominis, M. pneumoniae or M. penetrans. Consistent with previous results, patients in the current study (n=200) showed a high prevalence (overall 52%) of mycoplasmal infections. Using forensic polymerase chain reaction we also examined whether these same patients showed evidence of infections with Chlamydia pneumoniae (overall 7.5% positive) and/or active human herpes virus-6 (HHV-6, overall 30.5% positive). Since the presence of one or more infections may predispose patients to other infections, we examined the prevalence of C. pneumoniae and HHV-6 active infections in mycoplasma-positive and -negative patients. Unexpectedly, we found that the incidence of C. pneumoniae or HHV-6 was similar in Mycoplasma-positive and -negative patients, and the converse was also found in active HHV-6-positive and -negative patients. Control subjects (n=100) had low rates of mycoplasmal (6%), active HHV-6 (9%) or chlamydial (1%) infections and there were no co-infections in control subjects. Differences in bacterial and/or viral infections in CFS patients compared to control subjects were significant. Severity and incidence of patients' signs and symptoms were compared within the above groups. Although there was a tendency for patients with multiple infections to have more severe signs and symptoms (p<0.01), the only significant differences found were in the incidence and severity of certain signs and symptoms in patients with multiple co-infections of any type compared to the other groups (p<0.01). There was no correlation between the type of co-infection and severity of signs and symptoms. The results indicate that a large subset of CFS patients show evidence of bacterial and/or viral infection(s), and these infections may contribute to the severity of signs and symptoms found in these patients. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12887507
Multiple mycoplasmal infections detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients Nasralla M, Haier J, Nicsolosn GL - European Journal of Clinical Microbiology and Infectious Diseases 1999; 18: 859-65 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/10691196
Multiplex PCR for the detection of Mycoplasma fermentans, M hominis and M penetrans in patients with Chronic Fatigue Syndrome, Fibromyalgia, Rheumatoid Arthritis and Gulf War Syndrome Vojdani A, Franco AB - Journal of Chronic Fatigue Syndrome Chronic Fatigue Syndr 1999; ¾ : 187-97 Cfr. : http://www.thearthritiscenter.com/pub_multiplex.htm
Multiplex PCR for the detection of Mycoplasma fermentans, M. hominis and M. penetrans in cell cultures and blood samples of patients with Chronic Fatigue Syndrome Choppa PC, Vojdani A, Tagle C et al. - Mol Cell Probes 1998; 12: 301-308 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/9778455
Mycoplasma infection and rheumatoid arthritis - Analysis of their relationship using immunoblotting and an ultrasensitive PCR Hoffman RW, O’Sullivan FX, Schafermeyer KR, Moore TL, Roussell D, Watson-McKown R et al. - Arthritis and Rheumatism 1997; 40: 1219-28 Cfr. : http://compkarori.com/arthritis/pi16004.htm
No serological evidence that fibromyalgia is linked with exposure to human parvovirus B19 Narváez J, Nolla JM, Valverde J - Joint Bone Spine. 2005 Dec;72(6):592-4. Epub 2005 Mar 22 - PMID: 16376806 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/16376806
Olanzapine for the treatment of fibromyalgia symptoms Kiser RS, Cohen HM, Freedenfeld RN, Jewell C, Fuchs PN, Texas Pain Medicine Clinic, 5327 N. Central Expressway, Dallas, TX 75205, USA - J Pain Symptom Manage. 2001 Aug;22(2):704-8 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/11495717
Patients with rheumatoid arthritis are more tender than those with psoriatic arthritis Buskila D, Langevitz P, Gladman DD, Urowitz S, Smythe HA, University of Toronto Rheumatic Disease Unit, Wellesley Hospital, ON, Canada - J Rheumatol. 1992 Jul;19(7):1115-9 - PMID: 1512768 Articular and nonarticular tenderness was examined in 51 patients with rheumatoid arthritis (RA) and 50 patients with psoriatic arthritis (PsA) by scored palpation and dolorimeter readings. Fifty-seven percent of patients with RA had 10 or more tender fibrositic points vs 24% of patients with PsA (p = 0.0008). Thresholds of tenderness measured by dolorimetry of 6 fibrositic point sites were 3.97 (1.99) [mean (SD)] for RA vs 5.95 (2.28) for PsA (p less than 0.0001). Thresholds over actively inflamed joints were 4.19 (1.53) for RA vs 6.78 (2.55) for PsA (p less than 0.0001). In both RA and PsA, fibrositic sites were more tender than actively inflamed joints (p less than 0.0001). Nonarticular control sites were also more tender in subjects with RA with dolorimeter thresholds at 5.99 (1.96) in RA vs 7.58 (1.60) in PsA (p less than 0.0001). These data demonstrate that actively inflamed joints, fibrositic and control nonarticular sites were all more tender in patients with RA than PsA. Both groups were similar in their disease duration and clinical assessments of joint inflammation and damage. We suggest that there may be a disease specific diffuse increase in tenderness in patients with RA, which is not related to joint inflammation. Similarly, the severity of articular inflammation may be underestimated in subjects with PsA. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/1512768?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleIt emSupl.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed
Phagocytes transmit Chlamydia pneumoniae from the lungs to the vasculature Gieffers J, van Zandbergen G, Rupp J, Sayk F, Krüger S, Ehlers S, Solbach W, Maass M, Institute for Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany : email@example.com - Eur Respir J. 2004 Apr;23(4):506-10 - PMID: 15083745 Chlamydia pneumoniae, a major cause of community-acquired pneumonia, primarily infects the respiratory tract. Chronic infection of nonrespiratory sites, such as the vascular wall, the brain or blood monocytes, requires evasion from the lungs and spreading via the bloodstream. The cell types involved in dissemination are insufficiently characterised. In this study, New Zealand White rabbits were infected intratracheally with C. pneumoniae, and lung manifestation and systemic dissemination were monitored by polymerase chain reaction and immunohistochemistry. Infection of the lungs was characterised by an early phase dominated by granulocytes and a late phase dominated by alveolar macrophages (AM). Granulocytes, AM and alveolar epithelial cells acted as host cells for chlamydiae, which remained detectable for up to 8 weeks. AM transported the pathogen to the peribronchiolar lymphatic tissue and subsequently C. pneumoniae entered the spleen and the aorta via dissemination by peripheral blood monocytes. In conclusion, Chlamydia pneumoniae-infected alveolar macrophages transmigrate through the mucosal barrier and give the pathogen access to the lymphatic system and the systemic circulation. Infected peripheral blood monocytes are the vector system within the bloodstream and transmit the infection to the vascular wall. This is the first description of granulocytes acting as a reservoir for Chlamydia pneumoniae early in infection. Cfr. : http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=15083745&cmd=showdetailview&indexed=google Also read the comment on this article : Chlamydia pneumoniae - Crossing the barriers ? Blasi F, Centanni S, Allegra L - Eur Respir J. 2004 Apr;23(4):499-500 - PMID: 15083742 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/15083742?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
Pioneering fibromyalgia doctor continues to advance understanding The MiFio Network Fibromyalgia, a chronic, widespread pain in muscles and soft tissues accompanied by fatigue, is a fairly common condition that does not manifest any structural damage in an organ. Twenty-five years ago, Muhammad B. Yunus, MD and colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome. That seminal article, published in Seminars in Arthritis and Rheumatism, led directly to formal recognition of this disease by the medical community. In the June 2007 issue of Seminars in Arthritis and Rheumatism, Dr. Yunus once again makes an important contribution to the field of chronic pain and fatigue by meticulously synthesizing and interpreting the extensive body of scientific literature on fibromyalgia and his own insights into the concept of central sensitivity syndromes (CSS). Fibromyalgia, affecting approximately 2% of the US population, is an example of a class of maladies called CSS. These diseases are based on neurochemical abnormalities and include irritable bowel syndrome, migraine and restless legs syndrome. Incorporating a critical review of over 225 publications and the author's broad experience in fibromyalgia and related diseases, Dr. Yunus describes 13 separate conditions that are related to central sensitization (CS), where the central nervous system (spinal cord and brain) becomes extremely sensitized on certain parts of the body, so that even mild pressure or touch would cause much pain. Such hypersensitivity may also be associated with other symptoms such as poor sleep and fatigue. According to Dr. Yunus : "CSS are the most common diseases that are based on real neurochemical pathology and cause real pain and suffering. In some patients stress and depression may contribute to the symptoms but they are all based on objective changes in the central nervous system". Dr. Norman L. Gottlieb, Editor of Seminars in Arthritis and Rheumatism, believes that this article "advances our understanding of fibromyalgia, unifies and advances concepts and suggests that this and several other common disorders have much in common in terms of their biopsychosocial development. This, hopefully, will expand both clinical and research interest in this group of diseases and lead to advances in therapy for many of them". In an accompanying editorial John B. Winfield, MD, comments : "Without question, Muhammad Yunus is the father of our modern view of fibromyalgia.... Yunus, who took a rather more biological approach to fibromyalgia in the past, now emphasizes a biopsychosocial perspective. In my view, this is tremendously important because it is the only way to synthesize the disparate contributions of such variables as genes and adverse childhood experiences, life stress and distress, posttraumatic stress disorder, mood disorders, self-efficacy for pain control, catastrophizing, coping style and social support into the evolving picture of central nervous system dysfunction vis-a-vis chronic pain and fatigue ....Science and medicine now have a rational scaffolding for understanding and treating chronic pain syndromes previously considered to be 'functional' or 'unexplained.' ...Neuroscience research will continue to reveal the mechanisms of CS, but only if informed through a biopsychosocial perspective and with the interdisciplinary collaboration of basic scientists, psychologists, sociologists, epidemiologists and clinicians". Dr. Yunus concludes that CSS is an important new concept that embraces the biopsychosocial model of disease. He advocates further critical studies to fully test this concept which seems to have important significance for new directions for research and patient care involving physician and patient education. "Each patient, irrespective of diagnosis," says Dr. Yunus, "should be treated as an individual, considering both the biological and psychosocial contributions to his or her symptoms and suffering". The article is "Fibromyalgia and overlapping disorders - The unifying concept of central sensitivity syndromes" by Muhammad B. Yunus, MD, Professor of Medicine, Section of Rheumatology, The University of Illinois College of Medicine at Peoria, Peoria, Illinois (cfr. : http://cat.inist.fr/?aModele=afficheN&cpsidt=18834754 -). The accompanying editorial is "Fibromyalgia and related central sensitivity syndromes - Twenty-five years of progress" by John B. Winfield, MD, University of North Carolina School of Medicine. Both appear in the June issue of Seminars in Arthritis and Rheumatism, Vol. 36:6, published by Elsevier (cfr. : http://www.ncbi.nlm.nih.gov/pubmed/17303220 -). Cfr. : http://cache.mifio.com/healthmatters006.html
