FM research: Collagen structure in skin

Discussion in 'Fibromyalgia Main Forum' started by tansy, Dec 30, 2005.

  1. tansy

    tansy New Member

    from fibromyalgia patients.

    Int J Tissue React. 2005;27(3):75-82.

    Ribel-Madsen S, Gronemann ST, Bartels EM, Danneskiold-Samsoe B, Bliddal H.

    The Parker Institute, Department of Rheumatology, Frederiksberg Hospital,
    H:S University Hospital, Denmark. [log in to unmask]

    PMID: 16372472

    The distribution and amount of collagen in skin from a non-tender-point
    area from fibromyalgia patients was assessed by quantitative analysis of
    amino acids and by electron and light microscopy. Skin biopsies were
    obtained from the front of the thigh of 27 females who fulfilled the
    American College of Rheumatology criteria of fibromyalgia and from eight
    control subjects who were matched for gender, age and physical activity.
    Amino acids were determined by high-performance liquid chromatography.
    Electron and light microscopic investigations were carried out to examine
    tissue structure.

    Among the collagen-related amino acids, the mean number of hydroxyproline
    residues per 1,000 residues was 52.5 and 63.4 in fibromyalgia patients and
    control subjects, respectively (p = 0.050); proline residues were 81.7 and
    110.0 (p = 0.006); and hydroxylysine residues were 14.7 and 10.1 (p =
    0.002). The total amount of skin protein in proportion to dry tissue weight
    was 83.4% and 72.6% in fibromyalgia and controls, respectively (p = 0.037).
    The overall microscopic picture was normal. The lamellar structure of the
    perineurium and a deficiency in collagen packing in the endoneurium was
    observed more frequently and to a larger extent in fibromyalgia patients
    than in controls.

    In conclusion, there are some differences between the amino acid
    composition of skin proteins in fibromyalgia patients compared with
    controls. The amount of collagen may be lower in skin from fibromyalgia
    patients, and collagen packing in the endoneurium may be less dense.
  2. Cromwell

    Cromwell New Member

    ....maybe this is why I don't seem to have much in my face and get wrinkles easily/!!!!! Interesting report though, thanks!

  3. tansy

    tansy New Member

    in various research projects in ME/CFS and FM. Hereditary hypermobility syndromes are present in a significant % with FM and some with ME/CFS, they are just a few of the connective tissue disorders found in people with these DDs.

    When we look at what is being reported by posters here we can see conditions and skeletal problems related to low levels of collagen.


  4. tansy

    tansy New Member

    who's 3 years younger than I said that's why her face is showing her age. She too has a hypermobility syndrome and was born with a dislocated hip, another classic sign. The incidence on my mothers side is high, 50% and 66.6% per generation.

    Adrenal and thryoid problems can have an adverse effect upon collagen leading to increased wrinkles and loose skin. Low oestrogen can contribute to low collagen levels, this led to HRT being used to help prevent the outwards signs of ageing like wrinkles.

    love, Tansy[This Message was Edited on 12/30/2005]
  5. tansy

    tansy New Member

    that these DDs can accelerate ageing; that's why many benefit from dietary changes, supps, herbs etc that are recommended to address the adverse effects of ageing. These DDs feature high levels of oxidative stress; these contribute to the ageing process.

    We had a family get together on the 27th; my sister and SIL (a GP) commented that I looked younger than I did last year. It may just be that I am getting more restorative sleep now, but even so I have no doubt my mostly self prescribed Tx are having a positive global effect.

    love, Tansy
  6. tansy

    tansy New Member

    Collagen and muscle pathology in fibromyalgia patients.

    Rheumatology (Oxford). 2003 Jul 16 [Epub ahead of print].

    Gronemann ST, Ribel-Madsen S, Bartels EM, Danneskiold-Samsoe B, Bliddal H.

    The Parker Institute, Department of Rheumatology, Frederiksberg Hospital,
    H:S University Hospital.

    PMID: 12867573

    OBJECTIVE: To measure collagen concentration and search for muscle
    pathology in muscle non-tender-point areas from fibromyalgia (FM) patients.

    METHODS: Muscle biopsies were obtained from m. vastus lateralis of 27
    carefully selected, female fibromyalgia patients, and from eight
    age-matched female control subjects. Amino acids were determined by HPLC
    and electron microscopy was performed.

