Intestinal Bacteria Found in CFS Patients-article

Discussion in 'Fibromyalgia Main Forum' started by ulala, Jul 2, 2009.

  1. ulala

    ulala New Member

    This article backs up what Dr. Kenny De Meirier has found. He found enterococcus and streptococcus bacteria in stool samples of CFS patients. These doctors have found it in the intestines of CFS samples. Several people on this site have found these bacteria in their stool samples.

    Increased D-Lactic Acid
    Intestinal Bacteria in Patients
    with Chronic Fatigue Syndrome

    1. JOHN R. SHEEDY1,
    4. PAUL R. GOOLEY1,
    5. DONALD P. LEWIS3,
    8. HENRY L. BUTT5 and

    +Author Affiliations

    1 Bio21 Institute of Biotechnology and
    Molecular Science, Department of Biochemistry and
    Molecular Biology, The University of Melbourne,
    Parkville, Victoria

    2 Bio21 Institute of Biotechnology and
    Molecular Science, The University of Melbourne,
    Parkville, Victoria

    3 Donvale Specialist Medical Centre, Donvale,
    Victoria, Australia

    4 Bio21 Institute of Biotechnology and
    Molecular Science, Faculty of Medicine, Dentistry and
    Health Sciences, The University of Melbourne,
    Parkville, Victoria

    5 Bio21 Institute of Biotechnology and
    Molecular Science, Bioscreen, The University of
    Melbourne, Parkville, Victoria

    6 Human Physiology, Faculty LK, Vrije
    Universiteit Brussel, Brussels, Belgium

    1. Correspondence to:
    Kenny L. De Meirleir, Vrije Universiteit Brussel, MFYS,
    Pleinlaan 2, 1050 Brussels, Belgium. e-mail:


    Patients with chronic fatigue syndrome (CFS) are
    affected by symptoms of cognitive dysfunction and
    neurological impairment, the cause of which has yet
    to be elucidated.

    However, these symptoms are strikingly similar to
    those of patients presented with D-lactic acidosis.

    A significant increase of Gram positive facultative
    anaerobic faecal microorganisms in 108 CFS patients
    as compared to 177 control subjects (p<0.01) is
    presented in this report.

    The viable count of D-lactic acid producing
    Enterococcus and Streptococcus spp. in the faecal
    samples from the CFS group (3.5×107 cfu/L and
    9.8×107 cfu/L respectively) were significantly higher
    than those for the control group (5.0×106 cfu/L and
    8.9×104 cfu/L respectively).

    Analysis of exometabolic profiles of Enterococcus
    faecalis and Streptococcus sanguinis, representatives
    of Enterococcus and Streptococcus spp. respectively,
    by NMR and HPLC showed that these organisms
    produced significantly more lactic acid (p<0.01) from
    13C-labeled glucose, than the Gram negative
    Escherichia coli.

    Further, both E. faecalis and S. sanguinis secrete
    more D-lactic acid than E. coli.

    This study suggests a probable link between
    intestinal colonization of Gram positive facultative
    anaerobic D-lactic acid bacteria and symptom
    expressions in a subgroup of patients with CFS.

    Given the fact that this might explain not only
    neurocognitive dysfunction in CFS patients but also
    mitochondrial dysfunction, these findings may have
    important clinical implications.


    * Intestinal bacteria
    * D-lactic acid
    * chronic fatigue syndrome


    o Received July 23, 2008.
    o Revision received March 31, 2009.
    o Accepted April 17, 2009.

    * Copyright © 2009 International Institute of
    Anticaner Research (Dr. John G. Delinassios), All
    rights reserved

  2. ulala

    ulala New Member

    D-lactic acidosis: Turning sugar into acids in the gastrointestinal tract

    Kidney Int (Jan) 49:1-8 1996

    D-lactic acidosis is an uncommon but biochemically fascinating disease process. It is seen almost exclusively in patients following jejunoileal bypass or small bowel resections (and in ruminants), often following the use of antibiotics or a large meal of simple sugars. Halperin and Kamel's review focuses on the specific metabolic pathways and stoichiometry involved in the production and metabolism of various organic acids such as acetic, butyric, propionic and especially L- and D-lactic acids. As these organic acids are produced even in healthy individuals, the normal metabolism of these acids is reviewed. Focus is given to the normal production of butyrate by colonic bacteria and the utilization of this organic acid by the colonic mucosa as a required metabolite.