Population study of tender point counts and pain as evidence of fibromyalgia Croft P, Schollum J, Silman A, Arthritis and Rheumatism Council Epidemiology Research Unit, University of Manchester - BMJ. 1994 Sep 17;309(6956):696-9 - PMID: 7950521 Objective - To determine the relation between tender points, complaints of pain and symptoms of depression, fatigue and sleep quality in the general population. Design - Two stage cross sectional study with an initial questionnaire about pain to classify those eligible for an examination of tender points. Setting - Two general practices in north west England. Subjects - Stratified random sample of adults from age-sex registers. Of the responders, 250 were selected for examination of tender points on the basis of their reported pain complaints; 177 subsequently participated. Main outcome measures - Tender point count (0 to 18) grouped into four categories with the highest (> or = 11) corresponding to the criteria of the American College of Rheumatology for fibromyalgia. Assessment of pain (chronic widespread, regional, none). Measures of depression, fatigue and difficulty with sleeping. Results - Women had a higher median tender point count (six) than did men (three). Counts were higher in those with pain than in those who had no pain and in those with widespread compared with regional pain. Most subjects with chronic widespread pain, however, had fewer than 11 tender points (27/45; 60%). Two people with counts of 11 or more were in the group reporting no pain. Mean symptom scores for depression, fatigue and sleep problems increased as the tender point count rose (P value for trend < 0.001). These trends were independent of pain complaints. Conclusions - Tender points are a measure of general distress. They are related to pain complaints but are separately associated with fatigue and depression. Sleep problems are associated with tender points, although prospective studies are needed to determine whether they cause tenderness to develop. Fibromyalgia does not seem to be a distinct disease entity. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/7950521?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Single ItemSupl.Pubmed_Discovery_RA&linkpos=3&log$=relatedarticles&logdbfrom=pubmed Also read the comment ons this article : Chronic fatigue syndrome and fibromyalgia Ho-Yen DO - BMJ. 1994 Dec 3;309(6967):1515 - PMID: 7804073 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/7804073?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
Positron emission tomography in patients with fibromyalgia syndrome and healthy controls Muhammad B. Yunus 1 *, Carter S. Young 2, S. Atezaz Saeed 1, James M. Mountz 3, Jean C. Aldag 1 - 1University of Illinois College of Medicine at Peoria - 2Methodist Medical Center of Illinois, Peoria, Illinois - 3School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania - E-mail : Muhammad B. Yunus : Yunus@uic.edu - *Correspondence to : Muhammad B. Yunus, Department of Medicine, University of Illinois College of Medicine at Peoria, PO Box 1649, Peoria, IL 61656 Objective - Abnormal brain findings have previously been described in fibromyalgia syndrome (FMS) by single-photon-emission computed tomography. Our goal was to investigate change in regional cerebral glucose metabolism in people with FMS by positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG). Methods - Twelve patients with FMS and no comorbid psychiatric diagnosis and 7 healthy pain-free controls were studied with FDG-PET in a blinded manner. Those with a psychiatric diagnosis were excluded. Brain scans were obtained using a PET scanner. Semiquantitative analysis of regional 18F-FDG uptake was performed in both cortical and subcortical brain structures. Results - In the resting state, there were no significant differences in 18F-FDG uptake between patients and controls for all brain structures measured. Conclusion - FDG-PET scan findings in FMS were not significantly different from healthy controls. Normal results in our study may be explained by discordance between regional cerebral blood flow and regional cerebral glucose metabolism. Cfr. : http://www3.interscience.wiley.com/journal/109582522/abstract?CRETRY=1&SRETRY=0
Review of juvenile primary fibromyalgia and chronic fatigue syndrome Breau LM, McGrath PJ, Ju LH, Department of Psychology, Dalhousie University, Halifax, Canada - J Dev Behav Pediatr. 1999 Aug; 20(4):278-88 - PMID: 10475602 This article reviews the current literature on childhood fibromyalgia and chronic fatigue syndrome. In doing so, it questions assumptions about the presumed nature of the disorders-that they are distinct from each other and are duplicates of their adult counterparts. It also attempts to synthesize the available data to reach some preliminary judgments about these disorders : that fibromyalgia and chronic fatigue syndrome may be related in children and may not be duplicates of the adult disorders; that psychological and psychosocial factors are unlikely contributors to the etiology of these disorders; and that the evidence is increasingly pointing to a role for genetic factors in their etiology. A discussion of the research into treatments for childhood fibromyalgia and chronic fatigue syndrome highlights the lack of well-designed, controlled studies. Finally, directions for future research are offered where results of the current literature are unclear. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/10475602?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleIt emSupl.Pubmed_Discovery_RA&linkpos=4&log$=relatedreviews&logdbfrom=pubmed
The "Chronic Active Epstein-Barr Virus Infection" Symdrome and Primary Fibromyalgia D Buchwald, DL Goldenberg, JL Sullivan, AL Komaroff - Arth & Rhu, 1987; 30:10, 1132-1136 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2823835
The chlamydia pneumoniae handbook Cpnhelp.org This "Handbook" is an attempt to organize and pull together information on Chlamydia pneumoniae, it's impact on human diseasesi and it's treatment via combined antibiotic protocolsi into a more easily accessible, organized and up to date format. Some of the material has already been posted on www.cpnhelp.org - website and is simply linked here in a more organized way. Some of the material in this handbook is new and represents the most current, state of the art information on Cpn, CAPi, and the various supplementsi which have been found helpful in clinical experience. We will endeavor to update and expand the Cpn Handbook as new information becomes available. Cfr. : http://www.cpnhelp.org/book/export/html/408