    RESULTS: The FM patients had lower hydroxyproline and lower total
    concentration of the major amino acids of collagen than the controls. No
    significant difference was seen in the concentration of the major amino
    acids of myosin or of total protein. Electron microscopy showed no
    significant differences between FM patients and controls although atrophied
    muscle fibrils occurred in FM patients only, but frequencies were not
    significantly different.

    CONCLUSION: Fibromyalgia patients had a significantly lower amount of
    intramuscular collagen. This may lower the threshold for muscle
    micro-injury and thereby result in non-specific signs of muscle pathology.


    Collagen crosslinks in fibromyalgia.

    Sprott H, Muller A, Heine H.

    University of Jena, Germany.

    OBJECTIVE: To determine if abnormal collagen metabolism is a characteristic of fibromyalgia.

    METHODS: The diagnosis of fibromyalgia was made according to the American College of Rheumatology criteria. Skin biopsy samples were obtained from the trapezius region of 8 patients with fibromyalgia. Urine was collected under standardized conditions from 55 control subjects and 39 patients with fibromyalgia, and serum was obtained from 17 controls and 22 patients with fibromyalgia. Pyridinoline (Pyd), an indicator of connective tissue disease, and deoxypyridinoline (Dpyd), an indicator of bone degradation, both of which represent products of lysyl oxidase-mediated crosslinking in collagen, were analyzed by ion-paired and gradient high-performance liquid chromatography (HPLC) methods with fluorescence detection. Levels of hydroxyproline (Hyp), a collagen turnover marker, were also measured. The findings were related to creatinine levels, and the Pyd:Dpyd ratio was determined.

    RESULTS: Highly ordered cuffs of collagen were observed around the terminal nerve fibers by electron microscopic examination of biopsy tissue from all 8 patients with fibromyalgia, but were not observed in any of the control skin samples. The Pyd:Dpyd ratios in the urine and serum and the Hyp levels in the urine were significantly lower in patients with fibromyalgia than in healthy controls.

    CONCLUSION: Decreased levels of collagen crosslinking in fibromyalgia may contribute to remodeling of the extracellular matrix and collagen deposition around the nerve fibers, and may contribute to the lower pain threshold at the tender points. Analysis of altered collagen metabolism either by histologic examination on biopsy, or preferably, by HPLC analysis of collagen metabolites in urine or serum may aid in understanding more about the pathogenesis of fibromyalgia.

    PMID: 9259425 [PubMed - indexed for MEDLINE] [This Message was Edited on 12/30/2005]
  7. tansy

    tansy New Member

    extract from an article on the how stuff works web site

    **here is a list of the five types of collagen, and where they are used in the body.

    Type 1 - Connective tissue of skin, bone, teeth, tendons, ligaments, fascia, organ capsules

    Type 2 - Cartilage

    Type 3 - Connective tissue of our organs (liver, spleen, kidneys, etc.)

    Type 4, 5 - The separating layer between epithelial and endothelial cells as well as between skeletal or smooth muscle cells (basal lamina), kidney glomeruli, lens capsule, and Schwann and glial cells of the nervous system.

    As you can see, collagen is everywhere in the body, and vitamin C plays a role in the formation of collagen. So, how is vitamin C involved in collagen synthesis?

    When collagen is produced, there is a complex series of events, some occurring inside of the cell, and some outside of the cell. Vitamin C is active inside of the cell, where it hydroxylates (adds hydrogen and oxygen) to two amino acids: proline and lysine. This helps form a precursor molecule called procollagen that is later packaged and modified into collagen outside of the cell. Without vitamin C, collagen formation is disrupted, causing a wide variety of problems throughout the body.**
  8. tansy

    tansy New Member

    Extract from another web site

    **Beneficial omega-3 fatty acids in fish may play a role in the healing process by conferring an anti-inflammatory effect, which may soothe discomfort from swelling in joints.

    Laboratory studies indicate that omega-3 fatty acids may increase healing of ligaments injured by sprains by accelerating the entry of new cells into the damaged area and speeding up collagen synthesis.

    Fish are a natural source of vitamin D, which is required by the body for calcium absorption and is also needed for the maintenance of healthy cartilage and bones.**
  9. tansy

    tansy New Member

    From the body and fitness web site

    Grape seeds are the primary commercial source of a group of antioxidant, collagen-protective pigments called oligomeric proanthocyanidins (OPCs or PCO), which are concentrated in pine bark and grapes. OPCs and related phenolic flavonols are also found in berries, blackcurrant, green tea, black tea, and many other plants.