    Normally only minute amounts of D-lactate are produced endogenously. The abnormal intestinal anatomy in these patients causes undigested sugars to be delivered distally and bacteria to migrate proximally, allowing prolonged contact between the two with consequent fermentation. When overproduction and absorption of D-lactate occurs, metabolic acidosis may be produced associated with an elevation in the anion gap, unless urinary excretion of the D-lactate anion occurs faster than the depleted bicarbonate can be regenerated. In the past it was thought that the limited ability of the enzyme D-2-hydroxyacid dehydrogenase to metabolize D-lactate was an important pathegenic factor in its accumulation. More recent data suggest that D-lactate is metabolized at a significant rate, though only about 1/5th as rapidly as L-lactate (the latter is metabolized by the stereospecific enzyme L-lactate dehydrogenase. Therefore, it is likely that in patients predisposed to developing D-lactic acidosis, it is the marked overproduction of D-lactate rather than limited metabolism which leads to the syndrome of dizziness, confusion and other typical neurological symptoms.

    D-lactate is metabolized in humans to pyruvate which may be metabolized to acetate and then to ATP via oxidative phosphorylation. Free fatty acids exist in serum in inverse proportion to insulin, and compete with pyruvate as substrate for oxidative phosphorylation. Because of this, the authors speculate, though without substantiating evidence, that insulin administration to patients with D-lactate would decrease free fatty acid levels, promoting metabolism of D-lactate.

    Comment: This excellent analysis of D-lactic acidosis emphasizes the biochemistry of intestinal production of organic acids by bacteria and the elimination of D-lactate by metabolism and urinary excretion. Other observers have noted that thiamine deficiency inhibits pyruvate metabolism and causes D-lactate accumulation. Alternative means of D-lactate production exist: D-lactate can be produced from ketones in cats (and presumably humans) with diabetes and during the metabolism of propylene glycol in patients with an overdose of this hydrocarbon. The clinical aspects of this disease received little attention, so we must still ponder whether the neurologic symptoms seen during exacerbations of D-lactic acidosis are due to the accumulation of D-lactate or perhaps to the coproduction of other noxious organic acids. (Greg Cowell, M.D, Chicago, IL)

  3. ulala

    ulala New Member

    so badly. If I eat sugar I literally pass out into an almost coma type sleep.

    Dietary management of D-lactic acidosis in short bowel syndrome
    Article Abstract:

    Short bowel syndrome can be caused by a congenital disorder or by surgical removal of a section of the intestines. Patients with short bowel syndrome may have difficulty digesting certain carbohydrates. The non-absorbed carbohydrates are fermented by one type of normal intestinal bacteria called lactobacilli, producing D-lactic acid. Since the D-lactic acid cannot be metabolized, it is absorbed by the body to cause severe metabolic acidosis (acidic blood). Administration of antibiotics or oral administration of bacteria flora are two types of treatment. The experience of an nine-year-old girl with D-lactic acidosis who was treated with an altered carbohydrate diet is reported. The patient had previous intestinal resection in which 14 centimeters of her intestines were removed. She was maintained on parenteral nutrition for nine months, and then released with a normal diet and energy supplements. Six months later, after she ingested a large amount of sugar, signs of acidosis developed, such as uncoordinated movements, slurred speech and confusion. Similar episodes of metabolic acidosis occurred every time she ingested large amounts of sugar. The number of episodes were increasing, and growth failure was noted. In an effort to identify which carbohydrates produced acid, two strains lactobacilli isolated from the patient's stool were evaluated. It was discovered that the lactobacilli in the patient's intestines was unable to make D-lactate, essential for the metabolism of D-lactic acid. Therefore, the patient's diet could be altered to eliminate the offending carbohydrates. The altered diet, which included carbohydrates that were mainly in the polymeric form (mono and oligosaccharides), were given through a tube inserted into the nose and feed directly into the stomach. There have been no further acidotic episodes in the 30-month period that followed. The child continues to grow normally. (Consumer Summary produced by Reliance Medical Information, Inc.)

    author: Preece, M.A., Booth, I.W., Mayne, A.J., Handy, D.J., George, R.H.
    Publisher: British Medical Association
    Publication Name: Archives of Disease in Childhood
    Subject: Health
    ISSN: 0003-9888
    Year: 1990

    Case studies, Malabsorption syndromes, Diet therapy, Lactic acidosis
  4. Jayna

    Jayna New Member

    For years, as part of my post-exertional malaise symptoms, I have had stools so acidic they burned passing out (sorrry to be gross). All my dr's looked at me blankly and dismissed this symptom immediately when I brought it up.

    Now I'm going to do some research on what carbs won't trigger this reaction, and see what happens if I avoid any that do.
    [This Message was Edited on 07/02/2009]
  5. ulala

    ulala New Member

    I don't know if you've read any posts by catseye (karen) or MATN. Karen has been os on target in her posts and thinking. She has been posting about juicing and cutting out all carbohydrates, except vegetables. She also said that drinking baking soda was helping her.
    Many people here attacked her about that, but she was right on target. When I google D-lactic acidosis they treat it with antibiotics, and sometimes IV sodium bicarbonate and oral sodium bicarbonate. Also thiamine can be low and supplemenation will help.

    MATN doesn't post here anymore, but she put herself into remission with a very strict organic diet. If you can read her posts they are very informative.