The chronic fatigue syndrome - Definition, current studies and lessons for fibromyalgia research Komaroff AL, Goldenberg D, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115 - J Rheumatol Suppl. 1989 Nov;19:23-7 - PMID: 2691680 Chronic fatigue syndrome (CFS) is characterized by chronic, debilitating fatigue lasting greater than 6 months. Frequent chronic and recurrent findings include fever, pharyngitis, myalgias, adenopathy, arthralgias, difficulties in cognition and disorders of mood. In the majority of patients, the illness starts suddenly with an acute, "flu-like" illness. The following laboratory abnormalities are seen with some frequency, although none are seen in all patients: lymphocytosis, atypical lymphocytosis, monocytosis, elevation of hepatocellular enzymes, low levels of antinuclear antibodies, varying levels of antithyroid antibodies, partial hypergammaglobulinemia, elevated CD4:CD8 ratio, decreased cytolytic activity of natural killer cells and low levels of immune complexes. Clinical and serologic studies suggest an association of CFS with all of the human herpesviruses, particularly Epstein-Barr virus (EBV) and the recently discovered human B lymphotropic virus (HBLV) or human herpesvirus 6; neither EBV nor HBLV has yet been shown to play a causal role in the illness. Preliminary evidence suggests that many of these features of CFS also are seen in patients with fibromyalgia. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2691680
The Fibromyalgia Syndrome, Primer on the Rheumatic Diseases B Freundlich, L Leventhal - Arthritis Found, 1993; 247-249
The immune system, atherosclerosis and persisting infection Pigarevskii P V; Mal'tseva S V; Seliverstova V G, Vestnik Rossiiskoi akademii meditsinskikh nauk - Rossiiskaia akademiia meditsinskikh nauk 2005;(2):17-22 The paper demonstrates that lymph nodes situated in the vicinity of magistral blood vessels are the source of immune and inflammatory response to LDL as the main pathogenetic factor in atherosclerosis. The activation of T-cell-mediated immunity takes place in them at the very early stages of the disease, resulting in forming of CD4+T-lymphocytes, activated mononuclear cells and immunostabilizing B-lymphocytes. The cell changes in lymph nodes correlate with the severity of atherosclerotic lesions in the vessel intima and closely reflect the peculiarities of immune inflammation development in fatty streaks and atherosclerotic plaques in human atherogenesis. A paradoxical reaction was observed in cases with Chlamydia pneumoniae found in the wall of aorta and paraaortal lymph nodes. No evident immune response on the part of immunocompetent cells took place, but, on the contrary, the function of mononuclear cells, including T-lymphocytes, was suppressed. This phenomenon may be explained by the fact that intracellulari localization of Chlamydia pneumoniae hides it from immune system control or by the possible microorganism capability of direct immunosuppressive influence on lymphoid cells both in the blood vessel wall and in regional lymph nodes. Cfr. : - http://www.cpnhelp.org/?q=node/129 - http://www.biomedexperts.com/Abstract.bme/15776961/The_immune_system_atherosclerosi s_and_persisting_infection
The importance of B-cells and ecto-5'nucleotidase in Mycoplasma fermentans infection and the relevance to rheumatoid arthritis Johnson SM, Department of Basic Medical Sciences, St. George's University of London, London, UK : firstname.lastname@example.org - Immunology. 2008 Feb;123(2):187-96. Epub 2007 Aug 4 - PMID: 17680797 The aim of this work was to discover if Mycoplasma fermentans, which is known to infect B cells, could be the cause of the raised ecto-5'-nucleotidase observed in the synovial fluid of rheumatoid arthritis patients. The ecto-5'-nucleotidase activity in the patients' serum has been shown to correlate with the erythrocyte sedimentation rate and DNA from the mycoplasma has been found in the synovial fluid. B lymphoblastoid cell lines were exposed to 16 strains of Mycoplasma fermentans and their ecto-5'-nucleotidase, CD73, was measured both biochemically and by mouse antibodies to human ecto 5'-nucleotidase using the fluorescence activated cell sorter. The type strain, PG 18, did not grow with the B cells. Some of the mycoplasma strains (9/15) increased the cellular ecto-5'-nucleotidase activity from twice to 17 fold, and usually showed 5'-nucleotidase activity themselves. At least one strain, M106, induced human 5'-nucleotidase on the normally 5'-nucleotidase negative Daudi and Raji Burkitt's lymphoma cell lines, and increased sevenfold the 5'-nucleotidase on the monocyte/macrophage cell line THP-1. Growing the cells in aged medium increased the level of mycoplasma infection. This mycoplasma-induced enzyme showed a conformational change and an increase in activity with a glycosylation change involving mannose groups. The other group of strains, mostly of respiratory or cell culture origin, usually did not have any 5'-nucleotidase of their own and decreased the B-cell enzyme activity by about half. Electron microscopy and flow cytometry showed that the strain M106 was filamentous and could be found inside the B-cells. The 5'-nucleotidase-inducing strains of M. fermentans may be important in the aetiology of rheumatoid arthritis. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/17680797?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_Single ItemSupl.Pubmed_Discovery_PMC&linkpos=1&log$=citedinpmcarticles&logdbfrom=pubmed
The Role of Chronic Infections in the Maintenance and Progression of Chronic Fatigue Syndrome, Fibromyalgia Syndrome, Rheumatoid Arthritis, Immune Deficiency Syndromes and Gulf War Illness G.L. Nicolson et al. - ME/CFS Congress, Sydney, Australia, 1999 Cfr. : http://www.immed.org/illness/fatigue_illness_research.html
Infection as one possible cause of fibromyalgia - Part IX
Infection as one possible cause of fibromyalgia