    Traditional use

    There are no traditional medicinal uses of OPCs, except to the extent that berries, grapes, and other food sources have been perceived as generally healthful.

    Modern perspective

    For more than 50 years, European biochemists have been conducting research into OPCs, which are also generically termed pycnogenol. (When capitalized, the term Pycnogenol refers to a patented pine bark extract.) Supplemental OPCs are used in Europe to treat weak blood capillaries (chronic venous insufficiency), post-surgical edema (swelling), cirrhosis, varicose veins and diabetic retinopathy.

    OPCs restore the antioxidant function of vitamin C molecules worn out by their free radical scavenging activities. In one experiment, OPCs boosted vitamin C activity by 1,000%. Test tube studies indicate that OPCs are 18 times more effective than vitamin C, and 50 times more potent than Vitamin E, for neutralizing free oxygen radicals.

    OPCs’ anti-inflammatory properties have been proved in laboratory studies on test animals and in human clinical trials involving sports injuries and post-surgical recovery. Given their mode of anti-inflammatory action and affinity for collagen, OPCs may be useful in reducing rheumatic inflammations.

    OPCs promote healthy cartilage by normalizing "collagen cross-linkage." Collagen consists of twin, ladder-like spirals of proteins connected by step-like cross links. In osteoarthritis and rheumatoid arthritis, excess cross-linkage is caused by internal production of excess free radicals, and release of excess amounts of collagenase enzyme.

    Daily requirement

    Flavonols, including grape seed OPCs and green tea catechins, are not classified as essential nutrients, since their absence does not produce a deficiency state. However, OPCs may have many health benefits, and anyone not eating a wide variety of plants will not derive these benefits.
    Medically, OPCs are usually prescribed at a dosage level of 300 mg per day, and a reasonable preventive health regimen would range from 50 to 100 mg per day.

    Types of products: Currently, pine bark extracts rich in OPCs (i.e., Pycnogenol) dominate the U.S. market. But grape skin/seed extracts contain equivalent amounts, including a unique antioxidant (B2-3’-o-gallate) that makes them a more desirable source of OPCs. Most research has been done on grape skin/seed extract, and it is less expensive.

    OPCs are reported to produce better antioxidant effects in body tissues when packaged in a patented chemical envelope called a phytosome. OPC phytosomes may be twice as effective as straight OPC extract, but this enhanced efficiency per milligram must be weighed against the cost differential.

    Facts About Grape Seed and Aging

    Grape Seed Extract contains oligomeric proanthocyanidins (OPCs) which are a class of flavonoids (water-soluble compounds) found in a wide variety of plants. OPCs have powerful antioxidant activity and destroy free radicals.* Free radicals are highly reactive compounds generated by air pollution, cigarette smoke and many other sources and also naturally-occurring in the body.* Free radicals can damage fats, protein, and DNA in the body disturbing normal function in the process.*26

    Collagen and elastin are critical structural proteins in connective tissue, blood vessels, and muscle. OPCs help maintain healthy collagen and elastin and contribute to the integrity and strength of blood vessels and capillaries.*32, 28 OPCs inhibit potentially harmful enzymes, such as hyaluronidase and histidine decarboxylase, which are implicated in the breakdown of muscle fiber and the release of histamine in the inflammation process.*33 OPCs also inhibit several glycosidases and glucosidases, enzymes which help break down synovial fluid in the joints.*27 This ability to inhibit these destructive enzymes helps to reduce the body's natural inflammatory response.*28

    The abnormal accumulation of fluid in the body's tissues can result from malfunction of the capillaries (the smallest of the blood vessels).* Grape seed extract supports normal circulation in the veins, according to human clinical trials.*29 Other human research adds evidence that OPCs strengthen the capillaries when compared to placebo. *30 Animal research reinforces the idea that grape seed extract inhibits fluid accumulation by preventing abnormal capillary permeability.*31 According to preliminary laboratory research, grape seed extract has been shown to inhibit the binding of cholesterol to blood vessel walls.*32

    Recent findings

    In test tube and animal experiments published in 1998, which compared grape seed proanthocyanidin extract (GSPE) to vitamin C, Vitamin E succinate and beta carotene (Bagchi D et al.), GSPE showed significantly more antioxidant activity—results consistent with and expanding upon earlier experiments (see Abstract, below).