The role of gender in fibromyalgia syndrome Muhammad B. Yunus, College of Medicine at Peoria, University of Illinois, One Illini Drive, PO Box 1649, 61656 Peoria, IL, USA : Yunus@uic.edu - Current Rheumatology Reports, Volume 3, Number 2 / March, 2001 Fibromyalgia syndrome (FMS), characterized by widespread pain and tenderness on palpation (tender points), is much more common in women than in men in a proportion of 9:1. Two recent studies have shown important gender differences in various clinical characteristics of FMS. In a community and a clinic sample, women experienced significantly more common fatigue, morning fatigue, hurt all over, total number of symptoms and irritable bowel syndrome. Women had significantly more tender points. Pain severity, global severity and physical functioning were not significantly different between the sexes, nor were psychologic factors eg, anxiety, stress and depression. Gender differences have also been observed in other related syndromes eg, chronic fatigue syndrome, irritable bowel syndrome and headaches. The mechanisms of gender differences in these illnesses are not fully understood, but are likely to involve an interaction between biology, psychology and sociocultural factors. Cfr. : http://www.springerlink.com/content/82v826m3090471w0/
Treatment with staphylococcus toxoid in fibromyalgia/chronic fatigue syndrome – A randomised controlled trial Zachrisson O, Regland B, Jahreskog M, Jonsson M, Kron M, Gottfries CG, Psychiatry Section, Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden : email@example.com - Eur J Pain. 2002;6(6):455-66 - PMID: 12413434 We have previously conducted a small treatment study on staphylococcus toxoid in fibromyalgia (FM) and chronic fatigue syndrome (CFS). The aim of the present study was to further assess the efficacy of the staphylococcus toxoid preparation Staphypan Berna (SB) during 6 months in FM/CFS patients. One hundred consecutively referred patients fulfilling the ACR criteria for FM and the 1994 CDC criteria for CFS were randomised to receive active drug or placebo. Treatment included weekly injections containing 0.1 ml, 0.2 ml, 0.3 ml, 0.4 ml, 0.6 ml, 0.8 ml, 0.9 ml and 1.0 ml SB or coloured sterile water, followed by booster doses given 4-weekly until endpoint. Main outcome measures were the proportion of responders according to global ratings and the proportion of patients with a symptom reduction of > or =50% on a 15-item subscale derived from the comprehensive psychopathological rating scale (CPRS). The treatment was well tolerated. Intention-to-treat analysis showed 32/49 (65%) responders in the SB group compared to 9/49 (18%) in the placebo group (P<0.001). Sixteen patients (33%) in the SB group reduced their CPRS scores by at least 50% compared to five patients (10%) in the placebo group (P< 0.01). Mean change score on the CPRS (95% confidence interval) was 10.0 (6.7-13.3) in the SB group and 3.9 (1.1-6.6) in the placebo group (P<0.01). An increase in CPRS symptoms at withdrawal was noted in the SB group. In conclusion, treatment with staphylococcus toxoid injections over 6 months led to significant improvement in patients with FM and CFS. Maintenance treatment is required to prevent relapse.Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12413434
Challenges to conventional thinking about mind and body
‘‘When an ordinary person is contacted by a painful feeling, he feels two feelings — a bodily one and a mental one’’
Challenges to conventional thinking about mind and body
Paul Grossman, Freiburg Institute for Mindfulness Research, Konradstrasse 32, 79100, Freiburg, Germany - E-mail address : BreathingSpace@t-online.de - Journal of Psychosomatic Research 55 (2003) 491–492 - D 2003 Elsevier Inc.
The notion that physical symptoms of sane individuals may sometimes bear little or no relationship to measurable physiological functioning is counterintuitive to most us, whether we are lay people, psychologists, physicians or even psychosomatic experts. Such an idea profoundly violates nearly everyone’s ordinary view of reality and challenges our sense of safety in the world : if we cannot trust those filtered cortical transmissions telling us that something is happening to our body, what can we believe ?
If our bodily perceptions are so error-prone, how do we know when we ought to be truly alarmed by somatic symptoms ? If we possess a nervous or fearful disposition, does this mean we are doomed to ‘invent’ or ‘amplify’ physical symptoms and are even more unable than less anxious types to distinguish between genuine physiological alterations and misperceptions ?
Precisely, these kinds of issues are raised by the research in this issue by Houtveen et al.
The authors report that the extent of self-rated somatic symptoms during mental stress and CO2 rebreathing was generally unrelated to a variety of cardiovascular, autonomic and ventilatory measures, but it was, on the other hand, strongly and positively associated with trait anxiety and a history of physical complaints.
These findings correspond to a number of studies that have found no exaggerated physiological reactivity to relevant laboratory stressors among individuals marked by a heightened proclivity to physical complaints and/or chronic anxiety. However, it remains unclear why still other investigations of anxiety accompanied by extreme physical symptoms, as in panic disorder, sometimes do find concurrent evidence of atypical physiological levels or reactivity.
Do these other findings represent real distinctions between normal individuals and patients with distinct types of anxiety disorder, as suggested by differences in laboratory studies of cardiovascular autonomic control between panic patients and normal controls (e.g., Ref. ) or by Klein’s suffocation alarm theory of panic disorder  in which impaired central regulation of respiration is proposed as a primary cause of the disorder ? Or could it merely be that most studies have taken place not in the real world, but in a laboratory environment, often without sufficient time for subjects to adapt themselves to the unfamiliar setting and physiological measurement devices.
One might reasonably assume that particularly under nonadapted conditions, chronically anxious patients may display greater laboratory physiological responses than nonanxious controls, but that these variations may not necessarily reflect real-life, neurophysiological differences between the groups, as so often suggested in the literature.
Regarding panic disorder, such laboratory specificity of response is supported by several studies : for example, Stein and Asmundson [3,4] found no autonomic or cardiovascular differences during rest or challenge between panic patients and controls after they employed an extended acclimatization phase. An ambulatory study of panic disorder patients and healthy controls also found no differences in cardiac activity between groups under reallife conditions . Still other research reviewed by Houtveen et al. indicates that even under typical laboratory conditions, highly relevant stressors, such as public speaking, often produce no exaggerated physiological reactions among social phobics, although somatic symptom reporting and anxiety are greatly elevated. Furthermore, even when we consider those publications where differences between patient and control groups are reported, there are always large proportions of the patient groups who produce no atypical physiological baseline levels or reactions to stressors, although subjective reports of physical symptoms and anxiety are consistently elevated among these patients. When such diverse evidence is considered, incongruence between physiology and experience of anxiety and somatic complaints seems very credible.
But how can we understand this lack of concordance between physiology and symptomatology ?
In general, the literature has primarily focused upon the cognitive–behavioral explanation that chronically anxious individuals manifest a tendency toward increased attention to and amplification of bodily symptoms related to consequences of negative, often catastrophic appraisal of somatic sensations. However, equally plausible is the possibility that states of anxiety actually alter the central nervous system circuitry so that visceral perceptions are, indeed, more unpleasant or painful. Subsequent negative appraisal and aversive responses to bodily sensation may be epiphenomenal to this altered central processing of somatic sensation. Increasing support for this second hypothesis has been gathered by imaging and pharmacological studies in recent years, especially by investigations examining relations between pain and anxiety.
Interactions between serotonergic and endorphinic systems and chemical–perceptual mapping of cortical regions, provide evidence of central links between anxiety and interoceptive experience [6,7]. Also, emotion-related limbic functioning has been tied to central sensory up-regulation  and specific hippocampal networks that exacerbate pain under anxiety-provoking conditions have been identified .
These are just a few examples of the growing body of evidence that indicate that the experience of unpleasant or painful bodily sensations does, in fact, reflect accurate perception during anxious times, despite the lack of heightened peripheral physiological activity.
Should such an intimate connectedness of emotion and somatic experience continue to be supported by future investigation, we may need to rethink current ideas about mind–body relations. At least in terms of interpreting subjective experience of psyche and soma, it may be useful to reexamine pre-Cartesian, even ancient Buddhist views of an inseparable mind/body, in which emotional state (among other things) centrally conditions our every perception. For example, the simple wisdom : ‘‘When an ordinary person is contacted by a painful feeling, he feels two feelings — a bodily one and a mental one’’ . In this light, one may gain courage to attempt to answer the questions posed at the beginning of this commentary : unpleasant somatic symptoms may always tell us something is awry, but only sometimes is peripheral physiological functioning the problem.
Paying close and impartial attention to our bodies during emotional states may also teach us that we store much of our emotional dysphoria in our bodily sensations, even if these sensations are mainly located at the top of our heads : we ought not to forget that physical symptoms constitute major diagnostic criteria for almost all clinical psychiatric disorders and these symptoms are rarely accompanied by convincing evidence of actual physiological dysfunction. Studies like that of Houtveen et al. force us to step out of our perhaps dated scientific paradigms and consider other ways of understanding the embodied mind.
Psychophysiological response patterns in panic disorder Hoehn-Saric R, McLeod DR, Zimmerli WD, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 - Acta Psychiatr Scand. 1991 Jan;83(1):4-11 - PMID: 2011954 To determine whether panic disorder patients exhibit physiological hyperarousal during rest or during mild, non-panic-inducing stress, 18 patients who experienced frequent panic attacks were compared with nonanxious controls on a battery of physiological assessments. During baseline, patients with panic disorder exhibited higher forehead electromyographic activity, higher systolic blood pressure and higher heart rates than non-anxious volunteers. During psychological stress, heart rate and systolic blood pressure rose more in patients with panic disorder than in nonanxious controls. The skin conductance response, however, was greater and more variable in the nonanxious controls. The results suggest that panic disorder patients with frequent panic attacks exhibit heightened cardiovascular arousal and decreased electrodermal flexibility than nonanxious people, even in nonthreatening situations. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2011954