    A large body of research documents the antioxidant abilities of flavonoids in general,*23 while a growing number of studies have focused exclusively on OPCs. Research shows that grape seed extract inhibits the formation of free radicals and neutralizes existing free radicals.*23 In fact, one study found grape seed extract to have a stronger antioxidant effect than vitamin E.*24 An animal experiment validates this antioxidant capability of OPCs by suggesting that it is equivalent to vitamin E for preventing lipid peroxidation of liver cells.*25


    Flavonols, including proanthocyanidins, are free of side effects. As water-soluble nutrients, unusable excess intake is eliminated through urination.

    Authors: Bagchi D et al.

    Title: Protective effects of grape seed proanthocyanidins and selected antioxidants against TPA-induced hepatic and brain lipid peroxidation and DNA fragmentation, and peritoneal macrophage activation in mice.
    Source: Gen Pharmacol 1998 May;30(5):771-6.

    Treatment of mice with GSPE (100 mg/kg), vitamin C, VES and beta-carotene decreased TPA-induced production of reactive oxygen species, as evidenced by decreases in the chemiluminescence response in peritoneal macrophages by approximately 70%, 18%, 47% and 16%, respectively, and cytochrome c reduction by approximately 65%, 15%, 37% and 19%, respectively, compared with controls. 3. GSPE, vitamin C, VES and beta-carotene decreased TPA-induced DNA fragmentation by approximately 47%, 10%, 30% and 11%, respectively, in the hepatic tissues, and 50%, 14%, 31% and 11%, respectively, in the brain tissues, at the doses that were used. Similar results were observed with respect to lipid peroxidation in hepatic mitochondria and microsomes and in brain homogenates. 4. GSPE exhibited a dose-dependent inhibition of TPA-induced lipid peroxidation and DNA fragmentation in liver and brain, as well as a dose-dependent inhibition of TPA- induced reactive oxygen species production in peritoneal macrophages. 5. GSPE and other antioxidants provided significant protection against TPA-induced oxidative damage, with GSPE providing better protection than did other antioxidants at the doses that were employed.