Autonomic function in panic disorder - Cardiorespiratory and plasma catecholamine responsivity to multiple challenges of the autonomic nervous system Presented in part at the 1992 Annual Meeting of the American College of Neuropsychopharmacology, San Juan, Puerto Rico, December 16, 1992 and at the 48th Annual Meeting of the Society for Biological Psychiatry, San Francisco, CA, May 20, 1993 Murray B. Steinab, Gordon J.C. Asmundsonab – a From the Anxiety Disorders Research Program, Department of Psychiatry, University of Manitoba, Winnipeg, Manitoba, Canada – b Department of Pharmacology, University of Manitoba, Winnipeg, Manitoba, Canada - Address reprint requests to : Murray B. Stein, MD, FRCPC, Anxiety & Traumatic Stress Disorders Research Program, Department of Psychiatry, University of California, San Diego Veterans Administration Medical Center, 3350 La Jolla Village Drive, San Diego, California 92161, USA - Biol Psychiatry 1994;Volume 36, Issue 8, Pages 548-558 (15 October 1994) We are grateful to Mariette J. Chartier, RN, BSc, for help in conducting the autonomic function studies, to Thomas W. Millar BSc(Eng) for his development of the data acquisition and reduction software, to Ken Dhalla and Dr. Naranjan S. Dhalla for providing the catecholamine assays, to Doug Tataryn, PhD for his assistance with data analysis and to Anjala Bharadwaj for her help in setting up and piloting the autonomic testing procedures. We are also indebted to Meir H. Kryger, MD for the use of his clinical laboratory facilities. This investigation was supported in part by grant MA-11344 (to MBS) and a Scholarship Award (to MBS) both from the Medical Research Council of Canada and a Postdoctoral Fellowship Award (to GJGA) from the Manitoba Health Research Council. Panic disorder has been widely hypothesized to be associated with dysfunction of the autonomic nervous system. In this study, 24 patients with panic disorder and 26 healthy control subjects took part in a broad battery of autonomic function tests, each designed to stress the autonomic nervous system in a particular fashion. Testing consisted of postural challenge, isometric exercise, cold pressor and Valsalva maneuver. Dependent measures included heart rate, vagal tone, blood pressure, respiratory frequency, end-tidal CO2 levels and plasma norepinephrine and epinephrine levels. The testing procedures reliably produced changes in autonomic output in the expected directions, but patients with panic disorder were not found to differ from healthy controls in their cardiorespiratory or plasma catecholaminergic responses. This pattern of normal autonomic responsivity in the patients with panic disorder was evident across multiple test conditions with varying autonomic demand characteristics, thereby supporting the integrity of autonomic regulatory systems in this illness. These data run counter to a simple notion of autonomic dysfunction in panic disorder. Cfr. : http://www.journals.elsevierhealth.com/periodicals/bps/article/PII000632239490619X/abstract
Vagal attenuation in panic disorder - An assessment of parasympathetic nervous system function and subjective reactivity to respiratory manipulations Asmundson GJ, Stein MB, Department of Psychiatry, University of Manitoba, Winnipeg, Canada - Psychosom Med. 1994 May-Jun;56(3):187-93 - PMID: 8084962 We examined the effects of hyperventilation and other manipulations of respiratory pace on parasympathetic nervous system function and subjective reactivity in 15 patients with panic disorder, 15 patients with social phobia and 15 healthy control subjects. After a 30-minute rest period subjects completed a 2.5-minute trial of each of hypoventilation, normoventilation and hyperventilation. Trials were separated by a 3 minute inter-trial interval. Incidence of panic attacks, symptom severity, vagal tone, heart rate, end-tidal carbon dioxide level and respiratory frequency were measured throughout. Resting physiological measures did not differ between groups. Each respiratory manipulation resulted in the expected physiological changes (e.g., hyperventilation attenuated vagal tone), however, groups did not exhibit differential physiological reactivity to the manipulations. There were no panic attacks reported during either the hypoventilation or normoventilation phases; however, two social phobic subjects (13.3%) and two panic disorder patients (13.3%) reported panic attacks during hyperventilation. Although both groups of anxiety patients reported greater severity of hyperventilation-induced symptoms than did control subjects, symptom severity did not correlate significantly with vagal tone or heart rate. These results suggest that parasympathetic function is unlikely to be aberrant in PD patients and that diminished parasympathetic activity is not sufficient for the experience of panic attacks. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8084962 -&- http://www.psychosomaticmedicine.org/cgi/content/abstract/56/3/187 Also read the comment on this article : Inferring vagal tone from heart rate variability Jennings JR, McKnight JD - Psychosom Med. 1994 May-Jun;56(3):194-6 - PMID: 8084963 Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/8084963?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract
Motor activity and tonic heart rate in panic disorder Clark DB, Taylor CB, Hayward C, King R, Margraf J, Ehlers A, Roth WT, Agras WS, Western Psychiatric Institute and Clinic, University of Pittsburgh, PA 15213 - Psychiatry Res. 1990 Apr;32(1):45-53 - PMID: 2349312 Motor activity and tonic heart rate were monitored in 62 drug-free panic disorder patients and 40 normal control subjects. Mean daily activity, mean waking heart rate controlled for activity and mean sleeping heart rate were determined. Panic disorder patients without phobic avoidance showed higher activity than control subjects or patients with limited or extensive avoidance. Similarly, an "inverted U", relationship between trait anxiety and activity was observed. On the other hand, neither mean waking nor sleeping heart rate showed significant differences between patients and controls, suggesting that the differences previously reported in laboratory studies result from anticipatory anxiety. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/2349312?dopt=Abstract
Brain chemistry reflects dual states of pain and anxiety in chronic low back pain Grachev ID, Fredrickson BE, Apkarian AV, Department of Anesthesiology, SUNY Upstate Medical University, Syracuse, NY, USA : firstname.lastname@example.org - J Neural Transm. 