    Bagchi D et al. Protective effects of grape seed proanthocyanidins and selected antioxidants against TPA-induced hepatic and brain lipid peroxidation and DNA fragmentation, and peritoneal macrophage activation in mice. Gen Pharmacol 1998 May;30(5):771-6.
    Bagchi D et al. Oxygen free radical scavenging abilities of vitamins C and E, and a grape seed proanthocyanidin extract in vitro. Res Commun Mol Pathol Pharmacol 1997 Feb;95(2):179-89.
    Mitcheva M, et al. Biochemical and morphological studies on the effects of anthocyans and vitamin E on carbon tetrachloride induced liver injury. Cell Mol Bio 1993;39(4):443-8.
    Maffei F. et al. Free radical scavenging action and anti-enzyme activities of procyanidines from Vitis vinifera. A mechanism for their capillary protective action. Arzn Forsch 1994;44:592-601.
    Gabor M, Razga Z. Effect of benzopyrone derivatives on simultaneously induced croton oil ear oedema and carrageenin paw oedema in rats. Acta Physiol Hung 1991;77(3-4):197-207.
    Dubos G, et al. La Revue de la Gériatrie, Tome 5, no. 6, September 1980 — Schwitters p. 112;
    Beylot C, et al. Gaz Med de France - 87, no. 22, June 13, 1980.
    Pfister A, et al. Acta Therapeutica no. 8, 1982.
    Masquelier J, et al. Acta Therapeutica no. 7, 1981 101-105.
    Tixier, JM, et al. Laboratoire de Biochimie du Tissue Connectif, Univ of Paris, June 25, 1984.
    Kuttan, R, et al. Collagen treated with (+) catechin becomes resistant to the action of mammalian collagenases. Experientia 37, 1981, Berhauser Verlag, Basel, Switzerland.
    Tixier, JM, et al. Laboratoire de Biochimie du Tissue Connectif, Univ of Paris, June 25, 1984.
    Kakegawa, et al, Inhibitory effects of tannins on hyaluronidase activation and on the degranulation from rat mesentry mast cells. Chem Pharm Bulletin, 33(11)5079-3082, 1985.
    Mori, et al. Med Sci Res 1987, 15, 831-2.
    US Patent # 4,698, 360. Oct 6, 1987.
    Masquelier J, Michaud J, Laparra J, Dumon MC. [Flavonoids and pycnogenols]. Int J Vitam Nutr Res 1979;49(3):307-11 [Article in French]
    Laparra, et al, Travaux originaux, Université de Bordeaux, 1976.
    Parienti J, et al. Means of controlling post traumatic edema in sports injuries with l’Endotélon [OPCS]. Gaz Med de France - 90, No. 3, Jan 21, 1983.
    " Pycnogenols: Recent Advances in the Therapeutical Actitivy of Procyanidins," by Prof. Jacques Masquelier, Hyppocrates Verlag, 1981.
    Blaszo G, Gabor, M. Edema-inhibiting effect of procyanidin. Acta Physiologica Academiae Hungaricae, Tomus 65 (2), 235-240,1985.
    Kakegawa, et al, Inhibitory effects of tannins on hyaluronidase activation and on the degranulation from rat mesentry mast cells. Chem Pharm Bulletin, 33(11)5079-3082, 1985.
    Bombardelli E, et al. Botanical derivatives in functional cosmetics. Drug Cosmet Ind 1994, (155) 44-51.
    Rice-Evans CA and Miller NJ. Antioxidant activities of flavonoids as bioactive components of food. Biochem Soc Trans 1996;24:790-795.
    Maffei F, Facino R, Carinin M, et al. Free radicals scavenging action and anti-enzyme activities of procyanidines from Vitis vinifera. A mechanism for their capillary protective action. Arzn Forsch 1994;44(5):592- 601
    Mitcheva M, Astroug H, Drenska D, et al. Biochemical and morphological studies on the effects of anthocyans and vitamin E on carbon tetrachloride induced liver injury. Cell Mol Bio 1993;39(4):443-8
    Ames BN, Shigenaga MK, and Hagen TM. Oxidants, antioxidants, and the degenerative diseases of aging. Proc Natl Acad Sci USA 1993;90:7915-1922
    Jonadet M, et al. Flavonoids extracted from Ribes nigrum L. and Alchemilla vulgaris L.: 1. In vitro inhibitory activities on elastase, trypsin and chymotrypsin. 2. Angioprotective activities compared in vivo. Journal de Pharmacologie 1986;17:21-27
    Delacrois P. Double-blind study of endotelon in chronic venous insufficiency. La Revue de Medecine 1981;27:28-31
    Lagrue G, et al. A study of the effects of procyanidol oligomers on capillary resistance in hypertension and in certain nephropathies. Semaine des Hopitaux 1981;57:33-36
    Zafirov D, et al. Antiexudative and capillaritonic effects of procyanidines isolated from grape seeds (V. vinifera). Acta Phys Pharm Bulg 1990;16(3):50-54
    Wegrowski J, et al. The effect of procyanidolic oligomers on the composition of normal and hypercholesterolemic rabbit aortas. Biochem Pharm 1984;33:3491-3497
    Tixier J, et al. Evidence by in vivo and in vitro studies that binding of pycnogenols to elastin affects its rate of degradation by elastases. Biochem Pharm 1984;33:3933-3939
    Kakegawa H, Matsumoto H, Endo K, et al. Inhibitory effects of tannins on hyaluronidase activation and on the degranulation from rat mesentery mast cells. Chem Pharm Bull 1985;33(11):5079-5082 7. Bombardelli E and Morazzoni P. Vitis vinifera L. Fitoterapia 1995;LXVI(4):291-317
  10. lolee

    lolee New Member

    When I first started this journey it was because I had a +ANA and +RNP, which is indiciative of MCTD (Mixed Connective Tissue Disease) the second set of tests, from a different lab did show high amounts but not "positive".

    MCTD is an overlap of Lupus, Schleroderma (sp?) and Shogruen's (again, sp?)

    The main "thing" was that in MCTD the body produces too much collagen and elastin, (ie: ligament's are collagen) and this creates "fibrodes" in the muscles.

    I further researched and found where you can have high but yet still negative labs in the beginning of this disease, the labs can also be effected by whether or not you are in a flare.

    The rhuemy is the one said he didn't think it was MCTD, was positive it was Fibro. And quite frankly, I hope so. MCTD kills you. Carried THAT around for a month, talk about stress!

  11. Mikie

    Mikie Moderator

    As always, you bring new info for us which is so valuable and interesting. It's good to know that so much research is now being done. These are all pieces of the puzzle which may someday lead to a cure.

    Happy New Year to you.

    Love, Mikie
  12. sydneysider

    sydneysider Member

    I'm interested in this connection.

    A physio told me recently that I am hypermobile. I did some research on the internet and found that if this was so, then I must have a very mild case, as I didn't even come close to the Beiton scale for hypermobility.

    I questioned the physio the next time I saw her about what made her think that I was hypermobile. She pointed out that my thumbs curve backward, and my fingers curve backwards more than normal.

    Due to the fact that this year I was found to have a damaged disk in my neck, plus having a friend who went into hospital for a fibroid operation, later became very sick, and was eventually found to have two slipped disks in the neck+FM, I'm really starting to wander if there's a connection here.

    I'm wandering if some of us have forms of hypermobility that make us suseptible to spinal damage, which triggers the FM.

    Some recent posts on Ehlers-Danlos Syndrome, and also a post on Dr Whitcombe's theory are making me wander even more.
  13. tansy

    tansy New Member

    Having posted this research I felt I should also post more information including non-Rx agents that may help adress problems with collagen. As you know I try to keep my mind on the bigger picture because there are overlaps in these DDs and other chronic illnesses.

    Love, Tansy
  14. tansy

    tansy New Member

    there is a high incidence of inherited hypermobility syndromes in these DDs. There is very likely a connection, I know this problem contributed to my levels of physical disability and pain, it was an unfortunate combo.

    Until I became ill keeping my muscles strong helped, but then my muscles became exercise intolerant. After over 22 years I was finally able to rebuild both muscle bulk and strength in my core, pelvic, and thigh muscles; as a result not only can I sit and stand better but pain from problems in this area is less severe now.

    My neck is another matter though, it may be they left it too long before arranging a MRI, and two of the exercises I was given 14 years ago were making matters worse. I have the classic swan neck found in hypermobility syndromes and other typical signs too.

    Love, Tansy[This Message was Edited on 12/31/2005]
  15. tansy

    tansy New Member

    From the altmedicine about web site

    What is Glucosamine?

    Alternate names: Glucosamine sulfate, Glucosamine hydrochloride, N-acetyl glucosamine.

    Glucosamine is a molecule made of glucose and an amine that is produced naturally in the body. It stimulates cartilage cells to produce two proteins that help to hold joint tissue together, proteoglycans and collagen. It may also prevent the breakdown of collagen.

    As people age, their bodies are less able to produce glucosamine, which results in cartilage being less flexible.
  16. tansy

    tansy New Member

    Hi Nancy

    I have just had some of the scariest days of my illness; the increased almost non stop heart flutters, lack of oxgygen, and dizziness were the worst I'd had. A few nights ago I woke up choking in a way that had never happened before; this time it was very difficult to clear. All triggered by a virus.

    Last week I saw a GP reported my increased dizziness which my PT thought was to do with Tx for my cervical spine and the increased heart flutters since late November. He just reacted as he always used to, in fact the only time his patronising verbal pats on the head stopped was when he asked after my son, they belong to the same rugby club and he'd not seen him there this season.

    Despite all I tried to discuss with him, my son's current problems, and the ground I covered, I might just as well have been talking to a brick wall.

    So last night I sat here wondering whether to go to A&E (ER) or not, realised it was physically beyond me, and knowing the odds are my Dx would mean nothing being checked out I opted to take care of myself.

    Today things are better. Turns out sinusisits was part of the problem, but due to having lost all feeling in that area, I had not realised I had it until my son told me the virus going around was causing severe sinusitis and dizziness. Bingo!

    So today it's big doses of vitamin C, OLE, and garlic; I've just ordered some wild oregano oil cos that worked great for my sinuses in the past. This is the first bout of sinusitis I've had since the summer of 2004, so it just did not occur to me. Explains the glued up brain feeling as well.

    In light of past and family problems with hypermobility, the heart, etc I want this checked out, just getting past the barriers is going to need some working out. The ME/CFS and lyme specialist who is treating my infections is well aware of these problems but he's being ignored too. This is why the UKers get so fed up with the all in the mind lobby, my frustrations are far too common here.

    Well that's my 2005 vent over.

    Hope your Xmas was at least as enjoyable as mine was. Happy New Year

    love, Tansy

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