2002 Oct;109(10):1309-34 - PMID: 12373563 The neurobiology of the interaction between pain and anxiety is unknown. The present study examined interrelationships between : regional brain chemistry (as identified by in vivo proton magnetic resonance spectroscopy [(1)H-MRS] in dorsolateral prefrontal cortex [DLPFC], orbitofrontal cortex [OFC], cingulate and thalamus), pain (as measured by short form of the McGill Pain Questionnaire [SF-MPQ]) and anxiety (measured by the State-Trait Anxiety Inventory) in chronic low back pain (CLBP) patients and contrasted to the relationship between brain chemistry and anxiety in sex and age-matched normal subjects. The results show that brain chemistry depends on a 3-way interaction of brain regions examined, subject groups (normal vs. CLBP) and anxiety levels (high vs. low). The concentration of N-Acetyl aspartate (the largest peak in (1)H-MRS) in OFC could distinguish between anxiety levels and between subject groups. Chemical-perceptual relationships were analyzed by calculating correlations between regional chemicals and perceptual measures of pain and anxiety. To isolate pain from anxiety, these maps were subdivided based on anxiety and, in the CLBP patients along anxiety-more-related vs. anxiety-less-related pain descriptors and along sensory vs. affective pain descriptors. There was a precise relationship between perception and brain chemistry. The chemical-perceptual network best related to pain in CLBP patients was comprised of the DLPFC and OFC; the chemical-anxiety network was best related to the OFC chemistry in normals and to all four regions studied in CLBP patients; and the cingulate was best related to the affective component of pain. We conclude that the chemical-perceptual mapping differentiates between closely related perceptual states of pain and anxiety in chronic pain and provides a brain regional-chemical-perceptual description of the long-term reorganization that occurs with chronic pain. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12373563
Serotonin-mediated increases in the extracellular levels of beta-endorphin in the arcuate nucleus and nucleus accumbens - A microdialysis study Zangen A, Nakash R, Yadid G, Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel - J Neurochem. 1999 Dec;73(6):2569-74 - PMID: 10582620 Although the involvement of both endogenous opioid and serotonergic systems in modulation of pain and emotion was suggested, the neurochemical interaction between these systems in the brain has not previously been studied directly. Herein, the effects of the local application of serotonin (5-HT) and fluoxetine (a 5-HT reuptake inhibitor) on extracellular levels of beta-endorphin in the arcuate nucleus and nucleus accumbens were assessed in freely moving rats using in vivo microdialysis. The mean basal concentrations of beta-endorphin in dialysates obtained from the arcuate nucleus and nucleus accumbens were 259.9 and 143.3 pM, respectively. Specific lesion of the serotonergic system by 5,7-dihydroxytryptamine (5,7-DHT) caused a significant decrease in these dialysate beta-endorphin levels. When 5-HT (0.25-5 microM) was added to the perfusion solution, the levels of beta-endorphin in the dialysate from the arcuate nucleus increased (186-296% of baseline), in a concentration-dependent manner. In the nucleus accumbens, 0.5 and 2 microM 5-HT in the perfusion fluid did not affect the levels of beta-endorphin in the dialysate, whereas 5 and 10 microM 5-HT caused an increase of approximately 190% of baseline. When fluoxetine (250 microM) was present in the perfusing solution, the levels of beta-endorphin in the dialysates from the arcuate nucleus and nucleus accumbens increased two- to threefold. This effect was not obtained in the 5,7-DHT-lesioned rats. Thus, 5-HT, either endogenously or exogenously delivered, appears to facilitate the release of beta-endorphin in the arcuate nucleus and nucleus accumbens. This indication of an interaction between serotonergic and endorphinic systems may be relevant for assessing pain and mood disorder circuits and the mode of action of antidepressant drugs. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/10582620
Role of the brain and sensory pathways in gastrointestinal sensory disorders in humans Mertz H, Vanderbilt University Medical Center, Nashville 37232-5340, USA : howard.Mertz@mcmail.vanderbilt.edu - Gut. 2002 Jul;51 Suppl 1:i29-33 - PMID: 12077061 Several features of the irritable bowel syndrome (IBS) suggest involvement of the emotional limbic system in the brain. Abnormalities which upregulate afferent (sensory) signal intensity anywhere in this system, from the gastrointestinal tract to the brain, could induce hypersensitivity, leading to the pain and discomfort that characterise IBS and other functional disorders. Functional gastrointestinal disorders are likely to be heterogeneous given the complexity of the afferent system and a number of different perturbations are possible. Intestinal hypersensitivity to pain and discomfort and associated reflex alterations in motility might explain the symptoms of functional bowel diseases. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12077061
Role of the brain and sensory pathways in gastrointestinal sensory disorders in humans Mertz H, Vanderbilt University Medical Center, Nashville 37232-5340, USA : howard.Mertz@mcmail.vanderbilt.edu - Gut. 2002 Jul;51 Suppl 1:i29-33 - PMID: 12077061 Several features of the irritable bowel syndrome (IBS) suggest involvement of the emotional limbic system in the brain. Abnormalities which upregulate afferent (sensory) signal intensity anywhere in this system, from the gastrointestinal tract to the brain, could induce hypersensitivity, leading to the pain and discomfort that characterise IBS and other functional disorders. Functional gastrointestinal disorders are likely to be heterogeneous given the complexity of the afferent system and a number of different perturbations are possible. Intestinal hypersensitivity to pain and discomfort and associated reflex alterations in motility might explain the symptoms of functional bowel diseases. Cfr. : http://www.ncbi.nlm.nih.gov/pubmed/12077061
The Connected Discourses of the Buddha – A Translation of the Samyutta Nikay Bikkhu Bodhi - Wisdom Publications (2nd edition), September 25, 2002 - ISBN-10: 0861713311 - ISBN-13: 978-0861713318 This is a complete translation of the Samyutta Nikaya, containing all of the important suttas ('Discourses of the Buddha') on such key Buddhist concepts as the Four Noble Truths, dependent origination, the seven factors of enlightenment and the Noble Eightfold Path. 'The Connected Discourses of the Buddha' ranks as one of the most inspiring compilations in the Buddhist canon. Bhikkhu Bodhi's distinguished and precise translation, his insightful introductory materials and his extensive notes guide the reader through this vast collection of the Buddha's ancient teachings. This is the third title in Wisdom Publications' award-winning Teachings of the Buddha Series, following 'The Long Discourses of the Buddha' and 'The Middle Length Discourses of the Buddha'. Like its two predecessors and 2005's anthology of 'Discourses of the Buddha', this volume belongs in the library of every student of Buddhism Cfr. : http://www.amazon.com/Connected-Discourses-Buddha-Translation-Samyutta/dp/0861713311